homeonews - Farmacia Natural

Transcripción

HOMEONEWS
Edición N° 6
Setiembre/Octubre de 2006
Director: Farm. Fernando Estevez Castillo
PUBLICACION BIMESTRAL
DISTRIBUCION GRATUITA
PARA PROFESIONALES DE LA SALUD
Homeonews
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Edición N° 6 – Setiembre-Octubre de 2006
Edición n° 6
Setiembre / Octubre de 2006
Registro de la Propiedad Intelectual n°: 505276
Director: Fernando Oscar Estevez Castillo
Propietario: Fernando Oscar Estevez Castillo (C.I.: 10.103.605)
Dirección postal: Pte. Quintana 414 – Lanús Oeste – Pcia de Buenos Aires
(B1824NVJ), Argentina
Tel.: (54-11) 4241-4441
E.Mail: [email protected] ó
[email protected]
Director: Fernando Estevez Castillo
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INDICE
1- Editorial, pág. 4.
2- Fitoterapia:
Estudios de las actividades antiinflamatoria, antibacteriana y antioxidante
de medicamentos fitoterápicos utilizados para el tratamiento de la
hiperplasia prostática benigna y la prostatitis, pág. 5.
3- Alopatía:
Onicocosmecéuticos, pág. 14.
4- Homeopatía:
-Efectos de los medicamentos homeopáticos Eupatorium perfoliatum y
Arsenicum album en la parasitemia de ratones infectados por Plasmodium
berghei, pág. 24.
-La agregación plaquetaria en la hipertensión portal y su modificación por
dosis ultra bajas de aspirina; pág. 25.
5- Nutrición:
El consumo de leche y su relación con el acné en niñas; pág. 34.
6- Notas de interés:
-Jornada Nacional de Medicamentos Fitoterápicos; pág. 47.
- Jornada; ¿Existe el ADHD?: mitos, realidades y alternativas; pág. 48.
7- Novedades:
-Nuevos productos: Biolip®; pág. 53.
-Libros: CHIA, redescubriendo un olvidado alimento de los aztecas; pág.
54.
8- Cursos, Seminarios y Ateneos:
-Seminario de Clínica Médica y Farmacia Homeopática; SAIDAH; pág. 55.
-Ateneos de Homeopatía 2006, Facultad de Medicina, Univ. Maimónides;
pág. 56.
-Curso de alergia y alimentación en el niño; AAMENAT; pág. 57.
9- Formulario de suscripción, pág. 58.
Foto de tapa: Eupatorium perfoliatum L. (Compositae)
Las opiniones vertidas en los artículos firmados son responsabilidad de sus autores.
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EDITORIAL
Estimados colegas del equipo de salud:
Nuevamente nos volvemos a encontrar, luego de unos meses difíciles para mi
familia, ya que fuimos víctimas de la inseguridad que nos toca vivir en estos
tiempos, lo cual lamentablemente y muy a mi pesar, no me permitió desarrollar
en forma completa mi actividad profesional y por ende publicar algunos
números de Homeonews. Pero como dice el refrán, “No hay mal que dure
cien años”, es por eso que siento una inmensa alegría, con la aparición de este
nuevo ejemplar, que muchos de Uds. me estaban reclamando.
En este número podrá encontrar un trabajo de Fitoterapia para el tratamiento
de la hiperplasia prostática benigna y la prostatitis, realizado con Hypoxis
hemerocallidea y Epilobium parviflorum; la descripción de los medicamentos
utilizados para el tratamiento de las patologías y la estética de las uñas
(Onicocosmecéuticos); el estudio de dos medicamentos homeopáticos
(Eupatorium perfoliatum y Arsenicum album) para su aplicación en la
malaria: un trabajo muy interesante con la aspirina en dosis ultra bajas,
modificando la agregación plaquetaria en la hipertensión portal. En el
capítulo NOTAS DE INTERES, las repercusiones de la Jornada Nacional de
Medicamentos Fitoterápicos y los resúmenes de la actividad realizada en
el Auditorio de Lab. Madaus, cuyo título fue: ¿Existe el ADHD?: mitos,
realidades y alternativas, organizada por el Centro de Neurología Integral
de Bs. As., la Asociación Argentina de Fitomedicina, SAIDAH y
Farmacia+Natural. Con respecto a NOVEDADES, OMS presentó BIOLIP®,
una emulsión con poderosa acción lipolítica remodelante, eficaz en la reducción
del contorno corporal y en el tratamiento de nódulos adiposos, y Editorial Del
Nuevo Extremo publicó el libro: CHIA, redescubriendo un olvidado
alimento de los aztecas. En el capítulo CURSOS, SEMINARIOS Y
ATENEOS, se destacan el Seminario de Clínica Médica y Farmacia
Homeopática organizado por SAIDAH (Sociedad Argentina de
Investigación, Docencia y Asistencia Homeopática), los últimos Ateneos
del corriente año del Departamento de Homeopatía de la Facultad de
Medicina de la Universidad Maimónides y el Curso de Alergia y
Alimentación en el niño, de la Asociación Argentina de Médicos
Naturistas.
Me despido hasta el próximo número, esperando que puedan disfrutar, tanto
como yo, de toda la información publicada en Homeonews.
Farm. Fernando Estévez Castillo
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FITOTERAPIA
ESTUDIOS DE LAS ACTIVIDADES ANTIINFLAMATORIA,
ANTIBACTERIANA Y ANTIOXIDANTE DE MEDICAMENTOS
FITOTERAPICOS UTILIZADOS PARA EL TRATAMIENTO DE LA
HIPERPLASIA PROSTATICA BENIGNA Y LA PROSTATITIS
V. Steenkampa, M.C. Gouwsa, M. Gulumianb, c, E.E. Elgorashid and J. van
Stadend,
a
Department of Urology, Faculty of Health Sciences, University of Pretoria, P.O.
Box 667, Pretoria 0001, South Africa.
b
National Institute for Occupational Health, P.O. Box 4788, Johannesburg,
South Africa.
c
Haematology and Molecular Medicine Department, University of the
Witwatersrand, Parktown, South Africa.
d
Research Centre for Plant Growth and Development, School of Biological and
Conservation Sciences, University of KwaZulu-Natal Pietermaritzburg, Private
Bag X01, Scottsville 3209, South Africa.
[Journal of Ethnopharmacology, Vol 103, No 1, 2006: pp. 71-75]
RESUMEN
Se investigaron los extractos acuosos y etanólicos de cinco plantas medicinales
que aparecen en la literatura médica para el tratamiento tradicional de la
hiperplasia prostática benigna y/o prostatitis, por sus efectos sobre la actividad
secuestrante de hidroxilos, la actividad antibacteriana y la inhibición de la
ciclooxigenasa-1 y –2 (COX-1 and COX-2) en la biosíntesis de las
prostaglandinas. Ambos extractos (acuoso y etanólicos) de Hypoxis
hemerocallidea y Epilobium parviflorum inhibieron el crecimiento de Escherichia
coli. Los 10 extractos secuestraron los radicales hidroxilos pero con diferentes
potencias (32–93%). Los extractos etanólicos fueron los más activos en inhibir
la COX-1 en la biosíntesis de las prostaglandinas. El extracto etanólico de
Epilobium parviflorum mostró efectos inhibitorios sobre la COX-1 y -2 en la
biosíntesis de prostaglandinas, inhibió el crecimiento de Escherichia coli y
ejerció actividad antioxidante. Aunque estos resultados respaldan el uso
tradicional del Epilobium parviflorum para el tratamiento de la prostatitis y la
hipertrofia prostática benigna, se necesitan más investigaciones para esta
planta tan promisoria.
Palabras clave:
Antiinflamatorio, antibacteriano, antioxidante, hiperplasia
prostática benigna, medicamentos fitoterápicos, prostatitis.
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ARTICULO ORIGINAL
1. Introduction
Prostatitis, a general term for inflammation of the prostate, and benign prostatic
hyperplasia (BPH), enlargement of the prostate due to non-cancerous growth
within the gland, are common disorders of the prostate. Prostatitis can appear in
at least three forms: acute bacterial prostatitis, chronic bacterial prostatitis and
chronic non-bacterial prostatitis. Chronic non-bacterial prostatitis is the most
common form of prostatitis and is usually caused by infectious agents such as
fungi, mycoplasmas or viruses (Tanner et al., 1999). Acute bacterial prostatitis
occurs from a urinary tract infection, usually caused by Escherichia coli (E. coli),
which has spread to the prostate, whereas chronic bacterial prostatitis is usually
the result of partial blockage of the male urinary tract, as occurs with BPH,
promoting the harbouring of bacteria.
BPH is a condition that affects the majority of men over the age of 50 (Boyle
and Napalkov, 1996). This disorder has two phases, one that involves no
clinical signs and the other that manifests as disorders of urination resulting
from urinary tract obstruction by an enlarged prostate (Isaacs, 1994). A
hormone-induced chronic inflammation that results from the infiltration of
inflammatory cells and their signalling molecules such as prostaglandins,
leukotrienes and growth factors into the prostate is frequently associated with
BPH (Theyer et al., 1992). The risk of mortality and long-term morbidity,
associated with surgical procedures for symptomatic BPH has prompted
research into alternative medical therapies (Chapple, 1998).
Crude extracts of five herbal remedies reported in the literature for traditional
treatment of BPH and/or prostatitis were selected for investigation. These
included (i) Agathosma betulina (Berg.) Pillans. (Rutaceae) leaf preparations
which have a long history of use in traditional herbal medicine as a urinary tract
disinfectant and diuretic and are used to treat prostatitis (Watt and BreyerBrandwijk, 1962); (ii) corms of Hypoxis hemerocallidea Fisch. & C.A. Mey.
(Hypoxidaceae), used to treat bladder disorders including BPH and urinary
infections (Van Wyk et al., 1997) as well as rheumatoid arthritis, immune
system disorders and tuberculosis (Watt and Breyer-Brandwijk, 1962); (iii)
Pygeum africanum Hook. f. (Rosaceae) bark; (iv) Serenoa serrulata Hook. f.
(Arecaceae) berries and (v) Epilobium parviflorum L. (Onagraceae) leaves. The
last three plants are used in the treatment of both BPH and prostatitis (Treben,
1984 and Dvorkin and Song, 2002). All these remedies are traditionally
prepared as infusions (1–2 g in a cup of water), taken orally three to four times
daily.
In this study, the hydroxyl scavenging activity of the herbal remedies were
studied because free radicals and oxidative stress are known to be associated
with inflammation (Winrow et al., 1993). Moreover, hydroxyl radical scavengers
have been reported to suppress upregulation of cyclooxygenase (COX) and
subsequently reduce inflammation (Feng et al., 1995 and Kumagai et al., 2000).
Over-expression of COX-2 and a decrease in prostaglandin E-1 synthesis takes
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place in patients with BPH and prostatitis (Jang and Schaeffer, 2003 and Wang
et al., 2004). Therefore, the effect of plant extracts on COX-1 and -2 catalysed
prostaglandin biosynthesis was evaluated.
Antibacterial activity was determined against the Gram-negative bacteria,
Escherichia coli, which is in accordance with its function as a human pathogen
in cases of BPH and prostatitis.
2. Materials and methods
2.1. Plant material
Plant material of exotic species (Serenoa serrulata and Epilobium parviflorum)
was purchased from health stores while indigenous species were obtained
from, identity confirmed and voucher specimens lodged with, the South African
National Biodiversity Institute, Tshwane.
2.2. Preparation of extracts
Dried plant material (1 g; refer to plant part used in the introduction) was
suspended in 10 ml deionised water and brewed as a tea by boiling for 15 min.
Extracts were allowed to cool, centrifuged and the supernatants passed through
0.45 µm and 0.22 µm filters (Millipore, Bedford, MA), consecutively.
Alternatively, 1 g dried plant material was extracted with 10 ml ethanol at room
temperature for 24 h, after which the extracts were filtered. For the antibacterial
assay the ethanol extracts were dried and re-suspended in distilled water. The
extracts were diluted to a concentration of 2 mg/ml and thereafter serially
diluted (test range 1 mg/ml to 7.8 µg/ml). To determine hydroxyl scavenging
activity, the concentration of the extracts in the reaction mixture was 4 mg/ml.
For the COX assays, 1 g of dried plant material was extracted with 10 ml water
or ethanol in an ultrasound bath for 30 min after which extracts were filtered and
evaporated to dryness. The residues were then re-suspended in water or
ethanol to a final concentration of 250 µg/ml.
2.3. Antibacterial activity
Antibacterial activity was assessed using the micro-well dilution method as
described by Eloff (1998). Escherichia coli (ATCC 25922) was cultured and
maintained on bloodplates. An inoculum of the microorganism was prepared
from 24 h Mueller-Hinton broth (Mast Diagnostics, Merseyside, UK) cultures
and suspensions were adjusted to a 0.4 reading using a colorimeter
(Sherwood). The 96-well round-bottomed sterile plates were prepared by
dispensing 180 µl of the inoculated broth into each well. A 20 µl aliquot of the
plant extract was added. Dilutions of ciprofloxacin served as positive control
while broth without plant extract was used as a negative control. Plates were
covered and incubated for 24 h at 37 °C. Bacterial growth was determined by
visual scoring (0–3) after colour reaction with 50 µl of ρ-iodonitrotetrazolium
violet (0.2 mg/ml; Sigma Chemical Company, St. Louis, MO). Visual scoring of
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the colour intensity was carried out relative to the positive and negative controls.
Tests were carried out in triplicate and each experiment was repeated four
times.
