EDITORIAL ESPANOL:

====================

En esta revisión del mes de Abril año 2003, hay 10 nuevas publicaciones, y destaca, la salida al mercado, para esa década, la presentación del FINASTERIDE, en forma de crema tópica, para el tratamiento del HIRSUTISMO en la mujer. 

Primeramente salió el PROSCAR, de 5 mg y luego la PROPECIA  de 1 mg, (Laboratorio MERCK SHARP & DOHME), para uso oral, inhibidor de la enzima 5-alfa reductasa, que es la que evita la producción del metabolito DIHIDROTESTOSTERONA (DHT), responsable de la alopecia androgénica.

Posteriormente sacaron la presentación en crema tópica al 0.025% para el tratamiento del HIRSUTISMO EN LA MUJER con gran resultado, que son las publicaciones destacadas de este bloque (Referencias 10,11,12,13,14 y 15)

Debemos recordar que la FDA aprobó en el año 2001 la MOLÉCULA DUTASTERIDE, bajo el nombre de AVODART, (Lab. Sandoz y otros), también para el tratamiento de la ALOPECIA ANDROGÉNICA, e HIRSUTISMO, en forma oral, tópica y ampollas, para microinyecciones en el cuero cabelludo.

Pero estas medicinas, ambas, FINASTERIDE y DUTASTERIDE, fueron inventadas y descubiertas para el tratamiento de la HIPERPLASIA PROSTÁTICA BENIGNA (HPB), en el hombre, su efecto secundario, al inhibir la enzima 5-alfa reductasa se traduce en la regeneración de los folículos pilosos, luego fueron utilizadas en el HIRSUTISMO en la MUJER.

Hay que destacar que AMBAS MEDICINAS no tienen gran efecto en la ALOPECIA ANDROGÉNICA en la MUJER, se requieren DOSIS más altas y tratamientos mas prolongados, y en el caso de la ALOPECIA POSTMENOPÁUSICA, la efectividad es similar al placebo, es decir casi nula.

Hoy 2024 ambos medicamentos siguen en el mercado, tanto la FINASTERIDE como el DUTASTERIDE. La presentación en forma tópica, en algunos países es dificil de conseguir, o no esta disponible. Tienes que recurrir a mercados internacionales para acceder a ella.

Aqui te dejo dos enlace sobre: FINASTERIDE 5MG VS FINASTERIDE 1 MG EN LA ALOPECIA ANDROGÉNICA. 

El otro enlace, una medicina naturista: SERENOA REPENS Y FINASTERIDE EN LA ALOPECIA ANDROGÉNICA.

También destacan en esta revista, los efectos secundarios de los tatuajes y piercings: una ENDOCARDITIS BACTERIANA por un piercing en la lengua (7), y una infección por MICOBACTERIA ATÍPICA, luego de tatuaje (3).

Saludos,,,

Dr. José Lapenta R.,,,

 EDITORIAL ENGLISH:

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In this review of April 2003, there are 10 new publications, and the most notable is the launch of FINASTERIDE, in the form of a topical cream, for the treatment of HIRSUTISM in women.

First came PROSCAR, 5 mg, and then PROPECIA, 1 mg, (MERCK SHARP & DOHME Laboratory), for oral use, an inhibitor of the enzyme 5-alpha reductase, which prevents the production of the metabolite DIHYDROTESTOSTERONE (DHT), responsible for androgenic alopecia.

Later, they brought out the topical cream presentation at 0.025% for the treatment of HIRSUTISM IN WOMEN with great results, which are the highlighted publications of this block (References 10,11,12,13,14 and 15)

We must remember that in 2001 the FDA approved the DUTASTERIDE MOLECULE, under the name AVODART, (Lab. Sandoz and others), also for the treatment of ANDROGENIC ALOPECIA, and HIRSUTISM, in oral, topical and ampoule form, for microinjections in the scalp.

But these medicines, both FINASTERIDE and DUTASTERIDE, were invented and discovered for the treatment of BENIGN PROSTATIC HYPERPLASIA (BPH) in men, their side effect, by inhibiting the enzyme 5-alpha reductase, results in the regeneration of hair follicles, then they were used in HIRSUTISM in WOMEN.

It should be noted that BOTH MEDICINES do not have a great effect on ANDROGENIC ALOPECIA in WOMEN, higher DOSES and longer treatments are required, and in the case of POSTMENOPAUSAL ALOPECIA, the effectiveness is similar to placebo, that is, almost zero.

Today, in 2024, both drugs are still on the market, both FINASTERIDE and DUTASTERIDE. The topical presentation is difficult to obtain in some countries, or is not available at all. You have to resort to international markets to access it.

Here are two links about: FINASTERIDE 5MG VS FINASTERIDE 1 MG IN ANDROGENIC ALOPECIA.

The other link, a natural medicine: SERENOA REPENS AND FINASTERIDE IN ANDROGENIC ALOPECIA.

Also highlighted in this magazine are the side effects of tattoos and piercings: a BACTERIAL ENDOCARDITIS from a tongue piercing (7), and an ATYPICAL MYCOBACTERIA infection after a tattoo (3).

Greetings,,,

Dr. José Lapenta R. 

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REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES 

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1.) THE VIRUS OF THE SARS DIES FOR CLIMATOLOGICAL CHANGES.

2.) Smallpox Vaccination and Cardiac Complications / Vacunacion contra viruela y complicaciones cardiacas.

3.) A tattooed butterfly as a vector of atypical Mycobacteria / tatuaje en mariposa vector de una micobacteria atipica.

4.) Thalidomide for treatment of severe generalized discoid lupus lesions in two patients with systemic lupus erythematosus / Talidomida para el lupus.

5.) Cialis for impotency & erectile dysfunction / Cialis para la impotencia y disfuncion erectil

6.) Papaya, the Wonder Fruit / La lechosa fruta maravillosa.

7.) Haemophilus aphrophilus Endocarditis after Tongue Piercing / Endocarditis despues de piercing en la lengua.

8.) Is bupropion (Zyban) causing deaths? / medicina para dejar de fumar ocasiona muertes ?.

9.) Polycystic Ovary Syndrome.

10.) Finasteride cream in hirsutism / Finasteride en crema para el hirsutismo.

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1.) THE VIRUS OF THE SARS DIES FOR CLIMATOLOGICAL CHANGES

 Author: Lapenta JJ, Dermatologist, DERMAGIC/EXPRESS   April 2.003

The first thing that we have to think with this new VIRUS of THE ATYPICAL

PNEUMONIA, of the type coronavirus who the big scientists have classified as a

MUTATION of some type of virus of THE INFLUENZA, is the places where he appeared

and the countries that I contaminate and WHEN he APPEARED. Also the mortality of the

same one that doesn't arrive neither to 4% of the total of cases. The race but affected

the Asian.