2.4. Anti-inflammatory activity
Anti-inflammatory activity was determined using the COX-1 and COX-2 assays
as described by Jäger et al. (1996) and Zschocke and van Staden (2000),
respectively. Indomethacin a known COX-1 and -2 inhibitor was included as
control (Noreen et al., 1998). Concentrations of 7.14 µg/ml (20 µM) and
71.4 µg/ml (200 µM) of indomethacin were used in the COX-1 and -2 assays,
respectively. The results given are the mean ± S.E.M. of two experiments
carried out in duplicate (% inhibition).
2.5. Electron spin resonance (ESR) spectrometry
ESR measurements were carried out on a Bruker EMX, fitted with an AquaX
cell. The settings were as follows: 25 mW, scan time 40 s, scan width 10
Gauss. The ESR software was the Bruker WinAacquisition (version 3.04) with
integrated auto-sampler controlling software. Data analysis and construction of
graphs were carried out using Statistica (version 5.0). The HO radical was
generated by a Fenton-type reaction and was measured by the spin trapping
method of Janzen et al. (1992) using α-phenyl-N-tert-butylnitrone (PBN; Council
for Scientific and Industrial Research, Modderfontein, South Africa). The
scavenging activity was determined as the percent inhibition of the peak
intensity of the control. Vitamin C (20, 40, 80, 160 mg/l) was included as
positive control for the water extracts. The results are the mean ± S.E.M. of four
experiments carried out in triplicate. Glassware was washed in 30% nitric acid
to eliminate background production of HO .
3. Results and discussion
Escherichia coli growth was inhibited by both the water and ethanol extracts of
Hypoxis hemerocallidea and Epilobium parviflorum (Table 1) but the extracts
were less potent than the control compound, ciprofloxacin. When prepared as a
tea approximately 37 mg/ml of Hypoxis hemerocallidea and 24 mg/ml of
Epilobium parviflorum is consumed three times a day. We extrapolate that
should the extract be totally absorbed, the serum concentration of Hypoxis
hemerocallidea and Epilobium parviflorum will be 18.5 µg/ml and 12 µg/ml,
respectively. Since total inhibition of bacterial growth was found at
concentrations of 62.5 µg/ml and 1000 µg/ml for Hypoxis hemerocallidea and
Epilobium parviflorum aqueous extracts, respectively, these concentrations are
not physiologically relevant. Concerning the antibacterial activities of the crude
extract of Serenoa serrulata (Didry and Pinkas, 1982) and Agathosma betulina
(Lis-Balchin et al., 2001), our findings support earlier studies that these extracts
do not affect the growth of Escherichia coli.
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Table 1.
Antibacterial activity of the medicinal plants studied
Plant/Standard
Extract
Concentration (µg/ml) of extracts
inhibiting 100% of Escherichia coli
growth
Agathosma betulina (Berg.) Pillans.
Ethanol
>1000
Water
>1000
Ethanol
62.5
Water
62.5
Ethanol
>1000
Water
>1000
Ethanol
>1000
Water
>1000
Ethanol
125
Water
1000
Hypoxis hemerocallidea Fisch. & C.A. Mey.
Pygeum africanum Hook. f.
Serenoa serrulata Hook. f.
Epilobium parviflorum L.
Ciprofloxacin
0.1
The effects on COX-1 and COX-2 enzymatic activity show that in general the
ethanolic extracts exhibited higher inhibitory effects than the aqueous extracts
(Fig. 1). All five ethanolic extracts inhibited COX-1 catalysed prostaglandin
biosynthesis in a range between 88% and 98%. The inhibition of the COX-1
enzymatic activity by the ethanolic extracts of Hypoxis hemerocallidea is in
consistence with previous findings by Jäger et al. (1996). Hypoxis
hemerocallidea, Pygeum africanum and Epilobium parviflorum aqueous extracts
inhibited COX-1 catalysed prostaglandin biosynthesis in the range of 23–72%.
Of the ten extracts evaluated for COX-2 inhibitory effect, the ethanolic extracts
of Agathosma betulina and Epilobium parviflorum as well as the aqueous
extracts of Hypoxis hemerocallidea, Pygeum africanum, Serenoa serrulata and
Epilobium parviflorum, showed an inhibitory effect. Of these, the ethanolic
extract of Epilobium parviflorum was the most potent, inhibiting COX-2
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catalysed prostaglandin biosynthesis with 59%, whereas the ethanolic extract of
Agathosma betulina showed an inhibitory effect of 25%. Contrary to our results,
Hiermann et al. (1986) reported that the aqueous extract of Epilobium
parviflorum was inactive in the carrageenin-induced rat paw oedema model.
Ojewole (2002) found both the aqueous and methanolic extracts of Hypoxis
hemerocallidea to have an anti-inflammatory effect when using the albumininduced rat paw oedema model and similar to our finding using ethanol, that the
methanolic extract produced a greater anti-inflammatory effect than the
aqueous extract.
Fig. 1. Inhibition of COX-1 (■) and COX-2 ( ) catalysed prostaglandin biosynthesis by (A)
ethanol and (B) water extracts (250 µg/ml) of the remedies. A: Agathosma betulina; B: Hypoxis
hemerocallidea; C: Pygeum africanum; D: Serenoa serrulata; E: Epilobium parviflorum.
The HO radical scavenging ability is widely used as a criterion for the
antioxidant properties of plant materials. The percent reduction of the HO
radical due to the scavenging ability of water and ethanol extracts of the plants
is shown in Fig. 2. The water and ethanol extracts (4 mg/ml) of the majority of
herbal remedies showed scavenging activity above 80%, with the exception of
the water and ethanol extract of Serenoa serrulata and the ethanol extract of
Pygeum africanum. The control, vitamin C, showed scavenging activity of 76%
and 96% at concentrations of 80 mg/l and 160 mg/l, respectively. With the
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exception of the report on the interaction of rooperol (isolated from Hypoxis
hemerocallidea) with oxidative systems in human blood (Van der Merwe et al.,
1993), no literature on the antioxidant activities of the other remedies
investigated could be obtained.
Fig. 2. Percent reduction of the HO radical due to the scavenging ability of ethanol (■) and
water ( ) extracts of the remedies. A: Agathosma betulina; B: Hypoxis hemerocallidea; C:
Pygeum africanum; D: Serenoa serrulata; E: Epilobium parviflorum.
Many compounds found in plants are known to possess antimicrobial,
antioxidant and/or anti-inflammatory activity (Sohn et al., 2004). Epilobium
parviflorum has been reported to have a high antioxidant capacity, which is
attributed to the high concentration of flavonoids (Arredondo et al., 2004).
However, the macrocyclic tannin, oenothein B, isolated from the aqueous
extract has been identified as the compound responsible for the activity of the
extract in the treatment of prostate disorders (Lesuisse et al., 1996). It is evident
that any compound or a number of compounds could exert the observed
effects, and furthermore, it is possible that different compounds could be
responsible for the various activities observed.
This is the first report on the antibacterial activity of the crude extracts of
Epilobium parviflorum and Hypoxis hemerocallidea against Escherichia coli as
well as the first to determine anti-inflammatory activity by means of inhibition of
COX-2 catalysed prostaglandin biosynthesis. The ethanolic extract of Epilobium
parviflorum showed inhibitory effects on both the COX-1 and -2 catalysed
prostaglandin biosynthesis and exerted antioxidant activity, both which could
lead to suppression of the upregulation of cyclooxygenase and subsequently
reduce inflammation. Since both extracts of Epilobium parviflorum inhibited
growth of Escherichia coli these could be used in the treatment of patients with
acute bacterial prostatitis where Escherichia coli infection has spread to the
prostate. Although these results support the traditional use of Epilobium
parviflorum for treatment of prostatitis and BPH, further investigation is required,
for this promising plant.
Acknowledgement
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The National Research Foundation, Pretoria is thanked for financial support.
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ALOPATIA
ONICOCOSMECEUTICOS
Eckart Haneke1,2
1
Dermatology Practice, Freiburg, Germany.
Department of Dermatology, Medical Centre, St Radboud University,
Nijmegen, the Netherlands.
2
[Journal of Cosmetic Dermatology 5 (1) 2006, pp 95:100]
RESUMEN
La uña es el apéndice de la piel más grande. Además de su importancia
fisiológica y de sus funciones sensitivas, tiene una gran importancia estética.
Las quejas de uñas quebradizas o débiles son frecuentes, particularmente en
las mujeres. Existen a la venta innumerables preparaciones que se
promocionan para mejorar la calidad de las uñas, sin embargo, la mayoría no
alcanza el efecto benéfico deseado. La cirugía no puede mejorar la calidad de
las uñas, pero sí las anormalidades de forma y tamaño.
ARTICULO ORIGINAL
Introduction
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Beautiful nails have been the privilege of rich and noble people for more than
3000 years. Already in ancient China, long nails had been worn by the high
class. Nowadays, beautiful nails are affordable for almost everybody and in the
United States alone, nail care products were sold for $6.7 billion in 2002. Nail
care clinics and salons are opened everywhere with professional manicurists
who have their own schools and training centers. Many preparations are sold to
enhance nail quality and beauty; however, in reality, there are not many
possibilities to improve the appearance of the nails and it is often difficult to
distinguish facts from fictions.
The nail organ comprises the:
• nail plate;
• matrix and nail bed and;
• nail walls,
and forms a functional unit together with the
• digital pulp;
• distal interphalangeal joint;
•tendons and ligaments;
•innervation and blood supply.
This functional unit both acts as a mechanical tool, as a protective organ, as
well as an extremely important sensory organ. The nail plate protects the tip of
the digit against trauma, provides defense, and allows scratching, improves
dexterity, and enhances fine touch.
Nail growth is controlled by a variety of cell–cell, cell–matrix, and cell–tissue
interactions as well as signaling factors, many of which are not yet clearly
defined. It also depends on age, blood supply, intensity of mobilization,
dominance of the respective hand, a variety of diseases and drugs, as well as
hereditary factors, temperature, altitude, etc.
Nail beauty is defined by its:
•shape;
•size;
•shine;
•surface smoothness;
•consistency;
•periungual tissue and;
•integrity of the entire fingertip.
The fingernails are longer than wide, whereas most toenails are wider than
long.
The ideal fingernail appears as an oval-shaped, longer than wide, longitudinally
slightly curved, transversally more curved keratin plate. These ideal proportions
are no longer met if the nail is too wide, too narrow, overcurved, flat, or hollow.
The lunula is visible as a whitish fusiform structure right in front of the free
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margin of the proximal nail fold. In the nonmanicured finger, the lunula is very
narrow and often not visible in the ring and little fingers as well as in the lesser
toes. The nail plate surface is even without ridges and furrows; however,
longitudinal depressions and ridges, often with pearl-like nodes in longitudinal
arrangement, appear with age and have to be considered normal above
40 years. The size of the nail plate depends on that of the finger. The thumbnail
is almost as wide as it is long, but the other fingernails are clearly longer than
wide. Excessively large nails point at an abnormality of the underlying bony
phalanx, but often nails only appear larger than normal because of overzealous
manicure. Shortening of the distal phalanx leads to acquired brachyonychia, a
relatively common feature of chronic hemodialysis, which may cause secondary
hyperparathyroidism with resorption of the bony tip. The length of the free nail
margin depends on personal preferences, but is limited by anatomical factors.
Very long nails require artificial nails. Frankly, malformed nails are seen in a
number of inborn syndromes or as a sequel of trauma, infection, or tumor
formation.
None of these abnormalities can be improved by drugs or food additives,
although buffing and polishing can alleviate the ridged surface of the nails in
aged persons.
The nail is a shiny, transparent, even plate. With age, longitudinal ridges and
furrows appear in virtually every person, but transverse lines and ridges are the
result of a pathological process either in the matrix or the overlying proximal nail
fold. Pits with regular size in the nail surface are the most common sign of nail
psoriasis and are visible as small depressions. Pits in alopecia areata are
usually smaller; those in nail eczema are irregular in size. They may cause a
sandpaper appearance and loss of transparency. Even though the nail has
melanocytes, they remain inactive in fair-skinned persons. Thus the nail is
usually not pigmented in Caucasians. However, melanin production may be
stimulated by ultraviolet radiation (photochemotherapy), cytotoxic drugs,
malnutrition, or adrenal insufficiency. Brown to black, streaky nail pigmentation
in a fair complexioned Caucasian over 30 years should raise suspicion of
ungual melanoma.
Certain surface alterations can be camouflaged with nail varnish.
Healthy periungual tissues are a prerequisite for an esthetic nail. They include
the two lateral and the proximal nail fold with the cuticle. Chronic picking and
manipulation at the nail folds, often precipitated by hang nails but later
exacerbating them, cause thickening of the nail folds and interfere with the
integrity of the skin increasing the risk of periungual infections. The cuticle is of
utmost importance. It seals the space under the proximal nail fold, the so-called
nail pocket, and protects the nail matrix from penetration of foreign bodies and
pathogens. In order to make the lunula visible, many persons remove the cuticle
either with chemical cuticle removers or sharp instruments. These procedures
also loosen the tight connection between the underside of the proximal nail fold
and the underlying young nail plate allowing penetration of foreign materials,
allergens, bacteria, and fungi under the nail fold. Chronic paronychia with
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transverse ridging may develop; grayish or green nail discoloration hints at
infection with Proteus, Klebsiella spp., or Pseudomonas aeruginosa. Repeated
subacute flare-ups are characteristic for chronic Candida paronychia, which
may also be secondary to allergic contact dermatitis as a result of food
ingredients.
The sequelae of overzealous manicure should be prevented by thorough patient
education. Paronychia requires medical treatment in addition.
The nail plate is a cellularly derived, plate-like structure composed of keratin
fibers that are embedded in a sulfur-rich material. The nail substance is formed
by the nail matrix. The nail bed adds only a small amount of subungual keratin,
which is biochemically different from matrix-derived nail plate keratin. It allows
the plate to slide over it and is also responsible for the extremely firm
attachment of the nail plate to the nail bed. The nail shows continuous growth
over a lifetime with no cyclical growth except for slight perennial and circadian
rhythms. A hormonal regulation is not known. The growth rate depends on the
digit's length, activity, blood supply, temperature, etc., but apparently not on
food intake. Fingernails grow about three times faster than toenails; the middle
finger of the dominant hand of a young person grows about 0.1 mm per day,
which means that it takes approximately 1 month for 3 mm of a new nail. Any
effect of a drug or onychocosmeceutical will need several months to be visible
or perceptible and a drug that is perceived as one that cured brittle or fragile
nails within a few weeks may be a phantastic psychopharmacon but certainly
was not the reason for the "better nail." The consistency of the nail is genetically
determined, but can be modified by external influences. The normal nail is an
elastic plate with considerable physical strength. It is highly resistant to most
chemicals. The nail may be hard and brittle, or soft and fragile, show
onychorrhexis or onychoschizia.
Systemically administered substances to enhance nail growth and quality take
several months to become visible.
Finally, the shape of the entire tip of the digit is important for an esthetic look. It
may be too short, too wide, or even too long. Alterations of the terminal
interphalangeal joint often directly modify the corresponding nail, as is
commonly seen in degenerative osteoarthritis with Herbenden's nodes resulting
in overcurvature of the fingernails.
This brief introduction explains why so many claims about "nail drugs" have to
be taken with care or obviously cannot be true.
Onychocosmeceuticals
There are many preparations in the market made up of a variety of vitamins,
sulfur-containing amino acids or proteins, hormones, calcium, iron, zinc,
selenium, and other "essential" elements and minerals, medicinal yeast,
crushed egg shells, and even organic food. Their effect appears to be mainly
psychological as some patients report miraculous improvement within a few
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days or weeks, whereas most others do not see any effect. Even though some
overt deficiency states may cause brittle, fragile, or soft nails, this by no means
proves that the uncritical supplementation of these substances might improve
the nails of an otherwise healthy person.
Biotin
Biotin, also known as vitamin H, is often called the hair and nail vitamin. It is
part of many enzymes that play an important role in carboxylation processes.
Thus, it is important for gluconeogenesis, lipogenesis, propionate and leucin
metabolism. It stimulates epidermal differentiation and increases the amount of
those cytokeratins synthesized during terminal differentiation. Finally, it plays a
role in the metabolism of sulfur-containing amino acids of the matrix. Marked
biotin deficiency is associated with poor nail quality. It was shown to improve
the quality of hooves in horses and some studies in men reported a positive
effect in brittle nails.1 3 Biotin was also said to increase the nail growth rate.4
However, biotin is a substance synthesized to a great extent by intestinal
bacteria, and the true need of biotin intake per day is not known. Further, it is
even not clear whether the effect is the result of "vitamin doses" or
pharmacologic dosing exceeding the normal need several fold. Therapeutic
dosages are 2.5–10 mg daily. However, our own experience was rather
disappointing.
There may be a role for biotin in the treatment of brittle nails although the exact
dose needed is not yet exactly known.
Vitamin A
Hypovitaminosis A is associated with phrynoderma, lusterless hair, and night
blindness. Severe vitamin A deficiency was associated with egg shell nails.5
However, vitamin A overdoses have a considerable onychodestructive effect
comparable to that of synthetic retinoids.6 8 Patients who received mega doses
of vitamin A for cancer therapy developed desquamative erythroderma with hair
loss and severe nail destruction. Thus, preparations for nail improvement
should not contain high vitamin A doses.
Pyridoxine and ascorbic acid
A combination of evening primrose oil (two capsules three times daily),
pyridoxine 25–30 mg and vitamin C 2–3 g daily was recommended for brittle
nails.9 There is a lack of scientific evidence for either of these vitamins on nail
quality.
Thiamine
A preparation containing thiamine mononitrate 60 mg, calcium D-pantothenate
60 mg, medicinal yeast 100 mg, L-cystine 20 mg, keratin 20 mg, and p-amino
benzoic acid 20 mg is marketed under the name of Pantovigar® (Georg Simons
Ltd, Frankfurt). It is claimed to improve hair growth and nail quality.10,11 None of
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the substances, even not cystine and keratin, have a proven beneficial effect on
nail growth or quality.
Vitamin E
Vitamin E is widely used as an antioxidant. It has been given in the yellow nail
syndrome with some success provided the dose was high enough, usually
between 600 and 1200 EU daily, and it was given for many months.12 15 It was
also successfully used as a topical preparation dissolved in dimethyl sulfoxide.16
No beneficial effect on normal or brittle nails is documented in the scientific
literature.
Sulfur-containing amino acids and proteins
Because hair and nails are sulfur-rich structures, the addition of amino acids,
sulfur-rich proteins, and gelatin have been claimed to improve nail growth and
quality.4 However, the biochemical composition of the nail is genetically
regulated and widely independent from nutritional factors; this is clearly
evidenced by the fact that the quality of hair and nails is usually excellent even
in the poor people of developing countries, except for kwashiorkor and other
serious diseases. Although sulfur itself does not improve nail growth it was
found that cystine may have a positive effect on the growth of hyponychium
cells.17 Cystine was also claimed to be incorporated into growing hair and
nails.18 However, this has never been confirmed in humans.
Also, other proteins did not prove to enhance the cosmesis or quality of the
nails. Particularly, gelatin is not able to influence the nail positively. It is a
hydrocolloid formed from the degradation of collagenous tissues such as
tendons, bone, and skin. It contains 84–86% of protein and 2–4% of mineral
salts. It is rich in glycine (24%), proline (14%) and hydroxyproline (10%), but
poor in essential and particularly in sulfur-containing amino acids: cystine <
0.1%, methionine < 1%. A pharmacodynamic effect of those collagen amino
acids on the nail is not proven. Neither are hormones able to improve the
consistency of a nail.
Calcium
Calcium is apparently not responsible for nail hardness as the nail is relatively
poor in calcium.19 However, a study of daily calcium 1.0 g vs. evening primrose
oil 4.0 g, calcium 1.0 g and 440 mg marine fish oil (Efacal) over 1 year improved
the nail quality in both pre- and postmenopausal women.20
Iron
The amount of iron found in the nail reflects the iron content of the person.21 It
has long been observed that iron deficiency causes brittle nails, longitudinal
ridges, and koilonychias.22 Iron supplementation over a long time was found to
improve brittle nails even without an obvious iron deficiency.
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Zinc
Zinc deficiency is known to cause soft, fragile nails, longitudinal ridging,
striations, and gray discoloration in addition to periungual blistering and chronic
paronychias. Acute-onset zinc deficiency as observed in acquired zinc
deficiency syndromes also causes transverse leukonychia and/or Reil–Beau
lines.23,24 Prolonged treatment with zinc was said to improve brittle nails even
without a demonstrable zinc deficiency.
Selenium
Selenium is critical for the activity of glutathione peroxidase protecting DNA
against oxidation. Nail selenium levels reflect total body levels.25 Selenium
supplementation strengthened the nail in selenium deficiency.26 Selenium
intoxication caused transverse lines, nail loss, swelling of the fingertip, and
purulent discharge.27
Other essential or trace elements have not been proven to play an important
role in nail growth or quality.
Fluorides
Although fluorides are essential for enamel hardness of the teeth, nothing is
known about their effect on soft or brittle nails. The state of fluoridation did not
have an effect on thumb nail growth rate.28 Both alimentary and exogenous
fluorides can be measured in the nails, which reflect the exposure to fluorides.
Silica
Nails contain up to 16 mg silicium dioxide per 100 g (0.016%). It was claimed
that SiO2 would favor the cross-linking of keratins, thus lending firmness and
resistance to the nails. Although the compound is necessary for protein
synthesis in certain algae, nothing is known about human nails.
Silicilic acid, an instable compound with rapid polymerization to large silicates
was found to improve brittle nails29 and to clear psoriatic onychopathy in 5 of 10
evaluable patients.30
Rhodanides
A preparation containing rhodanides is marketed to improve hair loss and nail
quality. Nothing is known about its presumed mechanism of action, and the
"information" accompanying the product (Activogland, Strathmann Co.,
Germany) is extremely vague.
Nutrition
Overt malnutrition has a negative effect on nail growth. In severe cases in darkskinned people, multiple longitudinal pigmented bands may occur.31 Cachexia
and bulimia cause soft and brittle, often fissured nails,32 34 whereas severe nail
dystrophy is observed in kwashiorkor. These changes are all resulting from
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generalized protein deficiency and there is no relation between nail consistency
changes in normal-eating people and their food quality. In particular, so-called
organic or biologic food has no influence on the genetically determined nail
consistency.
Nail care oils
There are a lot of so-called nail oils containing jojoba oil, bisabolol, panthenol,
vitamins, and amino acids. They are claimed to penetrate the nail plate;
however, it is not clear what vitamins are to do in the nail. Some oils may help
to hold humidity. In general, oils as well as creams and ointments make the nail
more elastic and thus prevent nail splitting.
Cosmetically embarrassing nail disorders
A great variety of diseases affecting the nail can be treated pharmacologically.
The long-term cure rate in onychomycosis is between 40% and 60% and
combination therapy with an effective systemic antifungal (fluconazole,
itraconazole, terbinafine) plus a transungual antifungal delivery system
(amorolfine, ciclopirox nail lacquer) may decrease the failure rate by about onehalf.
Psoriatic nails respond to systemic antipsoriatic treatment and to a lesser
degree also to topical treatment and intralesional injections of corticosteroid
crystal suspension. Psoriatic pitting may be camouflaged with cosmetic nail
varnish or sculptured nails.
Chronic paronychia is treated according to its causes; either with antibacterial or
antifungal topical and systemic drugs or potent corticosteroids if an immediatetype contact dermatitis commonly resulting from food allergy, is the cause.
Eczema nails require identification of their cause and an etiological treatment.
Nail-specific conditions such as brittle or soft nails have been mentioned
previously. There are a number of cosmetic procedures that can harden a soft
nail. Painting with formaldehyde-containing or 5% aluminium chloride-containing
solutions make the nails less flexible, but also more prone to breaking upon
mechanical stress.
Conclusion
Certain cosmetic nail alterations are amenable to treatment. Considering the
genetically determined biochemical structure of the nail, a careful selection of
conditions to be treated may avoid unsuccessful treatments.
References
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1 Colombo VE, Gerber F, Bronhofer M et al. Treatment of brittle fingernails and
onychoschizia with biotin: scanning electron microscopy. J Am Acad Dermatol
1990; 23: 1127–32.
2 Floersheim GL. Behandlung brüchiger Fingernägel mit Biotin. Z Hautkr 1991;
64: 31–48.
3 Gehring W. The influence of biotin on nails of reduced quality. Akt Dermatol
1996; 22: 20–4.
4 Runne U, Orfanos CE. The human nail. Curr Probl Dermatol 1981; 9: 102–49.
5 Bereston ES. Diseases of the nails. Clin Med 1950: 238–40.
6 Positano RG, DeLauro TM, Berkowitz BJ. Nail changes secondary to
environmental influences. Clin Pod Med Surg 1989; 6: 417–29.
7 Baran R. Etretinate and the nails (study of 130 patients): possible
mechanisms of some side-effects. Clin Exp Dermatol 1986; 11: 148–52.
8 Baran R. Retinoids and the nails. J Dermatol Treat 1990; 1: 151–4.
9 Campbell AJ, McEwan GC. Treatment of brittle nails and dry eyes. Br J
Dermatol 1981; 105: 113.
10 Budde J, Tronnier H, Rahlfs VW, Frei-Kleiner S. Systemische Therapie von
diffusem Effluvium und Haarstrukturschäden. Hautarzt 1993; 44: 380–4.
11 Petri H, Pierchalla P, Tronnier H. Die Wirksamkeit einer medikamentösen
Therapie bei Haarstrukturschäden und diffusen Effluvien – vergleichende
Doppelblindstudie. Schweiz Rundschau Med (PRAXIS) 1990; 79: 1457–62.
12 Ayres S, Mihan R. Yellow nail syndrome. Response to vitamin E. Arch
Dermatol 1973; 108: 267–8.
13 Norton L. Further observations on the yellow nail syndrome with therapeutic
effects of oral alpha-tocopherol. Cutis 1985; 6: 457–62.
14 Rommel A, Havet M, Ball M et al. Syndrome des ongles jaunes: réponse à la
vitamine E. Ann Dermatol Vénéréol 1985; 12: 625–7.
15 Tosti A, Guidetti MS, Lorenzi S et al. La sindrome delle unghie gialli.
Esperienza di nove casi. G It Dermatol Venereol 1997; 132: 255–8.
16 Williams BC, Buffham R, du Vivier A. Successful use of topical vitamin E
solution in the treatment of nail changes in yellow nail syndrome. Arch Dermatol
1991; 127: 1023–8.
17 Schmiegelow PG, Berndt G, Lindner J, Puschmann M. Quantitative
autoradiographische Untersuchungen an Haaren, Haut und Nägeln mit den
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Vorläufern 36S-Cystin bzw. 35S-Methionin und 3H-Thymidin im Tierexperiment.
Therapiewoche 1981; 31: 8453–60.
18 Monganti P, Bruno C, Coleli G. Gelatin-cystine, keratogenesis and structure
of the hair. Boll Soc Ital Biol Sper 1983; 59: 20–5.
19 Forslind B. Biophysical studies of the normal nail. Acta Dermato-Venereol
1970; 50: 161–8.
20 Bassey EJ, Littlewood JJ, Rothwell MC, Pye DW. Lack of effect of
supplementation with essential fatty acids on bone mineral density in healthy
pre- and postmenopausal women: two randomized controlled trials of efacal v.
calcium alone. Br J Nutr 2000; 83: 629–35.