It is said that the VIRUS APPEARED in November of the 2.002 in the China, and he left

disseminating for different countries WHERE THE CLIMATE has allowed that the virus

MULTIPLIES, in other countries this has not happened. As example of this can mention to

SOUTH AMERICA where from MEXICO until the ARGENTINEAN until last week some

cases had been reported (less than 5). Neither in Venezuela, neither in Colombia, Peru, Chile,

Paraguay, Ecuador, Mexico, Cuba, Peru, and all South America, Brazil single 2 cases with

but of 165 million inhabitants.

Already Germany development a quick method to detect the Virus, which still continues being

disseminated, but the measures of sanitary control have avoided bigger wrongs.

In a program published by CNN in Spanish a scientist he says that to the VIRUS you should

not combat with antibiotics BECAUSE they don't RESPOND TO THESE

MEDICATIONS, but I PARTICULARLY don't AGREE, because when administering

antibiotics and or antivirales, THESE combatting a probable secondary infection, on the other

hand. It has been demonstrated that antibiotics as the ERYTHROMYCIN AND OTHERS

have the property of eliminating VIRAL infections, when modifying the person's immunologic

answer.

Another aspect to stand out in my opinion is that this it is A CREATED VIRUS IN A

LABORATORY, the genetic manipulation of the virus like BIOLOGICAL weapon is

something of what I have spoken for a long time. The VIRUS was TAKEN OUT before the

War from IRAQ, to prove its MORTAL CAPACITY.

For years the DERMAGIC comes denouncing a POSSIBLE biological WAR, THE VIRUS

OF THE SMALLPOCK could not come out to the street, they left it kept, because THE

ONE NUMBERS OF DIED it would reach the sky. They preferred to be played it with a

VIRUS OF LOW MORTALITY like that of the atypical Pneumonia that has alone a

mortality of 4%. IMAGINE THE SCANDAL with A VIRUS OF HIGH MORTALITY like

that of the SMALLPOCK

I find to believe in a GENETIC MUTATION RIDICULOUS, it is a virus of

LABORATORY. Who throw it to the street? Only GOD KNOWS IT.

But those that CREATED THE VIRUS, didn't think THAT THE CLIMATOLOGICAL

CONDITIONS will put an end to THE VIRUS. Because to Suramerica I don't arrive, and

not for SANITARY measures, I don't arrive because he doesn't HAVE CAPACITY OF

MULTIPLICATION IN OUR CLIMATE, and that will know it in Europe and those

affected countries when they change the stations. If the Virus RESISTS undoubtedly it was

confirmed that it is SUPER a CREATED VIRUS IN A LABORATORY.

My final recommendation for ALL THOSE AFFECTED are to go up the TEMPERATURE

OF THE ROOMS WHERE THE PATIENTS are, while more hot, BETTER, more cool, more survival for the VIRUS. Also not to forget to give antibiotics, and or antivirals with having proven capacity to modify the patient's immunologic answer.

greetings

Dr José Lapenta

EL VIRUS DEL SARS MUERE POR CAMBIOS CLIMATOLOGICOS

 Author: Lapenta JJ, Dermatologist, DERMAGIC/EXPRESS   April 2.003

Lo primero que tenemos que pensar con este nuevo VIRUS de LA NEUMONIA ATIPICA, del tipo coronavirus, quienes los grandes cientificos han catalogado como una MUTACION de algun tipo de virus de LA INFLUENZA, es los sitios donde aparecio y los paises que contamino y CUANDO APARECIO. Tambien la mortalidad del mismo que no llega ni a un 4% del total de casos. La raza mas afectada la Asiatica.

Se dice que el VIRUS APARECIO en Noviembre del 2.002 en la China, y se fue diseminando por diferentes paises DONDE EL CLIMA ha permitido que el virus SE MULTIPLIQUE, en otros paises esto no ha ocurrido. Como ejemplo de esto podemos mencionar a SUR AMERICA donde desde MEXICO HASTA la ARGENTINA solo hasta la semana pasada se habian reportado algunos casos (menos de 5). Ni en Venezuela, ni en Colombia, Peru, Chile, Paraguay, Ecuador, Mexico, Cuba, Peru, y toda Sur America, Brazil solo 2 casos con mas de 165 millones de habitantes.

Ya Alemania desarrollo un metodo rapido para detectar el Virus, el cual todavia sigue diseminandose, pero las medidas de control sanitario han evitado males mayores.

En un programa publicado por CNN en español un cientifico dice que al VIRUS NO se debe combatir con antibioticos PORQUE ellos NO RESPONDEN A ESTOS MEDICAMENTOS, pero YO PARTICULARMENTE NO ESTOY DE ACUERDO, pues al administrar antibioticos y o antivirales, ESTAS combatiendo una probable infeccion secundaria, por otra parte. Se ha demostrado que antibioticos como la ERITROMICINA Y OTROS tienen la propiedad de eliminar infecciones VIRALES, al modificar la respuesta inmunologica de la persona.

Otro aspecto a resaltar en mi opinion es que este ES UN VIRUS CREADO EN UN LABORATORIO, la manipulacion genetica de los virus como arma BIOLOGICA ES algo de lo que se viene hablando hace mucho tiempo. El VIRUS FUE SACADO antes de la Guerra de IRAK, para probar su CAPACIDAD MORTAL.

 

Desde hace años el DERMAGIC viene denunciando una POSIBLE GUERRA biologica, EL VIRUS DE LA VIRUELA no podia salir a la calle, lo dejaron guardado, pues LA MORTANDAD SERIA GRANDE. Prefirieron jugarsela con un VIRUS DE BAJA MORTALIDAD como el de la Pneumonia atipica que tiene solo una mortalidad del 4%. Imaginense el ESCANDALO QUE ESTO HA PRODUCIDO, que hubiese ocurrido si hubiese sido EL DE LA VIRUELA

Creer en una MUTACION GENETICA me parece RIDICULO, es un virus de LABORATORIO. Quien lo tiro a la calle ? Solo DIOS LO SABE.

Pero los que CREARON EL VIRUS, no pensaron QUE LAS CONDICIONES CLIMATOLOGICAS iban a acabar con EL VIRUS. Pues a Suramerica no llego, y no por medidas SANITARIAS, no llego porque NO TIENE CAPACIDAD DE MULTIPLICACION EN NUESTRO CLIMA, y eso lo sabremos en Europa y esos paises afectados cuando cambien las estaciones. Si el Virus RESISTE indudablemente quedara confirmado que es un SUPER VIRUS CREADO EN UN LABORATORIO.