21 Sobolewski S, Lawrence ACK, Bagshaw I. Human nails and body iron. J Clin
Pathol 1978; 31: 1068–72.
22 Djaldetti M, Fishman P, Hart J. The iron content of fingernails in iron deficient
patients. Clin Sci 1987; 72: 669–72.
23 Weismann K. Lines of Beau: possible markers of zinc deficiency. Acta
Dermato-Venereol 1977; 57: 88–90.
24 Nürnberger F. Zinkmangel bei künstlicher Ernährung. Z Hautkr 1987; 62
(Suppl. 1): 104–10.
25 Behne D, Gessner H, Kyriakopoulos A. Information on the selenium status of
several body compartments of rats from the selenium concentrations in blood
fractions, hair and nails. J Trace Element Med Biol 1996; 10: 174–9.
26 Vinton NE, Dahlstrom KA, Strobel CT et al. Macrocytosis and
pseudoalbinism: manifestations of selenium deficiency. J Ped 1987; 111: 711–
7.
27 Jenssen R, Closson W. Selenium intoxication. J Am Med Assoc 1984; 251:
1938.
28 McDonnell ST, O'Mullane D, Cronin M, MacCormac C, Kirk J. Relevant
factors when considering fingernail clippings as a fluoride biomarker.
Community Dent Health 2004; 21: 19–24.
29 Lassus A. Colloidal silicic acid for the treatment of psoriatic skin lesions,
arthropathy and onychopathy. A pilot study. J Int Med Res 1997; 25: 206–9.
30 Lassus A. Colloidal silicic acid for oral and topical treatment of aged skin,
fragile hair and brittle nails in females. J Int Med Res 1993; 21: 209–15.
31 Bisht DB, Singh SS. Pigmented bands on nails: a new sign in malnutrition.
Lancet 1962; 1: 507–8.
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32 Daniel CR, Sams WM, Scher RK. Nails in systemic disease. Dermatol Clin
1985; 3: 465–83.
33 Hediger C, Rost B, Itin P. Cutaneous manifestations in anorexia nervosa.
Schweiz Med Wochenschr 2000; 130: 565–75.
34 Ruymann FB. Juvenile polyps with cachexia. Report of an infant and
comparison with Cronkhite–Canada syndrome in adults. Gastroenterology
1969; 57: 431–8.
HOMEOPATIA
EFECTOS DE LOS MEDICAMENTOS HOMEOPATICOS EUPATORIUM
PERFOLIATUM Y ARSENICUM ALBUM EN LA PARASITEMIA DE
RATONES INFECTADOS POR PLASMODIUM BERGHEI
G. Lira-Salazar1, E. Marines-Montiel1, J. Torres-Monzón3, F. HernándezHernández3 and J.S. Salas-Benito2,
1
Especialización en Terapéutica Homeopática.
Programa Institucional de Biomedicina Molecular, Escuela Nacional de
Medicina y Homeopatía of Instituto Politécnico Nacional.
3
Departamento de Patología Experimental, Centro de Investigación y de
Estudios Avanzados of Instituto Politécnico Nacional, Mexico.
2
[Homeopathy, Volumen 95, Issue 4, October 2006, 223-228]
RESUMEN
La Malaria es una de las más importantes enfermedades parasitarias del
mundo y uno de los mayores problemas de la salud pública por las nuevas
cepas de Plasmodium resistentes a las drogas utilizadas. Actualmente están
siendo estudiados compuestos sintéticos y naturales para desarrollar drogas
antimaláricas más efectivas. Se investigaron los efectos de las preparaciones
homeopáticas de Eupatorium perfoliatum y Arsenicum album en la parasitemia,
utilizando un modelo de roedores afectados de malaria.
Se encontró un efecto inhibitorio significativo sobre la multiplicación del parásito
con ambos medicamentos, un 60% con Eupatorium perfoliatum a la 30 CH, y
un 70% con Arsenicum album 0/6 pero menos estable que el anterior. El
número de esquizontes fue más alto en los animales tratados con
medicamentos homeopáticos. Aunque el mecanismo de acción de estos
medicamentos es desconocido, podrían ser muy buenos candidatos como
25
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alternativa o complementarios de los medicamentos utilizados en el tratamiento
de la malaria.
Palabras clave: Plasmodium berghei; Eupatorium perfoliatum; Arsenicum
album; Ratones Balb/c; Medicamentos homeopáticos.
LA AGREGACION PLAQUETARIA EN LA HIPERTENSION PORTAL Y SU
MODIFICACION POR DOSIS ULTRA-BAJAS DE ASPIRINA
Francisco X. Eizayagaa,
outremepuichb.
Omar
Aguejoufb,
Philippe
Belonc,
Christian
a
Cátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, Universidad de
Buenos Aires, Buenos Aires, Argentina.
b
Laboratoire d’Hématologie, Université de Bordeaux 2, Victor Segalen,
Bordeaux.
c
Laboratoires Boiron, Sainte-Foy-les-Lyons , France.
[Pathophysiology of Haemostasis and Thrombosis 2005;34:29–34]
RESUMEN
La Aspirina (ASA) es ampliamente aceptada como una droga antitrombótica,
pero algunos reportes indican que en su utilización en dosis ultra-bajas (ULD)
tiene propiedades protrombóticas.
En este estudio, evaluamos el efecto de la hipertensión portal en ratas sobre la
agregación plaquetaria, en un modelo in vivo de trombosis arterial inducido por
láser. La hipertensión portal fue producida por una estenosis regulada de la
vena porta. La Aspirina en ultra-bajas dosis fue inyectada tanto al grupo control
como al de hipertensión portal.
Fueron evaluadas, la agregación plaquetaria inducida por ADP, el tiempo de
protrombina, el tiempo de activación parcial de tromboplastina, fibrinógeno y el
tiempo de hemorragia. Las ratas con hipertensión portal mostraron en el
ensayo con rayo láser, un número menor de émbolos y disminuida la duración
del tiempo de embolización y un incremento en el tiempo de hemorragia
inducida. Estos cambios fueron revertidos por una inyección de Aspirina en
dosis ultra-bajas. Esta observación podría ser de importancia para la
prevención primaria o el tratamiento de las hemorragias en el tracto digestivo
superior en pacientes con hipertensión portal.
Palabras clave: Hipertensión portal _ Agregación plaquetaria _ Aspirina _
Ultra-bajas dosis _ Estenosis de vena portal.
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ARTICULO ORIGINAL
Introduction
Portal hypertension is a major complication of chronic liver disease. As a
consequence of portal pressure rise, collateral portosystemic circulation
develops and hemorrhage becomes a frequent cause of death. Multiple factors
concur to complicate this often mortal disease. In the first place, hepatic and
portosystemic collateral circulation increased resistance and hyperdynamic
circulation. These changes are produced by vasodilating agents, such as
prostacyclin (PGI2) and nitric oxide (NO), and a diminished response to
vasoconstrictors. The alterations in vascular autonomic regulation also trigger
modifications in baroreflex response and the central nervous system [1–2].
Secondly, anatomic factors in the gastroesophageal junction make the
surrounding of this place the most frequent to start the hemorrhage. Thus,
pharmacologic treatment is usually aimed to modify hemodynamic forces. There
are also coagulation problems whose roles were never completely clarified.
Traditionally, as cirrhosis is the most frequent disease causing these alterations,
the hepatic synthesis of K vitamin-dependent factors was blamed. Lately, there
have been some reports trying to point out the role of platelet aggregation and
the importance of NO in its modifications [3]. There are few reports that
investigate platelet aggregation in vivo in portal hypertension, and none of them
utilize a prehepatic portal hypertension model. Aspirin (ASA) in ultra-low doses
(ULD) was reported as a potent enhancer of platelet aggregation in several
reports [4–7], in experimental and clinical research studies. The aim of this
study was to evaluate in vivo the changes in platelet aggregation in a model of
portal hypertension in the absence of liver damage and the modifications
observed after administering ASA in ULD.
Materials and Methods
Male Wistar rats (200–250 g) were housed separately and acclimatized before
use under conditions of controlled temperature (25 8 2 ° C) and illumination (12hour light/dark cycle). They were fed with standard rat chow and water ad
libitum. Animals received care in compliance with the European Convention of
Animal Care.
Surgical Procedures
After 1 week of acclimatization, rats were randomized and separated into two
groups: (1) sham-operated rats and (2) portal hypertensive rats. Portal
hypertension was induced by a calibrated portal vein stenosis, according to the
procedure described in Vorobioff et al. [8].
In brief, rats were anesthetized with ketamine (90 mg/kg body weight, i.m.), and
then, a midline abdominal incision was made. The portal vein was located and
isolated from the surrounding tissues. A ligature of 3-0 silk was placed around
the vein and snugly tied to a 20-gauge blunt-end needle placed alongside the
portal vein. The needle was subsequently removed to yield a calibrated stenosis
Homeonews
27
of the portal vein. Sham-operated rats underwent an identical procedure except
that portal vein was isolated but not stenosed.
Animals were housed for 14 days after the operation to develop portal
hypertension in the corresponding group.
Thrombus Formation Induction
After administering 200 mg/kg thiopental sodium, a median laparotomy was
made. The intestinal loop was placed on the microscope table and vascular
lesions were induced by Argon laser (Stabilite 2016, Spectra Physics, France).
The wavelength used was 514.5 nm and the energy was adjusted to 120 mW.
The laser beam is applied during 1/15 s. The dynamic course of the thrombus
formation was continuously monitored and recorded by placing the laser beam
coaxially into the inverted light beam path of the microscope (Axiovert, Zeiss,
France). Microscopic images were recorded through a video camera (DX L107,
color camera CCD) and were monitored on a television screen (Trinitron color
video monitor, PVM 144 2 QM, Sony, France). A schematic view of the
apparatus used has been previously described [9]. Arterioles between 15 and
25 µm in diameter were used. The parameters assessed were the number of
platelet emboli removed by blood flow and the duration of embolization (time
between the first and the last emboli occurring during a 10-min observation
period).
Biological Analysis
1-Platelet Aggregation Study
Platelet aggregation was made according to the method of Cardinal and Flower
on a Chrono Log 500 VS aggregometer (Coultronics, Margency, France) on the
whole blood obtained from the rat after laser experimentation. Platelet
aggregation was induced by ADP final concentration of 5 µM (Laboratoire
Diagnostica, Stago, France). Two parameters were determined: (1) impedance,
representing the maximum amplitude of aggregation expressed in ohms and (2)
velocity of aggregation expressed in ohms/minute.
2-Coagulation Tests
At the end of each experiment, blood was collected by cardiac puncture, mixed
with 3.8% sodium citrate (9 volumes blood/1 volume citrate) and centrifuged for
20 min at 4,000 rpm to obtain platelet-poor plasma. Activated partial
thromboplastin time (APTT) was performed with an automated coagulation
laboratory which permits the determination of APTT by the automatic addition of
CaCl2 to the plasma. The intrinsic factors of coagulation are activated by the
ellagic acid on an extract of bovine cerebral tissue, substitute of platelet factor
III. The coagulation is induced by the addition of CaCl2 (Instrumentation
Laboratory, Paris, France).
Prothrombin time (pTT) and fibrinogen were performed with an automated
coagulation laboratory which permits the simultaneous determination of pTT
and fibrinogen by using only the Ca-thromboplastin (Ca-thromboplastin high
28
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analytic sensibility: lyophilized
Instrumentation Laboratory).
extract
of
rabbit
cerebral
tissue
from
3-Induced Hemorrhagic Time
An experimental model of induced hemorrhagic time (IHT) was performed 10
min before thrombosis induction by laser. The tail of the rat was immersed for 5
min at 37 ° C and sectioned 6 mm from the extremity. IHT measured
corresponded to the time between the tail section and the end of bleeding,
expressed in seconds.
Statistical Analysis
Statistical analysis was carried out with Excel (Microsoft) and expressed as
mean 8 standard error. Data were compared using the Student’s parametrict
test (p < 0.05 was considered significant).
Drug Tested
ASA solution was purchased from Boiron Laboratories (Sainte- Foy-les-Lyons,
France). ASA in ULD was prepared as follows: 1 g of pure, finely powdered
ASA was suspended in 99 ml of alcohol (70 %). After being vigorously shaken,
1 ml of this dilution was mixed with 99 ml of distilled water and again vigorously
shaken.
The last process was repeated 13 times [4–7]. Sterilized water for injections
(Aguettant, Lyon, France) was used as control.
Protocol
Rats were randomly assigned in 4 groups. Group I: sham operated + placebo
(Sh); group II: sham operated + ASA (ShASA); group III: portal hypertensive +
placebo (PH), and group IV: portal hypertensive + ASA (PHASA). Each group
had between 5 and 9 rats in the pilot study (PS). A confirmatory study (CS) was
made for laser protocol, IHT and ex vivo platelet aggregation study. In this CS,
each group consisted of 25–32 rats.
Groups Sh and ShASA were submitted to a simulated operation. Groups PH
and PHASA to portal vein ligation as described above, in surgical procedures.
One hour previous to thrombosis induction, one dose of 1 ml/kg of ASA at ULD
or placebo was injected subcutaneously.
Results
In vivo Study
Number of emboli in the PS (n = 5–9/group): Sh 5.71+/-0.83, ShASA 8.33+/1.20, PH 2.44+/-0.50 and PHASA 4.17+/-1.4. Number of emboli in the CS (n =
25–32/ group): Sh 7.4+/-1.00, ShASA 8.52+/-5.92, PH 2.72+/-2.14 and PHASA
5.56+/-3.87. Portal hypertension produced a significant reduction in number of
emboli in the PS (p < 0.05) and the CS (p < 0.001) when compared with control
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29
(Sh). In the CS, there was also a significant rise in number of emboli when
comparing PH with PHASA.
Duration of embolization in the PS (n = 5–9/group): Sh 3.00+/-0.43 min, ShASA
4.17+/-0.70 min, PH 0.11+/-0.39 min and PHASA 2.00+/-0.81 min. Duration of
embolization in the CS (n = 25–32/group): Sh 3.12+/-0.31 min, ShASA 3.63+/0.51 min, PH 1.09+/-0.19 min and PHASA 2.77+/-0.36 min. Portal hypertension
produced a significant reduction in the duration of embolization in the PS (p <
0.05) and in the CS (p < 0.001). The duration increased towards normality when
comparing PHASA and PH (p < 0.001).
IHT in the PS (n = 5–9/group): Sh 114+/-9.47 s, ShASA 160+/-35.05 s, PH 289
+/-47.66 s and PHASA 156.67+/-52.76 s. IHT in the CS (n = 25–32/group): Sh
7.4+/-1 s, ShASA 8.52+/-1.12 s, PH 2.72+/- 0.38 s and PHASA 5.56+/-0.73 s.
Portal hypertension produced a significant rise in IHT in both studies (p < 0.05).
This rise was not observed in PHASA after ASA administration at ULD.
It should be noted that different means of IHT were observed in the two studies;
however, we found proportional differences in all the 4 groups studied in both
protocols.
Ex vivo Study
The changes observed in the ex vivo coagulation study (platelet aggregation
induced by ADP and expressed as amplitude and velocity, APTT, pTT and
fibrinogen) were not statistically significant when comparing the different groups
studied (data not shown).
Discussion
As shown in figures 1–4 , induction of portal hypertension significantly reduced
the number of emboli and the duration of embolization in both pilot and
confirmatory series in the in vivo thrombus formation study.
The addition of ASA at ULD induced a trend to normalize both parameters in
the PS. This trend turned into a significant difference in these parameters when
comparing groups PH and PHASA in the CS.
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30
In IHT, portal hypertension also showed a significant increase in tendency to
bleed. This tendency was not present after ASA administration (fig. 5, 6), thus
confirming its proaggregant effect.
This is the first report of changes of in vivo thrombus induction formation in a
model of prehepatic portal hypertension.
Although it is generally accepted that portal hypertension induces changes in
platelet function, there are not many experimental studies directed to clarify
these alterations. Albornoz et al. [3] , using the Borchgrevink method for
measuring platelet adhesion, documented similar changes in bile duct-ligated
cirrhotic rats, observing partial reversal of these alterations after blocking NO
production.
The partial portal vein ligation model of portal hypertension has been widely
used to clarify portal hypertension changes, especially related to
hemodynamics. Most of the changes observed in portal vein-ligated rats were
also observed in cirrhotic animals. In the classical papers of Vorobioff et al. [8]
and Benoit et al. [10] , a relative importance of 40% for hyperdynamic circulation
and 60% for increased vascular resistance of portal ligature and the portal
systemic collateral vascular bed in increased portal vein pressure, as well as an
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31
approximate portal pressure rise of 50%, were established . This animal model
with an almost normal liver function was chosen for the study of isolated platelet
activity alterations, ruling out, where possible, changes in coagulation factors
due to liver damage and because of its ability to reproduce the hyperdynamic
circulatory changes first described by Kowalsky and Abelman [11, 12]. It is
interesting to note that the alterations observed in platelet activity in vivo were
probably initially only triggered by hemodynamic changes such as pressure
alterations, increased portal inflow, endothelial stretch and shear stress.
Changes in platelet adhesion in cirrhosis have been widely reported [13, 14].
Alterations in coagulation have also been reported by Bajaj et al. [15] in patients
with noncirrhotic portal fibrosis and extrahepatic portal venous obstruction, both
conditions with portal hypertension and near-normal liver functions, in
pathophysiologic states similar to the animal model used in our study.
In this last paper, both groups had a decreased platelet aggregation and normal
platelet malondialdehyde levels.
The model of laser thrombus induction formation has the possibility of
evaluating in situ the platelet-endothelium interaction. In the past, numerous
studies have shown that platelets can adhere even to an intact endothelium and
substantially modulate endothelial cell function [16]. Normal endothelium is a
nonadhesive nonthrombogenic surface. When it is activated, it is proadhesive
and promotes the adhesion of circulating blood platelets even under conditions
of high shear stress. When a lesion is provoked in endothelial surface,
extracellular matrix proteins like collagen and von Willebrand factor are exposed
to the blood, triggering a reaction of platelet adhesion and activation. NO is a
potent vasodilating substance and inhibitor of platelet activity and is continually
secreted by the endothelium in response to shear stress. Evidence suggests
that elevated production of NO is essential to the development of portal
hypertension [17]. PGI 2 is another important endothelium-derived vasodilating
substance capable of modifying platelet function.
NO and PGI2 appear to act by separate pathways in promoting mesenteric
blood flow. It is possible that the absence of the endothelium could originate a
different response between platelet aggregation studies and laser thrombosis
production model. Moreover, in previous studies, the presence of a vascular
fragment was necessary to put in evidence the effect of ASA at ULD on platelet
aggregation [5, 6]. It should be noted that Kunihiro et al. [18] found differences
in platelet aggregation from blood samples obtained from systemic and portal
circulation in cirrhotic patients complicated with hepatocellular carcinoma, and
they attributed those differences to intraportal PGI2. For the above cited
elements, we could conclude that platelet aggregation ex vivo induced by ADP
and in vivo laser induction thrombus formation may not behave in an identical
way.
Although the pathophysiology of this animal model is more similar to
presinusoidal cases like noncirrhotic or idiopathic portal hypertension, these
observations may become useful in preventing the first episode of hemorrhage
or its recurrence in patients with portal hypertension of other origins.
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32
Hemorrhage is a major cause of death in portal hypertensive patients. Drug
therapy for this disease is aimed mainly at the prevention of variceal bleeding
and is done by β-blockers or vasodilators, with a predominant hemodynamic
action. NO blockers could modify portal pressure and increase platelet
aggregation, but the inhibition of intrahepatic NO could lead to an increased
hepatic resistance [17, 19]. In previous studies done in healthy volunteers with
ULD of ASA, no side effects were observed [4], and the effect of ASA in ULD
enhancing platelet aggregation in a laser-induced thrombosis model was
documented in the normal rat [7].
In the present study, the results obtained in the PS in experimental prehepatic
portal hypertension were repeated in a CS with more animals in each group.
This second study did not only show the significant difference observed in laserinduced thrombus formation when comparing Sham and portal hypertensive
groups, but also a significant difference between PH and ASA at ULD groups.
This tendency to normal platelet aggregation in the mesenteric bed was
confirmed by a trend to normalize IHT in the portal hypertensive group when
treated with ASA at ULD.
The factors normally considered to enhance the hemorrhage risk in patients
with portal hypertension are as different as anatomic factors [20], hyperdynamic
circulation, the degree of portal hypertension [21], endotoxininduced NO and
PGI2 [22] , altered synthesis of coagulation factors induced by liver damage or
by compensated mild disseminated intravascular coagulation in prehepatic and
hepatic portal hypertension [23] . It is difficult to point out the relative importance
of alterations of platelet aggregation in such a complex state, even though the
changes observed in IHT suggest that this platelet aggregation dysfunction
could be the fi nal pathway of some of these alterations through shear stress,
NO and PGI 2 production.
Further studies with other portal hypertension experimental models should be
performed to clarify if this effect remains when liver function is severely
compromised.
Conclusion
Prehepatic portal hypertension in the rat produces an altered platelet response
to endothelial damage in mesenteric circulation, as well as a prolonged IHT.
ASA in ULD normalized platelet activity and IHT.
The evidence provided by this study could be of importance for the primary
prevention or the treatment of recurrence of upper digestive tract hemorrhage in
patients with portal hypertension.
References
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Sanso G, Fernandez B: Prehepatic portal hypertension in rats modifi es
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2 Arranz CT, Balaszczuk AM, Costa MA, Eizayaga FX, Romay S, Mongelli C,
Lemberg A: Systemic barorefl ex alterations in prehepatic portal hypertensive
conscious rats. Arch Physiol Biochem 1995; 103: 422–426.
3 Albornoz L, Bandi JC, Otaso JC, Laudanno O, Mastai R: Prolonged bleeding
time in experimental cirrhosis: Role of nitric oxide. J Hepatol 1999; 30: 456–460.
4 Doutremepuich C, de Seze O, Le Roy D, Lalanne MC, Anne MC: Aspirin at
very ultra low dosage in healthy volunteers: Effects on bleeding time, platelet
aggregation and coagulation. Haemostasis 1990; 20: 99–105.
5 Lalanne MC, Doutremepuich C, de Seze O, Belon P: What is the effect of
acetylsalicylic acid at ultra low dose on the interaction platelets/vessel wall?
Thromb Res 1990; 60: 231–236.
6 Lalanne MC, de Seze O, Doutremepuich C, Belon P: Could proteolytic
enzyme modulate the interaction platelets/vessel wall in presence of ASA at
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7 Doutremepuich C, Aguejouf O, Pintigny D, Sertillanges MN, de Seze O:
Thrombogenic properties of ultra-low-dose of acetylsalicylic acid in a vessel
model of laser-induced thrombus formation. Thromb Res 1994; 76: 225–229.
8 Vorobioff J, Bredfeldt JE, Groszmann RJ: Hyperdynamic circulation in portalhypertensive rat model: A primary factor for maintenance of chronic portal
hypertension. Am J Physiol 1983; 244:G52–G57.
9 Vesvres MH, Doutremepuich F, Lalanne MC, Doutremepuich C: Effects of
aspirin on embolization in an arterial model of laser-induced thrombus
formation. Haemostasis 1993; 23: 8–12.
10 Benoit JN, Womack WA, Hernandez L, Granger DN: ‘Forward’ and
‘backward’ flow mechanisms of portal hypertension. Relative contributions in the
rat model of portal vein stenosis. Gastroenterology 1985; 89: 1092–1096.
11 Kowalski HJ, Abelmann WH: The cardiac output at rest in Laennec’s
cirrhosis. J Clin Invest 1953: 32; 1025–1033.
12 Groszmann R: Hyperdynamic circulation of liver disease 40 years later:
Pathophysiology and clinical consequences. Hepatology 1994; 20: 1359–1363.
13 Ordinas A, Escolar G, Cirera I, Vinas M, Cobo F, Bosch J, Teres J, Rodes J:
Existence of a platelet-adhesion defect in patients with cirrhosis independent of
hematocrit: Studies under flow conditions. Hepatology 1996; 24:1137–1142.
14 Younger HM, Hadoke PW, Dillon JF, Hayes PC: Platelet function in cirrhosis
and the role of humoral factors. Eur J Gastroenterol Hepatol 1997; 9: 989–992.
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15 Bajaj JS, Bhattacharjee J, Sarin SK: Coagulation profi le and platelet
function in patients with extrahepatic portal vein obstruction and non-cirrhotic
portal fi brosis. J Gastroenterol Hepatol 2001; 16: 641–646.
16 Gawaz M: Role of platelets in coronary thrombosis and reperfusion of
ischemic myocardium. Cardiovasc Res 2004; 61: 498–511.
17 Gupta TK, Chen L, Groszmann RJ: Pathophysiology of portal hypertension.
Clin Liver Dis 1997; 1: 1–12.
18 Kunihiro N, Kawai B, Sanjo A, Osaka K, Ohnishi A: Platelet aggregation and
coagulation and fi brinolysis parameters in both portal and systemic circulations
in patients with cirrhosis and hepatocellular carcinoma. Hepatol Res 2001; 19:
52–59.
19 Bosch J, Abraldes JG, Groszmann R: Current management of portal
hypertension. J Hepatol 2003; 38(suppl 1):S54–S68.
20 Vianna A, Hayes PC, Moscoso G, Driver M, Portmann B, Westaby D,
Williams R: Normal venous circulation of the gastroesophageal junction. A route
to understanding varices. Gastroenterology 1987; 93: 876.
21 Castaneda B, Debernardi-Venon W, Bandi JC, Andreu V, Perez-del-Pulgar
S, Moitinho E, Pizcueta P, Bosch J: The role of portal pressure in the severity of
bleeding in portal hypertensive rats. Hepatology 2000; 31: 581–586.
22 Goulis J, Patch D, Burroughs AK: Bacterial infection in the pathogenesis of
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in extrahepatic portal hypertension. Hepatology 1993; 18: 853–857.
NUTRICION
EL CONSUMO DE LECHE Y SU RELACION CON EL ACNE EN NIÑAS
Clement A Adebamowo1, Donna Spiegelman2, Catherine S Berkey3, F William
Danby4, Helaine H Rockett3, Graham A Colditz5, Walter C Willett5, Michelle D
Holmes3
1
Departments of Nutrition, Harvard School of Public Health, Boston, Division of
Oncology, Department of Surgery, University of Ibadan, University College
Hospital, Ibadan, Oyo State, Nigeria.
2
Departments of Biostatistics and Epidemiology, Harvard School of Public
Health, Boston.
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35
3
Channing Laboratory, Department of Medicine, Brigham and Women's
Hospital, Harvard Medical School, Boston.
4
Dartmouth Medical School, Hanover, NH.
5
Departments of Nutrition and Epidemiology, Harvard School of Public Health,
Boston Channing Laboratory, Department of Medicine, Brigham and Women's
Hospital, Harvard Medical School, Boston.