Mi recomendacion final para TODOS LOS AFECTADOS es subir la TEMPERATURA DE LAS HABITACIONES DONDE ESTAN LOS PACIENTES, mientras mas calor MEJOR, mas frio, mas supervivencia para el VIRUS. Tambien no olvidar suministrar antibioticos y o antivirales con probada capacidad de modificar la respuesta inmunologica del paciente.

Saludos

Dr Jose Lapenta

 

2.) Smallpox Vaccination and Cardiac Complications / Vacunación contra viruela y complicaciones cardiacas.

By John G. Bartlett M.D.

posted 03/27/2003

Source: CDC and NYC Department of Health Alert #11 (3/26/03)

The CDC has reported 7 adverse cardiac events among 25,645 persons vaccinated through 3/21/03. This includes 3 acute myocardial infarcts including 1 lethal MI, 2 cases of angina and 2 cases of myopericarditis. The onset of these complications is 2-17 days post-vaccination. The expected mortality without vaccination based on the age and number of vaccinia recipients is 2 deaths in 3 weeks. Causal relationship is not yet established.

Myopericarditis was reported in 2 of the 25,645 health care workers who received the vaccine, 10 of approximately 500,000 military recruits who were vaccinated, and 1 of 17,000 Israeli health care workers (who received the Lister strain vaccine).

As a result of these observations, the CDC is recommending that the vaccine should be deferred in people with known cardiac disease (myocardiopathy, prior MI, angina, or other evidence of coronary artery disease). The New York City Health Department recommends extension of this recommendation to defer vaccination in those with household or intimate contact with heart disease

3.) A tattooed butterfly as a vector of atypical Mycobacteria / tatuaje en mariposa vector de una micobacteria atipica

J Am Acad Dermatol 2003;48:S73-4.

Ronni Wolf, MDa,b

Danny Wolf, MDc

Tel Aviv and Kupat Holim, Israel

Abstract

We report the first case of cutaneous inoculation of atypical Mycobacteria secondary to tattooing. The diagnosis of atypical Mycobacteria infection of the skin was confirmed on the basis of the clinical and histologic appearance, the detection of acid-fast bacilli on Ziehl-Neelsen stain, and positive polymerase chain reaction. The medical complications of tattooing, which are manifold, are briefly summarized. This case emphasizes the need for federal regulation of tattooing, which is an invasive procedures associated with infectious and noninfectious complications.

4.) Thalidomide for treatment of severe generalized discoid lupus lesions in two patients with systemic lupus erythematosus / Talidomida para el lupus.

J Am Acad Dermatol 2003;48:S89-91.

Case Reports

Abdullah Alfadley, MD

Hanan Al Rayes, MD

Walid Hussein, MD

Abdullah Al Dalaan, MD

Khalid Al-Aboud, MD

Riyadh, Saudi Arabia

Abstract

We describe 2 patients with systemic lupus erythematous whose widespread discoid lupus erythematosus was unresponsive to systemic steroids and antimalarial agents. They showed dramatic improvement to thalidomide at a dose of 300 mg/d, with maximum benefit achieved within 15 weeks of therapy. Dosages of 50 to 100 mg/d were effective in maintaining remission for 1 year. However, thalidomide-induced neuropathy was observed in both cases.

5.) Cialis for impotency & erectile dysfunction / Cialis para la impotencia y disfuncion erectil

Source http://www.cialis-impotence-drug.com/index.html

What is Cialis?

Cialis is an emerging tablet-based oral treatment for impotency & erectile dysfunction (ED), which will soon be licensed for prescription, enabling you to buy online. Like Levitra, Cialis is proving highly successful in clinical trials and is generating major interest as a real alternative to Viagra and Uprima.

Cialis, being developed by Lilly, is currently undergoing approval and is competing with Levitra to be the next major treatment for ED on the market.

Where can I get Cialis?

It is not possible to obtain genuine Cialis yet or buy Cialis online, as it is still under its approval phase and won't be scheduled for release until early 2003. The delay in Levitra puts Cialis on equal or better competitive footing meaning that Cialis could reach the market first.

Activemed, the UK's leading online source for safe and genuine prescription medicines, is keeping a close eye on developments of this new impotency treatment, and will be the first to offer this medicine online once it is available. Check this information page for latest updates and information on Cialis.

How effective is Cialis in treating Erectile Dysfunction?

Cialis has seen major interest worldwide following the results of a recent clinical study on nearly 400 men with ED. The study was designed to evaluate the efficiency of Cialis at specific time points after dosing (24 or 36 hours). The case studies for Cialis showed that::

88 percent of men achieved erections in 30 minutes or less.

Cialis continued to stay in the system for up to 24 hours!

Cialis statically out performed the placebo at the two points of testing.

In secondary measures of efficacy - including the ability to penetrate, satisfaction with hardness of erection and overall satisfaction, Cialis was superior to the placebo at both 24 and 36 hours.

Does Cialis have side effects?

A small number (>5 percent) of those involved in the clinical trails reported mild side effects with the treatment, mostly including headaches, flushing and upset stomachs.

Cialis and cardiovascular side effects

These early tests seem to indicate that Cialis doesn't affect blood pressure as much as other ED drugs. The clinical trials showed that statistically there was no significant difference in cardiovascular side effects from the placebo. Tests are still in their early stages, but Activemed will keep you informed of any developments.

Is Cialis more effective than Viagra or Uprima?

There is currently no direct evidence from clinical trials or otherwise to compare the effectiveness of treatments such as Cialis and Levitra, against others such as Viagra and Uprima.

However, early findings do seem to indicate that Cialis may be especially effective in treating ED in patients at greater risk of cardiovascular events.

Can I mix Cialis with other medicines?

This will not be known until Cialis is fully licensed and legally available. Early tests have indicated that it should not be taken with nitrate-based medicines for heart conditions.

Can I take Cialis if I have a heart condition?

This will not be known until Cialis is fully licensed and legally available, although early findings do indicate that Cialis does not significantly affect blood pressure.

 

6.) Papaya, the Wonder Fruit / La lechosa fruta maravillosa

Source: http://www.europeanvegetarian.org/

Barbara Simonson -lecture given at the EVU Congress in Widnau 1999

from European Vegetarian, Issue 1/2000

Papaya Fruit

It was about 14 years ago, when I was in Maui, Hawaii, where for the first time I had the pleasure to enjoy the sweet taste of sun-ripened, organically grown papayas. In the health food store in Paista, I found dried papaya seeds in little glasses, called "Papaya Enzymes", for about $5 each glass. I was surprised. Why do people throw the seeds away when eating the fruit, and afterwards buy them again for a lot of money? How silly! So, when my then fiancé, Aeoliah, and I had a tropical breakfast, I ate my papaya like an apple - including the kernels! My fiancé was shocked. "This is not the way one eats papayas!" he shouted at me. This did not bother me, and since then I eat the papaya whole - including skin and seeds.

Now that I have written a whole 200-page book on this "wonder fruit", the Carica Papaya (that is its Latin name), I know why papaya seeds are so healthy, and why you should not throw the skin away either. The people on Cuba call the papaya "Fruta de Bomba", since it is shaped like a bomb. I discovered that the papaya is a "bomb" of vital nutrients! It is packed with enzymes, vitamins and minerals. The papaya-enzymes like Papain are mainly concentrated in the half green fruit the ripe seeds as well as in the leaves of this plant. So, do not throw the seeds away! If you do not like the bitter, spicy taste, dry them and use them like black pepper. They look like pepper, taste like pepper, yet are much healthier than pepper!

In Costa Rica and Mexico, the natives there call the papaya "Tree of Good Health" and regard it as a healing remedy for almost all diseases. The papaya tree grows very quickly, up to 10 meters in height. It doesn't need much care. In South America, its homeland, it grows like weeds. The red Indians of South and Middle America use the papaya not only for food, but also for healing wounds, for supporting a weak liver, for healing constipation, against worms and parasites, for healing inflammation and skin problems and even for treating cancer. They are the "inventors" of modern enzyme therapy! When you live on raw food, you can of course forget about papaya as a healing remedy. The more sensitive you get, the more you feel the purifying and nourishing effects of this tropical fruit, even while eating!

What are the main ingredients of the papaya, that grows as long as 120 centimeters in Venezuela (this species is called "Lechosa")? There are a lot of antioxidants in the papaya, as beta carotene- more than in carrots! - and Vitamin C - more than in kiwis! - and a lot of Bioflavonoids. The papaya contains a lot of minerals like Potassium, Magnesium and Calcium and is the most alkaline fruit we know. For anybody suffering from the effects of cooked food, sugar and meat consumption like "Acidosis" (the body gets too acid, and the person is irritable and depressed), it is recommended to start the day with a papaya breakfast. Some doctors recommend "papaya cures": Take at least one papaya everyday for four weeks. After a week or so, you experience the results: more energy, less sleep, a good mood and clear thoughts. Unbelievable?! Try it and see for yourself!

The papaya-enzymes help to digest proteins, fats and starches. Columbus discovered not only America, but also the papaya. When he reached the South-American shores, he was greeted by the natives with a feast. The sailors ate too much after the long journey, and the Indians took them to the rain-forest and offered them papayas for releasing their pain. And it worked! So, if you overeat the fruit Durian, which is a little hard to digest because of all the fat, you can eat a papaya afterwards to help digestion. Of course, it is better to eat moderately, even as a raw foodist! The papaya-enzymes help purify your intestines and help remove protein residue. Moreover, the papaya helps to nourish our endocrine system, as Norman Walker has written at length in his book on juicing.

Papaya helps the body to produce more Arginin, that is an essential amino acid that activates HGH, a growth hormone that is important for cell rejuvenation and rebuilding of cells in the liver, in muscles and in the bones. Even the skin benefits from Arginin - it gets smooth and is able to regenerate. The beautiful women in the Tropics use unripe papaya for getting rid of wrinkles and old skin cells. I tried it once, on the Canary islands - and had to scream, so much did this hurt! Our skin is probably much thinner than the skin of these women, who are exposed to the sun all day long. I recommend to dilute papaya juice for treating the skin, and have included several recipes for skin masks and creams in my papaya book.

The aborigines in Australia and the Kahunas on Hawaii use the papaya as a remedy for cancer. The papaya should be half-ripe then, between yellow and green. I have a friend, Halima Neumann, who was healed from stomach cancer by drinking the juice of papayas for six months, half a liter each day, and after that eating half-ripe papayas every day. Most of the enzymes are contained in the fruit flesh of the unripe papaya and the seeds of the ripe one. The unripe papaya tastes bitter, so I would not eat them normally. The unripe papaya is the only unripe fruit that alkalines the body! Good for her: After that cure, she decided to change her diet and become raw-foodist and started to meditate and heal her childhood. Now, she is 50 years old, enjoys vibrant health and has written some books in German about her experiences. She lives on the Canary Islands and gives seminars on how to live healthily with raw food and how to grow organic papayas.

On Maui, there is a funny guy living in Paia who calls himself "Papaya John". His normal name is John McCollum, and he has got a little shop called "Papaya John", selling only papayas and papaya products like dried papayas. He regards the papaya as medicine and is quoted in the "Maui News" with: "A Papaya a day keeps the doctor away". Papaya John is an organic farmer and surfer and turned papaya messiah. His mission: "My main interest is getting enzymes into you on a daily basis.", and calls the papaya "the tropical miracle fruit".

Papaya John learnt the secrets of the papaya from Dr. Koesel, one of the original California health food advocates, who moved to Maui in the '60s. There the two men met, and for John, the encounter was "magic": "I knew I had some kind of lifetime karma with this man." He studied all the health benefits of the papaya with him. When Dr. Koesel died in 1990, one week before his 90th birthday, for Papaya John it was obvious: "I have a commitment with God and Dr. Koesel. I believe in the papaya and it is my task to spread the good news." He began experiencing a level of radiant health and joy of life that he only dreamt of before. Now he grows 22 pound papaya fruits in his garden and would not live in a country where papayas do not grow. Papaya John smiles: "I am addicted to papaya enzymes!" Every morning, he drinks a lot of papaya juice and feels great. His surfboard is decorated with a huge papaya, and he takes his self-made papaya-bars, enzyme-active, wherever he goes or travels.

You do not have to center your life on the papaya in order to benefit from it. And, you can start trying out how much better you can feel even as a raw foodist by including papayas in your daily food choice! You can grow papayas easily in your backyard garden or, if you have, in a winter-garden for colder climate zones like Germany. In summer, I have my papaya trees outside, and take them in in the winter time. I even composed a hymn called "A Papaya A Day" I will share with you now. It is also included in my papaya book, including notes.

"Dismiss maya, eat papaya!" (David Wolfe)

A Papaya A Day

A papaya a day keeps the doctor away.

Take two or three and you will see:

You feel healthy and fine,

And you'll start to shine!