[Dermatology Online Journal 12 (4): 1]
RESUMEN
Existe una gran cantidad de evidencias para la asociación entre el acné y la
dieta. Nuestros estudios previos sugieren que existe una asociación entre el
consumo de leche y el acné adolescente. Este es un estudio de cohorte,
prospectivo, para evaluar dicha relación. Se estudiaron 6,094 niñas, de 9 a 15
años de edad (en 1996), quienes informaron su ingesta dietaria a través de
cuestionarios desde 1996 a 1998. La presencia y la severidad del acné fue
evaluada mediante cuestionarios en 1999. Se computaron las relaciones de
prevalencia multivariadas (PR) y los intervalos de confianza del 95% para acné.
Después de clasificar por edad, cantidad de veces y energía de la ingesta, los
PRs (95 % CI; valor p- para el ensayo de tendencia) para acné comparando la
más alta (2 o más ingestas por día) a la más baja (<1 por semana) categoría de
ingesta en 1996, fue 1.20 (1.09, 1.31; <0.001) para leche total, 1.19 (1.06, 1.32;
<0.001) para leche entera, 1.17 (1.04, 1.31; 0.002) para leche con baja
cantidad de materia grasa y 1.19 (1.08, 1.31; <0.001) para leche descremada.
Estos resultados no se modifican significativamente cuando se excluye a las
adolescentes que informaron el uso de anticonceptivos y cuando se restringe el
análisis a aquellas menores de 11 años. Se encontró una asociación positiva
entre el consumo de leche y el acné. Estos hallazgos respaldan los estudios
anteriores y sugieren que los efectos metabólicos de la leche son suficientes
para desencadenar respuestas biológicas en los consumidores.
ARTICULO ORIGINAL
Introduction
Teenage acne is a common, chronic and self-limiting skin disease that is
associated with physical and psychological morbidity in up to 90 percent of
adolescents and young adults [1]. In Western countries, acne affects all ages,
but its maximum prevalence peaks at 16-18 years when 75-98 percent of this
age group is affected [1]. Acne is more common in girls, both overall and below
the age 12 years.
Acne results from hyperkeratinization and obstruction of the pilosebaceous
follicles secondary to androgen-stimulated failure of normal desquamation of
the follicular epithelium, androgen-stimulated sebum production, subsequent
Homeonews
36
colonization of the follicles by Propionibacterium acnes and other organisms,
and variably, inflammation [2]. Ecological studies suggest an association
between the Western diet and acne [3], but the relevant dietary factors are
unclear. At least one clinical trial failed to find an association with chocolate
intake [4]. In another study, subjects were fed large quantities of foods that they
claimed worsened their acne but no acne flares occurred [5]. Robinson reported
that among 1,925 patients who kept a food diary, the majority implicated milk in
acne flares [6]. In a previous study of US female nurses who reported their high
school diet and the prevalence of physician-diagnosed severe teenage acne,
we found a positive association with intake of total and skim milk [7].
In this study, we examined data from a prospective study of US youth to
evaluate intake of dairy foods and other factors in relation to occurrence of acne
among girls. The study was approved by the Institutional Review Boards of the
Brigham and Women's Hospital and the Harvard School of Public Health.
Methods
Study population
The Growing Up Today Study (GUTS) is an ongoing cohort study of 9,039 girls
and 7,843 boys, aged 9-15 years at baseline in 1996. These patients were
followed by yearly questionnaire to ascertain lifestyle factors. Participants are
offspring of the women in the Nurses Health Study II (NHS II) cohort and have
been described in detail elsewhere [8]. In this analysis, we examined the
association between milk consumption and occurrence of acne among female
members of the cohort. After exclusion of participants who had implausible
values (<500 and >5000 kcal/day) for energy intake (n = 96), those who left
more than 70 response items blank (n = 33), and those who did not respond to
the 1999 questionnaires that contained the acne question (n = 2,945), there
were 6,094 girls who completed a detailed food frequency questionnaire (FFQ)
in 1996 and another FFQ in either 1997 or 1998.
Semi-quantitative food-frequency questionnaires and calculation of nutrient
intake
The development and validation of the GUTS food-frequency questionnaire has
been previously described [9, 10]. In brief, participants were asked how
frequently they used a typical portion size of specified foods on average during
the past year. The dairy food group included total milk, chocolate milk, instant
breakfast drink, ice cream, yogurt, cottage cheese, cream cheese, other (hard)
cheese, frappe (milkshake), and butter. In addition they were asked "What type
of milk do you usually drink" and the options were 'whole milk', '2 percent milk',
'1 percent milk', 'skim/nonfat milk', 'soy milk', 'don't know', and 'don't drink milk'.
Consumption of the specific types of milk was derived from the crossclassification of the responses to the usual type of milk consumed and the
frequency of total milk consumption. Whole milk and 2 percent milk were
grouped because of their similar fat content. Other food items that were studied
include French fries, pizza, and chocolate candy because these have often
37
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been perceived as causes of acne. The response categories for some of the
food items such as non-milk dairy foods, pizza, French fries and chocolate
candy were collapsed because of small cell sizes.
Nutrient intakes were computed by multiplying the frequency of consumption of
each unit of food and the nutrient content of the specified portions based on the
nutrient values in foods obtained from US Department of Agriculture sources
and food manufacturers [11]. In addition, portion sizes were determined by
reviewing the US Department of Agriculture Handbook No. 8 serving sizes [12],
the Nationwide Food Consumption Survey (NFCS) Foods Commonly Eaten by
Individuals (specifically for ages 9-18)[13] and the natural serving sizes for
foods like a slice of bread or one apple. Nutrients were energy-adjusted by
using the residuals from the regression of nutrient intake on total caloric intake
[14]. Total intake of vitamin D was calculated from all sources of vitamin D,
combining diet and supplements. Intake of vitamin D from foods was calculated
from all dietary sources without supplements. Dairy fat was computed from milk,
butter and cheese as a whole food and as ingredients in other foods reported in
the FFQs.
Validation of the food-frequency questionnaire was done in a random sample of
children of 399 participants in the Nurses Health Study II, of whom 305 agreed
to participate [10]. Most, 263 (86 %) returned the two food frequency
questionnaires administered at an interval of 1 year apart, and completed three
24-hour diet recalls over the same period. The mean of de-attenuated Pearson
correlation coefficients between the diet recalls and the food frequency
questionnaire was 0.54, which is similar to findings in adults [10]. To evaluate
the reproducibility of milk intake over the period of the study, we computed the
Spearman correlation coefficients for intake of types of milk at baseline in 1996
and in 1998. These correlations were 0.81 for total milk, 0.65 for whole milk,
0.54 for low fat milk, and 0.68 for skim milk. We note that reported intake can
reflect both true changes in intakes and error in reporting.
Assessment of non-dietary factors
Age, Tanner stage, use of oral contraceptives, weight and height were obtained
from the yearly mailed questionnaires. See Table 1.
Table 1: Age-standardized distribution of risk factors for acne by categories of total milk intake among GUTS participants
at baseline, 1996, USA
Servings (glasses)
≤1/week
2-6/week
1/day
2 or more/day
Number
370
824
720
1842
Mean Tanner stage
2.8
2.9
2.8
2.9
BMI (kg/m²)
19.2
19.1
18.9
18.9
Height (ins)
59.3
59.5
59.6
59.8
38
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Servings (glasses)
≤1/week
2-6/week
1/day
2 or more/day
Calorie intake, kcal
1736
1870
1964
2217
Calcium, mg
740
901
1040
1488
Total Vitamin D, IU
228
283
331
484
Vitamin D from foods, IU
147
220
269
421
Vitamin D from Supplements, IU
70.7
58.2
60.8
64.3
kg = kilograms; m = meters; ins = inches; kcal = kilocalories; mg = milligrams; IU = International Units
Identification of acne cases
In 1999, members of the GUTS cohort were asked "Compared to other people
your age, how would you describe your acne"; possible responses were 'I
almost never have any pimples', 'I sometimes get a few pimples', 'I usually have
a few pimples', 'I sometimes get a lot of pimples', and 'I usually get a lot of
pimples'.
Statistical analysis
To assess the potential for selection bias, we compared the girls who
responded to the 1999 questionnaire that included the item on acne with those
who did not, using the Wilcoxon rank-sum test for continuous variables and the
χ² test for categorical variables. Age-adjusted Mantel-Haenszel Prevalence
Ratios (PR)[15, 16] were used to identify variables that were significantly
associated with acne at p-value less than or equal to 0.1. These were then used
in multivariate stratified models to identify statistically significant predictors at a
p-value of 0.05 or less and those variables that changed the PR of the variables
of primary interest by 10 percent or more using the frequency procedure with
the Cochran-Mantel-Haenszel option in SAS [17].
In our primary analysis, to more clearly distinguish respondents with substantial
acne from those without, we excluded those who said they had "sometimes a
few" pimples and dichotomized the responses between the 'almost never' and
the combined categories of 'usually a few, sometimes a lot or usually a lot'
levels. This left 3,841 girls for our primary analysis. However we repeated our
analysis including all respondents, but dichotomizing the response to the acne
question at different levels in order to test the robustness of our findings.
Because we did not know the exact onset of acne and we desired to best
simulate a prospective study, we examined the association between diet
reported in 1996 and the history of acne that was reported in 1999. We also
examined diet responses for 1997 and 1998 separately and the cumulative
39
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average of the diet responses from 1996 to 1998 in relation to the occurrence of
acne. To further reduce the possibility that the results may be due to change in
milk intake as a result of having acne and to examine the association during a
period of low prevalence of contraceptive use, we repeated the analysis by
examining the association between diet reported by girls aged 11 years and
younger in 1996, and acne reported in 1999.
In multivariate analysis, we adjusted for age in months at baseline in 1996
(quintiles), energy intake (quintiles), height (quintiles), BMI (quintiles) and
Tanner's stage (Stages 1 and 2, 3, 4, and 5). The food items were modeled as
categories of servings per week or per day. The PR and 95 percent confidence
intervals (95% CI) were calculated for each category of intake and compared
with the lowest category of intake as the reference value. The lowest category
of intake for each type of milk included low intakes of all types of milk. In tests
for linear trend, food intake was modeled as continuous variables of servings
per day.
We categorized the energy-adjusted values of each nutrient into quintiles
(except for vitamin D from supplements which we categorized into quartiles)
and modeled the prevalence ratio for each quintile with the lowest quintile as
the reference category. In tests for linear trend across quintiles of nutrient
intake, ordinal scores were modeled as continuous variables. Missing value
indicators were created for those with missing covariates because we had few
missing data [18, 19]. We present two-sided 95 percent confidence intervals for
all PR.
Results
Girls who did not respond to the 1999 questionnaire that was used to define
acne were slightly older (mean age = 147 compared to 144 months) than those
who did, otherwise there was no notable difference between the two groups.
Most of the girls, 40 percent, drank whole or 2 percent milk, 23 percent drank
low fat milk, 33 percent drank skim milk, 0.4 percent drank soy milk and 4
percent didn't drink milk at baseline in 1996. Most, 80 percent reported
"sometimes a few" pimples or more and 43 percent reported "usually a few" or
more pimples. Table 1 shows the age-standardized prevalence of the risk
factors for acne according to categories of total milk intake in the cohort.
Calcium, total vitamin D, vitamin D from foods, vitamin D from supplements and
energy intake increased with increasing intake of total milk. The prevalence of
acne according to the intake of total milk was 0.60 for < 1 serving/week, 0.66 for
2-6 servings/week, 0.68 for 1 serving/day and 0.72 for 2 or more servings/day.
Table 2: Prevalence ratio (PR), 95% confidence intervals (95% CI) and p-value for test of trend for acne by
categories of milk intake among the girls in the GUTS cohort at baseline, 1996, USA
Servings (right)
<=1/week
2 - 6/week
1/day
2 or
more/day
220/370
542/824
490/720
1336/1842
Milk types(below)
Total milk
Cases/Total
p-value for test
of trend
40
Homeonews
Servings (right)
<=1/week
2 - 6/week
2 or
more/day
1/day
p-value for test
of trend
Milk types(below)
Age-adjusted PR
1.00
95% CI
Multivariate PR
1.00
95% CI
1.11
1.15
1.23
1.01, 1.23
1.05, 1.27
1.12, 1.34
1.13
1.17
1.2
1.02, 1.25
1.05, 1.29
1.09, 1.31
<0.001
<0.001
Whole milk
Cases/Total
Age adjusted PR
216/363
1.00
95% CI
Multivariate PR
1.00
95% CI
241/362
212/317
464/652
1.14
1.15
1.21
1.02, 1.27
1.02, 1.28
1.09, 1.33
1.17
1.22
1.19
1.04, 1.32
1.08, 1.37
1.06, 1.32
<0.001
<0.001
Low Fat milk
Cases/Total
Age adjusted PR
215/362
1.00
95% CI
Multivariate PR
1.00
95% CI
115/185
108/161
327/449
1.06
1.15
1.24
0.92, 1.22
1.01, 1.32
1.12, 1.37
1.04
1.16
1.17
0.89, 1.21
1.00, 1.35
1.04, 1.31
<0.001
0.002
Skim milk
Cases/Total
Age adjusted PR
215/361
1.00
95% CI
153/218
150/220
531/722
1.18
1.14
1.24
1.05, 1.34
1.00, 1.29
1.13, 1.37
<0.001
1.00
1.2
1.08
1.19
<0.001
1.04,
1.37
0.94,
1.24
1.08,
1.31
95% CI
PR = prevalence ratio; CI = confidence interval. Multivariate PR of acne for categories of intakes adjusted for
age, height and energy intake.