Life gets happy as could be,

Life gets happy as could be.

Papaya Fruit Salad

Mix pieces of ripe papaya with banana and mango slides. Serve with a little lemon juice.

Papaya Smoothie

For this Smoothie, you need five dried apricots, a big apple, half a papaya, pealed and cut into pieces. Soak the apricots overnight. Put everything into the Champion and mix until smooth. Makes a great breakfast, you also can use the Smoothie as a dressing for fruit salads.

Pina Colada

For this healthy drink, you need one cup of pineapple flesh, half a papaya, peeled and cut into pieces, one cup of cut fresh coconut flesh, and half a cup of pure water, if desired. Put the pineapple and papaya in the Juicer mix all the ingredients in the mixer. Serve with a leaf of peppermint. Simply delicious!

Papaya-Salsa

You need 1 1/2 cups of papaya, cut in pieces, the same amount of sweet, red peperoni, a teaspoon full of lemon juice, a teaspoon full of honey, very little ground red pepper. Mix all the ingredients. This makes a great dip for a raw food-salad.

My pocketbook "Papaya, healing with the Wonderfruit" will be available soon in the States. (Lotus Light Publications)

BARBARA SIMONSOHN,

HOLBEINSTR. 26

D - 22607 HAMBURG

TEL.: +49 40 - 89 53 38

FAX: +49 40 - 89 34 97

E-MAIL: BASIM@BARBARA-SIMONSOHN

7.) Haemophilus aphrophilus Endocarditis after Tongue Piercing / Endocarditis después de piercing en la lengua.

Source;http://www.cdc.gov/

Hossein Akhondi* and Ali R. Rahimi*

*Mercer School of Medicine, Savannah, Georgia, USA

Piercing invades subcutaneous areas and has a high potential for infectious complications. The number of case reports of endocarditis associated with piercing is increasing. We studied a 25-year-old man with a pierced tongue, who arrived at Memorial Health University Medical Center with fever, chills, rigors, and shortness of breath of 6 days' duration and had an aortic valvuloplasty for correction of congenital aortic stenosis.

Body piercing poses a risk for serious disease. Because it invades subcutaneous areas, piercing has a high potential for infectious complications. Such complications result from introduction of skin or mucous membrane microflora into subcutaneous tissue or from the ongoing presence of colonies of these microflora at the piercing site. Pain, edema, and prolonged bleeding may occur immediately after piercing (1), and a cyst, scar, or keloid may form at the piercing site. In various surveys, the rate of earlobe piercing infections alone has been estimated at 11% to 24%. Skin lesions or anatomic abnormalities at the site of piercing, as well as valvular heart disease, are risk factors for complications (2). Staphylococcal endocarditis of the mitral valve after nasal piercing (3), Neisseria endocarditis after tongue piercing (4), and Staphylococcus epidermidis endocarditis and mastitis following nipple piercing have been reported (5). Even though a consistent correlation is not known between piercing and endocarditis, the number of case reports is increasing, and a correlation may well exist.

Persons at high risk for complications should be treated with preventive antibiotics, just as persons at high risk for complications receive antibiotic treatment before dental procedures. The correlation between dental procedures and endocarditis has been reviewed by Van der Meer et al., who prospectively examined all cases of infective endocarditis in the Netherlands over a 2-year period (6). Of 427 patients who had been hospitalized, 64 had previous dental or other procedures in the preceding 3 months. Only 48 of the 438 patients met the qualification of having native-valve and

cardiovascular anomalies that increased their risk of getting endocarditis. Using these 48 patients as study cases, the researchers found no significant difference in presence of dental procedures between patients and matched controls without endocarditis (odds ratio 1.2, 95% confidence interval 0.03 to 2.3). Two other studies (7,8) reported similar results. No study has examined the correlation between piercing and endocarditis.

In the United States, body piercing, which is becoming increasingly common, is mainly performed by unlicenced practitioners. Only 26% of states have regulatory authority over tattooing establishments, and only six of these states exercise authority over body-piercing establishments. Piercing occurs in regulated and unregulated shops, department stores, jewelry shops, homes, or physicians’ offices. Generally no antibiotic is used, and sterilization methods vary. Studies show that ear piercing can cause cephalic tetanus (a local form of tetanus caused by wounds or other head and neck infections) (8), Pseudomonas infections, or perichondrial auricular abscesses, especially with Pseudomonas aeruginosa. Tongue or oral piercing can cause Ludwig’s angina (2,9,10) or may be complicated by normal oral flora, such as Haemophilus aphrophilus, as in this case. Genital piercing may result in Escherichia coli infection and may increase the risk for sexually transmitted diseases through tissue damage and exposure and unwanted pregnancy because of condom rupture (11). Systemic infections, such as toxic shock syndrome or sepsis, have also been reported (10). Among noninfectious cases, granulomatous perichondritis of the nasal ala, sarcoidlike foreign body reaction from multiple piercing, paraphimosis from a distal penis pierce, and speech impairment, together with difficulty in chewing and swallowing from oral jewelry, have been reported (1,2,9,10). Metal-associated problems include allergy (especially to nickel), eczematous rash, and lymphocytoma (2,9,10,12). We describe an incidence of H. aphrophilus endocarditis following tongue piercing.

Case Report

                    

The tongue piercing of the man from this case study....

A 25-year-old man arrived at Memorial Health University Medical Center with fever, chills, rigors, and shortness of breath of 6 days' duration. He had a history of aortic valvuloplasty at 8 years of age for correction of congenital aortic stenosis. At admission, the patient had fever of 38.9°C and a grade III/VI ejection systolic murmur accompanied by a grade II/VI diastolic blowing murmur best heard in the left sternal border area. The oral cavity was pink, and no inflammation or exudates were noticed on the pharynx. The middle portion of the tongue had been pierced, and a bispherical stud was in place (Figure). The piercing was performed 2 months before onset of illness. Extensive tattoos on the shoulders, arms, and upper torso dated back 3 years. The patient had previous dental work done but always with antibiotic prophylaxis.

Laboratory tests showed erythrocyte sedimentation rate of 41 mm/hr (normal rate, 0–15 mm/hr) and elevated C-reactive protein of 5.1 mg/dL (normal level 0–1). Transthoracic echocardiography was not conclusive; a transesophageal echocardiogram showed remnants of a bicuspid and deformed aortic valve with multiple vegetative lesions. Blood cultures were obtained, and the patient was started on triple antibiotics (ampicillin, nafcillin, and gentamycin). Wet preparation and acridine orange stain of the blood specimen showed gram-negative pleomorphic rods. Two of the conventional chocolate-agar cultures turned positive approximately 4 days after incubation and were consistent with H. aphrophilus (β-lactamase negative, lactose fermenting, and Mannose fermenting). The stud culture was also positive for H. aphrophilus. Antibiotics were modified because of sensitivity to ceftriaxone and gentamycin, and the patient was discharged to complete the 6-week course through a peripherally inserted central catheter line at home. Aortic valve replacement was recommended after completion of antibiotic therapy, but the patient did not return for treatment.

Conclusions

Our case demonstrates H. aphrophilus endocarditis possibly caused by tongue piercing (or as a complication of the ongoing presence of the stud) in a patient with congenital heart disease. Colonization around the stud likely caused bacteremia and endocarditis. H. aphrophilus is commonly isolated from the upper respiratory tracts of humans and animals; however, its prevalence is unknown. In a previous study of piercing complications in patients with congenital heart disease (13), 43% of the study population had earlobe piercing; of these, 6% took antibiotics before piercing. Twenty-three percent of patients had piercing-related infections 1 week to 3 years after piercing. Most infections were local skin infections; no endocarditis was reported in that study.

Until prospective randomized studies shed light on the relationship between piercing and endocarditis, prophylactic measures are indicated and should be formulated, particularly for persons at high risk, e.g., those with structural heart diseases.

Dr. Akhondi is a second-year resident with the Department of Internal Medicine at Mercer University School of Medicine, Savannah Campus at Memorial Health University Medical Center in Savannah, Georgia.

Dr. Rahimi is the associate director of Internal Medicine Education, chief of the Geriatrics Division, and professor of medicine at Mercer University School of Medicine, Savannah campus.

References

Braithwaite RL, Stephens T, Strek C, Braithwaite K. Risks associated with tattooing and body piercing. J Public Health Policy 1999;20:459–70.

Samantha S, Tweeten M, Rickman L. Infectious complications of body piercing. Clin Infect Dis 1998;26:735–40.

Ramage IJ, Wilson N, Thomson RB. Fashion victim: infective endocarditis after nasal piercing. Arch Dis Child 1997;77:187.

Tronel H, Chaudemanche H, Pechier N, Doutrelant L, Hoen B. Endocarditis due to Neisseria mucosa after tongue piercing. Clin Microbiol Infect 2001;7:275–6.

Ochsenfahrt C, Friedl R, Hannekum A, Schumacher BA. Endocarditis after nipple piercing in a patient with a bicuspid aortic valve. Ann Thorac Surg 2001;71:1365–6.

Van der meer JT, Thompson J, Valkenburg HA, Michel MF. Epidemiology of bacterial endocarditis in the Netherlands. II Antecedent procedures and use of prophylaxis. Arch Intern Med 1992;152:1869–73.

Lacassin F, Hoen B, Leport C, Selton-Suty C, Delahaye F, Goulet V, et al. Procedures associated with infective endocarditis in adults. A case control study. Eur Heart J 1995;16:1968–74.

Strom BL, Abrutyn E, Berlin JA. Dental and cardiac risk factors for infective endocarditis. A population-based, case-central study. Ann Intern Med 1998;129:761–9.

Koenig L, Carnes M. Body piercing, medical concerns with cutting-edge fashion. J Gen Intern Med 1999;14:379–85.

Folz BJ, Lippert BM, Kuelkens C, Wernaer JA. Hazards of piercing and facial body art: a report of three patients and literature review. Ann Plast Surg 2000;45:374–81

Fiumara NJ, Eisen R. The titivating penile ring. Sex Transm Dis 1983;10:43–4.

Ehrlich A, Kucenic M, Belsito DV. Role of body piercing in the induction of metal allergies. Am J Contact Dermat 2001;12:151–5.

Cetta F, Graham LC, Lichtenberg RC. Piercing and tattooing in patients with congenital heart diseases. J Adolesc Health 1999;24:160

 

8.) Is bupropion (Zyban) causing deaths? / medicina para dejar de fumar ocasiona muertes ?

Source: http://www.mja.com.au/

Simon C Chapman and Konrad Jamrozik

The Medical Journal of 21 January 2002 176 3: 134

©The Medical Journal of Australia ISSN: Australia0025-729X3 2002www.mja.com.au

To the Editor: From 1 February to 30 June 2001, 277 602 prescriptions for the smoking cessation drug bupropion hydrochloride (Zyban, GlaxoSmithKline) were processed. The Health Insurance Commission approved 343 737 prescriptions for bupropion between 1 February and 30 June.1 Comparing this figure with the 277 602 processed scripts, some 66 135 (19.2%) scripts went unfilled. One reason for this may have been extensive publicity given to reports of deaths and numerous adverse reactions following bupropion use.

The website of the Australian Drug Reactions Advisory Committee (ADRAC) reports that, as at 22 June, there had been 18 reports of deaths in patients aged from 30 years to 69 years who were using or who had recently stopped using bupropion.2 ADRAC summarised intelligence on these deaths thus:

... there were a variety of reported causes of death and not a single consistent mode of death. In addition to being smokers, several patients had other existing risk factors for unexpected death such as alcohol abuse, diabetes or cardiomyopathy. Eleven of the 18 patients had an alternative explanation for death that was at least as plausible as a possible effect of bupropion. In four reports, the available information was very limited and it was not possible to assess the cause of death. Further information is being sought on three cases to aid assessment of the cause of death.2

Smokers are at 3.1 times greater risk of dying (from any cause) than non-smokers and twice as likely to die from coronary disease and stroke.3 People with depression are three times as likely to be daily smokers4 and have double the suicide rate of non-smokers.5

In Australia, sudden coronary fatalities occur at a rate of about 450 per million people aged under 65,6 perhaps at a rate of 355 per million in non-smokers and about double that in smokers. In three months (the period of recommended bupropion use), one would expect 180 deaths per million smoker-users. Thus, among 277 602 Australian smokers, 50 might die during any given three-month period without any added risk from bupropion. This estimate helps to place the 18 fatalities reported to ADRAC in context.

The 277 602 scripts represent about 9.5% of Australia's 2.9 million regular smokers. These people, their families and doctors deserve to have their anxieties about the risks of using bupropion addressed. We would urge the government to commission urgently a case–control study of morbidity and mortality among smokers and their relationships to use or non-use of bupropion.

Competing interests: SC has received funding from SmithKlineBeecham (now GlaxoSmithKline) for the preparation of professional and public educational material on smoking in Australia.

Health Insurance Commission. Prescription data, item 8465M. 2001. <http: //www.hic.gov.au/statistics/dyn_pbs/forms/pbs_tab1.shtml#info>. Accessed 11 Sept 2001.