Multivariate PR
Table 2 shows the multivariate PR (95% CI; p-value for test of trend), adjusted
for age at baseline, height and energy intake comparing the highest (2 or more
servings per day) to lowest (<1 serving per week) categories of food intakes in
1996. These were 1.20 (1.09, 1.31; <0.001) for total milk, 1.19 (1.06, 1.32;
<0.001) for whole milk, 1.17 (1.04, 1.31; 0.002) for low fat milk and 1.19 (1.08,
1.31; <0.001) for skim milk. Additional adjustments for BMI or Tanner stage did
not alter the PRs appreciably. A weak inverse association was found with
intakes of cream cheese; the multivariate PR (95% CI; p-value for test of trend)
comparing intakes once a day or more with once a week or less was 0.66 (0.28,
1.55; 0.03). In our questionnaire, chocolate milk was asked as a separate item
and this was positively associated with prevalence of acne. The multivariate PR
(95% CI; p-value for test of trend) comparing intakes of 2 or more servings per
day with one serving or less a week was 1.29 (1.08, 1.53; 0.02). There were no
associations between acne and intakes of other dairy foods, chocolate candy or
pizza (data not shown). Intakes of total fat, specific types of fat and dairy fat
were not associated with acne.
The results for milk intake and the prevalence of acne using the questionnaires
completed in 1997, 1998 or the cumulative averaged intake from 1996 to 1998
were similar (data not shown). We tested the robustness of the findings to our
definition of acne by repeating the multivariate analysis, first by including the
'sometimes a few' as cases of acne (they were omitted entirely initially) and
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41
secondly by including them among the non-cases. The findings were similar to
what we reported above (data not shown). Furthermore, to reduce the likelihood
of reverse causation and possible interaction with use of oral contraceptives, we
examined these associations in a sub-cohort of participants who were aged less
than 11 years at baseline—a time of relatively low acne prevalence—and the
PR, 95% CI and p-value test for trend comparing extremes of intakes were
1.19, 1.08 - 1.31, <0.001. In addition, we repeated the analysis without those
girls who reported either use of oral (n = 188) or injectable contraceptives (n =
21) and the PR, 95 percent CI and p-value test for trend comparing extremes of
intakes of skim milk were identical, 1.19, 1.08 - 1.31, <0.001.
Conclusions
In this prospective study of US girls whose ages ranged from 9 to 15 years in
1996, we found that greater consumption of milk was associated with higher
prevalence of acne. We did not find an association with dairy fat. This suggests
that the fat content of milk is not important in comedogenicity. This finding is
consistent with the result of our previous study of US female nurses who
reported on their high school diet and prevalence of physician-diagnosed
severe teenage acne. In that study, we found a positive association with intake
of total and skim milk [7].
Milk intake may affect acne severity through the Insulin-like Growth Factor-1
(IGF-1) pathway. In two large cross-sectional studies, milk consumption was
positively associated with higher plasma IGF-1 levels [20, 21] and in both
studies, this was predominantly an association with skim milk. In a randomized
clinical trial of the effect of milk intake on bone remodeling, intakes of skim and
low fat milk were associated with increased serum IGF-1 levels in both sexes
[22]. It is not clear whether the increased IGF-1 is endogenous—released in
response to milk intake—or exogenous IGF-1 from milk. Human and bovine
IGF-1 share the same amino acid sequences [23] and several milk proteins,
including IGF-binding proteins (IGFBPs) protect IGF-1 from digestion in the gut
[24, 25]. Animal studies have shown that milk borne IGF-1 can be absorbed
after oral intake [24]. IGF-1 directly stimulates basal keratinocytes' proliferation
[26,27]. Although both serum androgens and IGF-1 levels rise at puberty, the
period of maximum prevalence of acne and the course of the condition follow
the levels of IGF-1 more closely than levels of androgens [28]. There is also a
stronger correlation in women between acne lesions and IGF-1 compared to
androgens [29].
Milk intake may influence comedogenesis because it contains several bioactive
molecules that can act on the pilosebaceous unit including androgens, 5αreduced steroids and other steroid hormones [30, 31]. Many of these bioactive
molecules survive processing and in the case of cheese, fermentation results in
the production of more testosterone from precursors in milk [31]. The level of
androgens in milk has generally been considered low and first-pass metabolism
in the liver may further reduce its bioavailability compared to the daily
endogenous production in young children and adolescents. However, recent
studies have questioned the methodology and assays on which estimates of
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42
daily production rates of endogenous steroid hormones in pre-pubertal children
are based [32]. Dietary intake may be a more significant source of androgens
than previously thought [33]. Milk also contains estrogens, some of which are
produced in the lactating bovine mammary gland and are direct suppressors of
sebaceous gland function [28].
Some hormones in milk are carried by whey proteins, including α-lactalbumin,
which also have intrinsic biological functions [34]. Animals fed α-lactalbuminenriched whey protein show increased will and capacity to engage in physical
activities, gains in lean body mass, improved efficiency of exercise training, and
decreased percentage body fat mass; all of which are similar to the effect of
androgens [35, 36, 37]. In addition, α-lactalbumin undergoes pressure-induced
conformational alteration, possibly because of centrifugation stresses during
processing; this leads to changes in biological function [38]. Whey proteins are
also added to low fat and skim milk to simulate the consistency of whole milk.
These proteins might therefore play a role in acne. We note an inverse
association with cream cheese, which may be due to reverse causation
because girls with acne may avoid cream cheese in the belief that it is
associated with acne. The group of girls who regularly eat cream cheese may
also be too small to draw conclusions. Alternatively, the fermentation phase of
cheese production is associated with changes in the relative concentration of
bioactive molecules in cheese that may explain this finding [31].
Vitamin D, present in milk because of fortification, plays an important role in
epidermal differentiation by inhibiting the proliferation of keratinocytes and this
could possibly affect acne risk [39]. However, supplemented vitamin D was not
associated with acne prevalence in this study (PR = 1.02, 95% CI = 0.96, 1.08
for highest compared to lowest quartile of intake, p-value for test for trend =
0.81). This suggests that vitamin D was not responsible for the observed
association with milk consumption.
Although some of the girls in this study did not respond to the questionnaire that
included the question on acne, we do not think that this is likely to bias our
result because this is a prospective study and response rate was not
appreciably related to milk consumption or to teenage acne. We did not have an
opportunity to validate the self-report of teenage acne but other studies have
shown that young people's perception of acne severity is closely related to
objective clinical assessment [40]. Our sensitivity analysis also shows that our
results are robust to different ways of classifying acne in our study population.
We did not exclude girls whose acne may be part of the symptom complex of an
underlying clinical disorder because we did not have data on this; had we, the
association with milk consumption may have been stronger. Our questionnaire
did not specify a body location for the acne. However, truncal acne, with
absence of a facial component occurs in less than 5 percent of sufferers [41].
The dietary assessment that we used has been well validated and the use of
energy-adjustment corrects for over- or under-reporting of overall dietary intake
[13]. We computed Mantel-Haenszel prevalence ratios, a method that
intrinsically controls for main effects and higher order interactions of all
confounders, whether these confounders are relevant or not. It leads to loss of
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43
statistical power and gives a conservative estimate of effect. For example, the
odds ratio (95% CI; p-value for test of trend) from the multivariate logistic
regression analysis adjusted for age at baseline, height and energy intake
comparing the highest (2 or more servings per day) to lowest (<1 serving per
week) categories of skim milk intakes in 1996, were 2.27 (1.47, 3.52; <0.001).
In conclusion, our study suggests that milk may have biological effects in the
consumer. Because milk contains androgenic hormones and other bioactive
molecules, moderation of milk intake may be useful as part of the management
of teenage acne. Furthermore, this finding raises the possibility that other
hormone-sensitive glands may be affected by the hormonal constituents of milk.
Because of the potential detrimental effect of milk products on acne, breast
cancer [42], and prostate cancer[43], these relationships should be evaluated
further.
Acknowledgment: The authors thank Gideon Aweh and Ellen Hertzmark for
their support with the data analysis, and the participants in GUTS who made
this work possible.
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NOTAS DE INTERES
JORNADA NACIONAL DE MEDICAMENTOS
FITOTERAPICOS
El día 10 de Agosto del corriente año, tuvo lugar en el Salón Belgrano del
Anexo de la Cámara de Senadores de la Nación, la JORNADA NACIONAL
DE MEDICAMENTOS FITOTERAPICOS. Esta actividad se desarrolló durante
todo el día, con una gran cantidad de asistentes y disertantes, tanto de nuestro
país como del exterior, quienes abordaron los siguientes temas:
-“Políticas de Salud con Plantas Medicinales en el mundo”.
-“Mercado de plantas medicinales y productos fitoterápicos en el mundo”.
-“Líneas de investigación con plantas medicinales en Universidades Argentinas
y ciencia y tecnología”.
-“Legislación, validación y producción de medicamentos fitoterápicos”,
-“Aspectos educativos y formativos en la temática fitoterápica”.
De acuerdo a lo indicado en el Programa entregado a los asistentes, “La
implementación de una Jornada Nacional de Fitoterápicos surge de la
necesidad de poder cubrir un segmento importante de patologías en
A.P.S. (Atención Primaria de la Salud) reduciendo en muchos casos los
altos costos que tienen algunos productos sintéticos, a la vez que se
intenta generar nuevos polos productivos regionales, dada la gran
biodiversidad que tiene nuestro país. A ello se debe agregar las importantes
investigaciones que realizan nuestras Universidades para validar
científicamente los usos de las plantas medicinales, y la necesidad de producir
estos productos por los propios laboratorios provinciales, todo lo cual podrá ser
volcado en el área social en la medida que exista una política nacional firme de
aplicación de fitoterápicos en salud humana. Un ejemplo de es el Proyecto
“Cultivando la Salud” que está desarrollando el Gobierno de Misiones,
conjuntamente con la Cooperación Italiana (COE) y la Asociación
Argentina de Fitomedicina, en el cual ya se han producido y registrado en
el ANMAT, medicamentos fitoterápicos con altos estándares de calidad y
que se están distribuyendo gratuitamente en la población cadenciada.
Finalmente es menester señalar la posibilidad de producción de nuevos cultivos
por parte del sector agroindustrial del país, el cual en los últimos diez años se
ha volcado en un altísimo porcentaje a la producción de monocultivos como la
soja. De esta manera se podrán generar nuevos polos productivos regionales,
dada la alta demanda que tienen a su vez estos productos en el exterior”.
Por último, quiero destacar la figura del Dr. Jorge Alonso, Presidente la
Asociación Argentina de Fitomedicina, quien fue el verdadero impulsor de
esta Jornada Nacional de Fitomedicamentos, como de otros tantos
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proyectos (“Cultivando la Salud”) y que gracias a su gran esfuerzo
personal y su calidad profesional, la Fitomedicina está comenzando a ser
reconocida por las Autoridades Oficiales de nuestro país, como un
elemento muy importante para la Atención Primaria de la Salud.
Felicitaciones, Dr. Jorge Alonso, por sus logros y éxitos!!!!!!!
¿EXISTE EL ADHD
Mitos, realidades y alternativas
JORNADA - DEBATE
El 14 y el 15 de Julio del corriente año, tuvo lugar en el Auditorio del
Laboratorio Dr. Madaus, la Jornada-Debate ¿Existe el ADHD? co-organizada
por el Centro de Neurología Integral de Buenos Aires, la Asociación
Argentina de Fitomedicina, SAIDAH (Sociedad Argentina de Investigación,
Docencia y Asistencia en Homeopatía) y Farmacia+Natural.
El Dr. León Benasayag (especialista en Neurología, Neuropediatría y electroencefalografía) durante su disertación.
El Dr. León Benasayag (Presidente del Centro de Neurología de Buenos
Aires), comenzó la Jornada presentando la Historia, el Diagnóstico y
Tratamiento del ADD y ADHD, mostrando las sustancias utilizadas
habitualmente por la comunidad médica para su tratamiento (metilfenidato y
otras) con sus respectivas consecuencias. Por tal motivo propuso como
Alternativas Terapéuticas:
! Partir de un diagnóstico exhaustivo realizado por un equipo
interdisciplinario.
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! Atención especializada según la característica o síntoma más
significativo: atención psicopedagógica, psicoterapia, etc.
! Otras actividades terapéuticas: terapia ocupacional que dirija los
juegos, regularización de los hábitos, cuidado de la alimentación.
! Artes marciales.
! Medicación cuando es necesaria : antihístamínicos, GABA y sus
derivados, CDPColina, Piracetam, Benzodiazepinas, etc.
La Lic. María Lucila Pazo (Lic. en Nutrición del Centro de Neurología de
Buenos Aires) presentó el tema desde su especialidad, asociando en muchos
casos estas conductas (escasa concentración, bajo rendimiento,
nerviosismo e inquietud, cansancio) con un déficit nutricional
(desnutrición encubierta: D.E.). Las consecuencias de la desnutrición
encubierta son: retraso del desarrollo psicomotor, trastornos madurativos y de
crecimiento y aumento de las infecciones. Estas carencias se encuentran en
niños de peso normal, con sobrepeso y obesos, en clases media y alta y
tienen origen en: la falta de conocimiento sobre que y como comer, los chicos
no desayunan, comen más afuera de la casa y a deshora, no realizan actividad
física y acuden al kiosco diariamente, consumiendo alimentos obesogénicos.
Por otro lado, recalcó que la alimentación correcta debe ser variada,
suficiente; bien distribuida e higiénica, siendo el desayuno de vital
importancia para la infancia; ya que de los alimentos que incluye depende el
rendimiento escolar, el análisis de la información, la capacidad de
concentración y la evocación de los conocimientos aprendidos. Por último dio
algunas recomendaciones para un desayuno saludable:
# Valorar el desayuno como momento para compartir en familia.
# Destinar de 15 a 20 minutos para realizarlo.
# Debe incluir: lácteos: leche, yogurt, quesos, cereales integrales sin
TRANS (copos, panes, etc.), frutas frescas (en trozos, jugos,
licuados), frutas secas (almendras, nueces, avellanas, etc.) y
semillas:de girasol, zapallo, chía y sésamo.