ADRAC update on buproprion (Zyban). Therapeutic Goods Administration website. <http: //www.health.gov.au/tga/docs/html/zyban.htm>. Accessed 21 Oct 2001.

Wald NJ, Hackshaw AK. Cigarette smoking: an epidemiological overview. Br Med Bull 1996; 52: 3-11.

Breslau N, Peterson EL, Schultz LR, et al. Major depression and stages of smoking. A longitudinal investigation. Arch Gen Psychiatry 1998; 55: 161-166.

Miller M, Hemenway D, Bell NS, et al Cigarette smoking and suicide: a prospective study of 300,000 male active-duty Army soldiers. Am J Epidemiol 2000; 151: 1060-1063.

Beaglehole R, Stewart A, Jackson R, et al. Declining rates of coronary heart disease in New Zealand and Australia, 1983-1993. Am J Epidemiol 1997; 145: 707-713.

Department of Public Health and Community Medicine,

 

9.) Polycystic Ovary Syndrome

Treatment with Insulin Lowering Medications ./ Síndrome del Ovario poliquistico, tratamientos con medicinas que disminuyen insulina.

Source:http http://www.ivf.com/pcostreat.html

by Mark Perloe, M.D.

INTRODUCTION:

Polycystic ovary syndrome is characterized by anovulation (irregular or absent menstrual periods) and hyperandrogenism (elevated serum testosterone and androstenedione). Patients with this syndrome may complain of abnormal bleeding, infertility, obesity, excess hair growth, hair loss and acne. In addition to the clinical and hormonal changes associated with this condition, vaginal ultrasound shows enlarged ovaries with an increased number of small (6-10mm) follicles around the periphery (Polycystic Appearing Ovaries or PAO). While ultrasound reveals that polycystic appearing ovaries are commonly seen in up to 20% of women in the reproductive age range, PolyCystic Ovary Syndrome (PCOS) is a estimated to affect about half as many or approximately 6-10% of women. The condition appears to have a genetic component and those effected often have both male and female relatives with adult-onset diabetes, obesity, elevated blood triglycerides, high blood pressure and female relatives with infertility, hirsutism and menstrual problems.

HYPER INSULIN & PCOS?

As of yet, we do not understand why one woman who demonstrates polycystic appearing ovaries on ultrasound has regular menstrual cycles and no signs of excess androgens while another develops PCOS. One of the major biochemical features of polycystic ovary syndrome is insulin resistance accompanied by compensatory hyperinsulinemia (elevated fasting blood insulin levels). There is increasing data that hyperinsulinemia produces the hyperandrogenism of polycystic ovary syndrome by increasing ovarian androgen production, particularly testosterone and androstenedione and by decreasing the serum sex hormone binding globulin concentration. The high levels of androgenic hormones interfere with the pituitary ovarian axis, leading to increased LH levels, anovulation, amenorrhea, and infertility. Hyperinsulinemia has also been associated high blood pressure and increased clot formation and appears to be a major risk factor for the development of heart disease, stroke and type II diabetes.

DIAGNOSIS

There is little agreement when it comes to how PCOS is diagnosed. Most physicians will consider this diagnosis after making sure you do not have other conditions such as Cushing's disease (overactive adrenal gland), thyroid problems, congenital adrenal hyperplasia or increased prolactin production by the pituitary gland. TSH, 17-hydroxyprogesterone, prolactin and a dexamethasone suppression test may be advisable. After reviewing your medical history, your physicians will determine which tests are necessary. If you have irregular or absent menstrual periods, clues from the physical exam will be considered next. Your height and weight will be noted along with any increase facial or body hair or loss of scalp hair, acne and acanthosis nigricans (a discoloration of the skin under the arms, breasts and in the groin). Elevated androgen levels (male hormones) androstenedione, DHEAS or testosterone confirm the diagnosis. A fasting insulin and glucose level will be obtained. Many physicians tell their patients that insulin values are normal, when in fact the value indicates that insulin may be playing a role in stimulating the development of PCOS. Most labs report levels less than 25-30 miu/ml as normal, while in fact, levels over 10 miu/ml on a fasting blood sample suggests that PCOS may be related to hyperinsulinism. As women with polycystic ovary syndrome may be a greater risk for other medical conditions, testing for blood lipids, diabetes and PAI-1 (a blood factor that promotes abnormal clotting).

NEWER METHODS OF TREATMENT

Traditional treatments have been difficult, expensive and have limited success when used alone. Infertility treatments include weight loss diets, ovulation medications (clomiphene, follistim, Gonal-F), ovarian drilling surgery and IVF. Other symptoms have been managed by anti-androgen medication (birth control pills, spironolactone, flutamide or finasteride).

Ovarian drilling can be performed at the time of laparoscopy. A laser fibre or electrosurgical needle is used to puncture the ovary 10-12 times. This treatment results in a dramatic lowering of male hormones within days. Studies have shown that up to 80% will benefit from such treatment. Many who failed to ovulate with clomiphene or metformin therapy will respond when rechallenged with these medications after ovarian drilling. Interestingly, women in these studies who are smokers, rarely responded to the drilling procedure. Side effects are rare, but may result in adhesion formation or ovarian failure if the procedure is performed by an inexperienced surgeon.

But recently promising new treatment options have become available. Drs. Velazquez, Nestler and Dunaif have shown that lowering serum insulin concentrations with metformin (Glucophage 1500 mg a day) or troglitazone (troglitazone, Rezulin has recently been withdrawn from the market because of life threatening side effects) ameliorates hyperandrogenism, by reduction of ovarian enzyme activity that results in male hormone production.

For women in the reproductive age range, polycystic ovary syndrome is a serious, common cause of infertility, because of the endocrine abnormalities which accompany elevated insulin levels. There is increasing evidence that this endocrine abnormality can be reversed by treatment with widely available standard medications which are leading medicines used in this country for the treatment of adult onset diabetes, metformin (Glucophage 500 or 850 mg three times per day or 1000 mg twice daily with meals), pioglitazone (Actos 15-30 mg once a day), rosiglitazone (Avandia 4-8 mg once daily) or a combination of these medications. These medications have been shown to reverse the endocrine abnormalities seen with polycystic ovary syndrome within two or three months. They can result in decreased hair loss, diminished facial and body hair growth, normalization of elevated blood pressure, regulation or menses, weight loss and normal fertility. We have seen pregnancies result in less than two months in woman who conceived in their very first ovulatory menstrual cycle. By six months over 90% of women treated with insulin-lowering agents will resume regular menses.