De izq. a der.: Dr. Jorge Alonso, Lic. Beatriz Janín, Dr. León
Benasayag, Dr. José L. Feldman, Lic. María Lucila Pazos y
Farm.Fernando Estevez Castillo.
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La Lic. Gabriela Dueñas (Licenciada en Ciencias de la Educación y
Psicopedagogía del Centro de Neurología de Buenos Aires) manifestó que se
está observando con gran preocupación un fenómeno que se puede
calificar de alarmante, refiriéndose al incremento de diagnósticos que entre otros- justifican el abuso de tratamientos con psicofármacos en la
población infanto-juvenil, entre ellos, el famoso ADD/ADHD. Los
diagnósticos que supuestamente justifican semejantes prescripciones médicas
pueden ser calificados – como mínimo- de “incompletos” dado que sólo
atienden a una evaluación de tipo “cuantitativa” de ciertos aspectos del sujeto
vinculados casi exclusivamente con sus funciones cognitivas haciendo
llamativa “omisión” de cualquier otro dato significativo vinculado a sus aspectos
afectivos, historia de vida, circunstancias familiares y escolares en las que se
haya inmerso el niño o el joven.
A la izq. la Lic. Gabriela Dueñas (Licenciada en Psicopedagogía)
Como respuesta a esta problemática propuso:
1-Diagnósticos abarcativos: en los que no se pierda de vista al sujeto,
niño u adolescente portador sí de un cuerpo, pero atravesado éste por una
historia, por emociones y experiencias de vida, cuya comprensión resulta
necesaria para entender su particular estilo de vincularse y aprender el mundo
que lo rodea, a los otros, a los objetos, etc.
2-Abordaje Terapéutico: el enfoque clínico debe atender a la singularidad
de cada niño u adolescente. Esto supone con frecuencia y de acuerdo a las
áreas y niveles de compromiso con el que nos encontremos, de: un
Tratamiento Clínico Psicopedagógico al niño con Orientación a padres y a la
escuela y un abordaje Psicoterapéutico al niño y a su familia.
El Dr. José Luis Feldman, (médico pediatra y homeópata, de SAIDAH Sociedad Argentina de Investigación, Docencia y Asistencia en Homeopatía-),
desde su amplia experiencia planteó:
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¿El ADHD es una entidad patológica individual o forma parte de un
trastorno de desarrollo social y emocional más amplio?
El ADHD forma parte de un grupo de síndromes que se encuentran bajo
sospecha, ya que depende en gran medida de la imagen deseada que se tiene
del niño y del umbral de tolerancia respecto de la desviación comportamental
que aceptan educadores, padres, maestros y profesionales de la salud.
Características psíquicas muy diversas son englobadas bajo un mismo
diagnóstico y tratamiento:
1) niños con dificultades transitorias para concentrarse (Por migraciones,
separación de la pareja parental, duelos, mala elección de la escuela o
didáctica inapropiada).
2) Niños cuya falta de concentración es efecto de una falla profunda en el modo
en que se constituyó su psiquismo (su pensamiento y sus afectos), y no logran
priorizar algunos estímulos e inhibir otros para poder prestar atención y
aprender
3) Niños con una buen armado psíquico que se encuentran bajo los efectos de
un traumatismo grave que atrapa toda su atención: maltrato infantil, abuso
sexual, violencia familiar, situaciones de catástrofe natural o social).
Para los pediatras la inquietud de los niños y las alteraciones de conducta son
las causas más frecuentes de consulta en el área de la salud mental. Hoy se
define como conducta, toda actividad fuera de las simples funciones fisiológicas
necesarias para mantener la vida. En cuanto al diagnóstico diferencial; el
motivo de consulta es el niño inquieto y se debe intentar definir si se trata de un
niño normal o si presenta alguna patología. Si se plantea que presenta una
patología, es necesario realizar algún grado de diagnóstico diferencial, para
saber adónde derivarlo, ya que la inquietud forma parte de varios trastornos
psíquicos, psiquiátricos, neurológicos y médicos.
Para realizar la evaluación correcta se debe determinar:
•
•
•
•
•
si la conducta inquieta significa peligro físico para el niño y los demás,
el grado de interferencia de esta inquietud con el aprendizaje del niño,
el grado de presión, por parte de los colegios, los padres u otros
profesionales, que necesitan que el niño sea tranquilo en sus actividades
o durante una hospitalización o procedimiento,
hasta qué punto se sitúa esta inquietud fuera de los límites normales
para el grupo de pares,
es importante conocer el contexto en el cual se desenvuelve este niño y
la posible reducción de la calidad de vida del niño y de la familia debido
a la inquietud.
¿Cuál es el riesgo de meter todo en una misma bolsa y medicarlos
indiscriminadamente?
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Además de que el metilfenidato no es inocuo ya que actúa como una
anfetamina, se pierde la oportunidad de que un niño y una familia exploren y
comprendan las causas de su sufrimiento y se alivien, permaneciendo intactas
las razones que lo llevaron a organizar el trastorno de atención y la
hiperactividad, aunque con la medicación disminuyan a veces transitoriamente
los síntomas.
El Dr. Jorge Alonso, médico clínico, Presidente de la Asociación Argentina de
Fitomedicina, comenzó su exposición, planteando si el ADHD siempre existió, ya
que entonces figuras tan reconocidas como Mozart, Einstein y Dalí, por sus
características tan particulares, podrían haber sido encuadrados como niños
ADHD. Luego siguió con el abordaje fitoterapéutico, para el cual citó a los
Adaptógenos, sustancias derivadas de plantas medicinales que permiten
enfrentar las situaciones traumáticas de un entorno desfavorable, tales como al
Eleuterococo (corteza de la raíz de Eleuterococcus senticosus) o el ginseng
norteamericano (raiz de Panax quinquefolius) entre otros; al Ginkgo biloba, por
producir mejorías del área cognitiva en general a través de lograr una mejor
oxigenación a nivel neuronal; la Valeriana officinalis por sus propiedades
sedantes sin generar adicción o dependencia y al Amaranto (Amaranthus
caudatus, Amaranthus mantegazzianus, Amaranthus sp.) por sus propiedades
nutritivas como alimento (una de las fuentes más importantes de proteínas,
contiene el aminoácido Lisina, además hierro y calcio. Por último aclaró que el
ADHD se trata con ADHD, es decir: A (AMOR, ALIMENTACIÓN ADECUADA,
ACTIVIDAD FÍSICA) D (DIÁLOGO FAMILIAR, DROGAS NO DAÑINAS) H
(HOMEOPATÍA,
HIERBAS
MEDICINALES)
D
(DIRECTRICES
PSICOPEDAGÓGICAS; DOCENTES PREPARADOS) y cerró su exposición
con palabras del Dr. Florencio Escardo “Mientras más escucho a mis
pacientitos, menos necesidad tengo de medicarlos”.
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El Farm. Fernando Estevez Castillo presentó el Informe del Indec
correspondiente a la facturación de la Industria Farmacéutica del primer
trimestre del año 2006 comparado con iguales períodos desde el 2001 al 2005,
donde se pudo ver que el rubro con mayor facturación y más crecimiento es
el correspondiente al Sistema Nervioso y específicamente aquel que
agrupa a las drogas utilizadas para tratar el ADHD, tales como el
metilfenidato. Además coordinó la Mesa Redonda final, que contó con la
importante participación de la Lic. Beatriz Janín (Directora de la Carrera de
especialización en Psicoanálisis en niños –UCES) quién volcó toda su
experiencia docente y profesional al responder todas las preguntas de los
asistentes, además de presentar su punto de vista coincidente con lo expresado
por todos los panelistas.
NOVEDADES
NUEVOS PRODUCTOS
BIOLIP®
OMS, División Cosmética de Laboratorios Dr. Madaus & Co., ha lanzado
BIOLIP®, una emulsión con poderosa acción lipolítica remodelante, eficaz
en la reducción del contorno corporal y en el tratamiento de nódulos
adiposos. Por los activos que contiene (Ciclolipase®, Spirulina, Cafeína,
Sepitonic M3®, Ruscus y Guaraná), tonifica y reduce la flaccidez en forma
sinérgica, actuando como renovador celular a la vez que revitaliza, hidrata y
mineraliza, mejorando la textura de la piel, promoviendo la eliminación de
agua y toxinas de los tejidos, reactivando la circulación.
BIOLIP® está libre de fragancias sintéticas y derivados animales, además
de ser hipoalergénico, como toda la línea de productos OMS.
Para más información:
OMS División Cosmética de Laboratorios Dr. Madaus & Co. S.A.
Av. Luis María Campos 585 – Buenos Aires – Argentina (C1426BOD)
Tel.: (54) (11) 4771-1734 / 4772-2428
Fax: (54) (11) 4775-4380
e.mail: [email protected]
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LIBROS
$ CHIA, redescubriendo un olvidado alimento de los aztecas, 1° Ed., año
2006. Ricardo Ayerza (h) y Wayne Coates. Editorial Del Nuevo Extremo.
La CHIA, uno de los cuatro cultivos principales de los aztecas cuando Colón
llegó al Nuevo Mundo, ofrece el mayor contenido de ácidos grasos omega-3
disponible en el reino vegetal. Las civilizaciones precolombinas usaron la chía
como materia prima para elaborar medicinas, compuestos nutricionales , y
como fuente energética en los viajes prolongados. En este libro, dos
ingenieros, uno en producción agropecuaria y otro en maquinaria agrícola,
revelan el potencial moderno de este olvidado cultivo, comparan los perfiles de
los ácidos grasos de la CHIA con los de otras fuentes importantes de omega-3:
aceite de pescado, semillas de lino y algas marinas y suministran evidencia de
que la chía es superior a ellas en numerosos aspectos.
Para más información:
Av. Luis María Campos 575 (C1426BOD)
Buenos Aires – Argentina
Tel.: 54-11-4774-5010
Web: www.farmaciamasnatural.com.ar
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CURSOS, SEMINARIOS Y ATENEOS
SEMINARIO
La Sociedad Argentina de Investigación, Docencia y Asistencia Homeopática
invita a los colegas, médicos, veterinarios y farmacéuticos homeopáticos al
próximo:
SEMINARIO DE CLINICA MEDICA Y FARMACIA HOMEOPATICA
a realizarse el próximo sábado 18 de noviembre de 9 a 14 hs. en el Salón
Auditorio del Laboratorio Madaus, sito en la Av. Luis María Campos 573 de la
Ciudad Autónoma de Buenos Aires.
Programa a desarrollar
09:00 a 10:00 hs.
POSIBILIDADES CONCRETAS DE APLICACIÓN DEL TRATAMIENTO
HOMEOPATICO EN LA ATENCION PRIMARIA EN COMUNIDADES DE
NUESTRO PAIS
Dr. José Luis Feldman
10:00 a 11:00 hs.
CRITERIO PARA EL EMPLEO DE MEDICAMENTOS “CHICOS”
EN ENFERMEDADES “GRANDES”
Dr. Ricardo J. Alvarez
11:00 a 11:30 hs.
PREGUNTAS DE LOS ASISTENTES.
11:30 a 12:00 hs.
INTERVALO
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12.00 A 13.30 hs.
MESA REDONDA
PRESCRIPCION Y DISPENSACION DEL MEDICAMENTO HOMEOPATICO.
POSIBILIDADES DE MALA PRAXIS MEDICA, VETERINARIA Y
FARMACEUTICA.
Coordinan:
Farm. Fernando Estevez Castillo – Dr. José L. Feldman
Invitados:
Médicos, Veterinarios y Farmacéuticos
(representantes de las diversas Instituciones Homeopáticas)
13:30 a 13:50 hs.
PREGUNTAS DE LOS ASISTENTES
13:50 a 14:00 hs.
CONCLUSIONES Y CIERRE DEL SEMINARIO
INSCRIPCION: Tel.: (011) 4432-1722 - 4774-5010 - 4632-1074
ARANCEL: $ 25,00.VACANTES LIMITADAS
ATENEOS
ATENEOS 2006
DEPARTAMENTO DE HOMEOPATIA
FACULTAD DE MEDICINA DE LA UNIVERSIDAD MAIMONIDES
Miércoles 15 de Noviembre de 12:30 a 14:00 hs
Ateneo bibliográfico. Tema: DSM-IV y semiología homeopática
Presenta: Dra. María Eva Badía
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Miércoles 6 de Diciembre de 12:30 a 14:00 hs
Ateneo Clínico (12:30 a 14:00)
Presenta: Dr. Juan Eizayaga
Lugar:
Universidad Maimónides, Hidalgo 775 Aula 504, Buenos Aires
Dirgidos a:
Médicos de todas las especialidades y estudiantes de medicina avanzados
(Entrada libre)
Informes e inscripción:
Departamento de Homeopatía
Facultad de Ciencias Médicas
Universidad Maimónides
Hidalgo 775, (1405), Buenos Aires, Argentina
Tel/Fax: (54-11)4905-1142
[email protected]
www.homeos.org
CURSOS
CURSO DE ALERGIAS Y ALIMENTACION EN EL NIÑO
Miércoles 8, 15, 22 y 29 de Noviembre de 2006, de 18:00 a 20:00 hs
Temario:
Alimentación en embarazo y lactancia. Alimentación infantil: trastornos del
aprendizaje y la conducta –ADD-Hiperactividad. Alergias alimenticias, dietas de
eliminación. Alimentación en el adolescente: cómo cubrir las necesidades
nutricionales.
Dictado por:
Dra. María Laura Aiello
(Médica pediatra, miembro de la SAP y de la Comisión de Lactancia Materna,
miembro de la Asociación Argentina de Médicos Naturistas)
Informes e inscripción:
Asociación Argentina de Médicos Naturistas
Serrano 669, Buenos Aires, Argentina
Tel/Fax: (54-11)4856-4443
[email protected]
www.aamenat.org.ar
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