The medical literature suggests that the endocrinopathy in most patients with polycystic ovary syndrome can be resolved with insulin lowering therapy. This is clinically very important because the therapy reduces hirsutism, obesity, blood pressure, triglyceride levels, elevated blood clotting factors and facilitates reestablishment of the normal pituitary ovarian cycle, thus often allowing resumption of normal ovulatory cycles and pregnancy. We know the polycystic ovary disease is associated with increased risk of heart attack and stroke because of the associated heart attack and stroke risk factors, hypertension, obesity, hyperandrogenism, hypertriglyceridemia, and these are to a large degree resolved by therapy with these medications.

ARE THESE MEDICATIONS SAFE?

Side effects are rare. Although metformin, rosiglitazone and troglitazone lower elevated blood sugar levels in diabetics, when given to non­diabetic patients, they only lower insulin levels. Blood sugar levels will not change. In fact, episodes of "hypoglycemic attacks" appear to be reduced.

METFORMIN (Glucophage):

When first starting this medication, people will often experience upset stomach or diarrhea which usually resolves after the first week. This side effect can be minimized by taking metformin with a meal and starting with a low dose. I recommend that our patients start with one 500 mg pill daily the first week and increase to twice a day during the second week. If after the second week GI side effects are minimal, the dose is increased to 850 mg twice daily. Patients with reduced renal function (creatinine >1.5 or creatinine clearance <60%) are at a higher risk for a rare side effect of metformin therapy called lactic acidosis, and the drug should be given cautiously, if at all, to such patients. Patients taking metformin should notify their physician and discontinue the medication:

48 hours before surgery

48 hours before an IVP Xray study or other Xrays where an intravenous dye is administered

If you experience shortness of breath, severe muscle weakness or chest pain

If you use alcohol excessively

TROGLITAZONE, (Rezulin) PIOGLITAZONE, (Actos), ROSIGLITAZONE, (Avandia):

These medications belong to a class of medications called PPAR gamma agonists. They enhance the ability of smooth muscle to metabolize sugar, thereby reducing insulin resistance.

The FDA has recently reviewed the safety of troglitazone ( and reports that 35 patients out of approximately 1.5 million have either died or required liver transplant.) Therefore Rezulin has been removed from the market.

As the new alternatives to troglitazone, (Rezulin), Rosiglitaone (Avandia) and pioglitazone (Actos) are metabolized by different liver enzymes experience has shown that these medications appear to pose less risk of hepatotoxicity.

HOW DO WE MONITOR THERAPY?

BBT charts are monitored and reviewed to determine if you are ovulating. With metformin, you will be asked to return three months after initiating therapy. If you have ovulated, therapy may be continued another three months to see if you will conceive. Women taking rosiglitazone or pioglitazone will be seen at two month intervals for monitoring liver function tests (ALT). BBT charts will be reviewed after four months. Re-evaluation will include measurements of lab tests that were abnormal at the initial evaluation. C-peptide levels, a measure of insulin secretion, may also be tested. If the laboratory studies are still abnormal, metformin may be increased up to 850 mg three times daily or rosiglitazone may be added. If the laboratory studies are normal but ovulation has not occured, a repeat trial of clomiphene may be considered. We have seen that women who were unable to ovulate on up to 250 mg ovulate when 50 mg of clomiphene is used in conjunction with metformin or PPAR gamma therapy.

Laparoscopic ovarian drilling may be considered for those women where other indications for laparoscopy are present.

PREGNANCY

While safety during pregnancy has not yet been established, three patients who continued on metformin during their entire pregnancy and one who remained on troglitazone have delivered normal babies. There are no reports of abnormal babies in women who conceived using metformin and all resulting babies were normal. Metformin is a category B medication. This means that insufficient human data is available but no credible animal data suggesting a teratogenic (could produce birth defects) risk. Although to the best of our present knowledge the risk of birth defects would be small, it must also be noted that maternal diabetes has been associated with an increased risk of birth defects and the underlying elevated insulin levels may lead to birth defects if not corrected.

While the most prudent policy may be to avoid the use of these medications during pregnancy until more data on pregnancy outcome is available, the risk of miscarriage may be reduced by continuing metformin during the pregnancy. We ask our PCOS patients taking insulin-lowering medications to monitor their basal body temperatures if pregnancy is a possibility. When the temperature remains elevated for more than 16 days, pregnancy is likely and a home pregnancy test should be performed. If positive, a medical consultation with the physician is scheduled. If the EPT is negative the BBT chart is reviewed by the physician or nurse to determine the appropriate course to follow.

MISCARRIAGE & PCOS

Women with PCOS who conceive either spontaneously or after ovulation induction have a much higher risk of miscarriage. Liddell has shown that polycystic appearing ovaries (on ultrasound) are more frequently seen in women with recurrent pregnancy loss, the presence of PCO on ultrasound did not predict the outcome in subsequent pregnancies. Hypersecretion of LH was thought to cause chromosomally abnormal eggs leading to an increased risk of miscarriage. But a Japanese study found that PCOS was more common in women whose prior loss was associated with normal chromosomes. Others have suggested that high androgen levels may be a contributory factor. Homburg has shown that miscarriage rates after ovulation induction or IVF is decreased when women are pretreated with a GnRH-agonist such as Synarel, Lupron or Zoladex.

Hyperinsulinemia may be a contributing factor in the higher rate of miscarriage. Elevated levels of insulin interfere with the normal balance between factors promoting blood clotting and those promoting breakdown of the clots. Increases in plasminogen activator inhibitor activity (PAI-Fx) associated with high insulin levels may result in increased blood clotting at the interface between the uterine lining (endometrium) and the placenta. This could lead to placental insufficiency and miscarriage.

There are no placebo-controlled clinical trials to indicate whether pregnancy outcomes are improved in pregnancies that result from the use of insulin-lowering medications or whether pregnancy outcomes are better in those who continue metformin throughout the pregnancy or those who discontinue. Coetzee has shown that use of metformin to manage non-insulin dependent diabetes during pregnancy can be accomplished safely. We have initially noted that women who conceive following metformin or troglitazone therapy have an unacceptably high (>30%) risk of miscarriage. Dr. Glueck notes similar increased risk of miscarriage following metformin therapy. He notes that the risk of miscarriage is increased in those patients with a prior history of miscarriage, those with high LH, high androgen levels, hyperinsulinemia or elevated PAI-Fx. Initial findings in a non-randomized trial suggest a decreased risk of miscarriage if metformin is continued throughout the pregnancy. At present there is insufficient data to routinely advise continuation of metformin during pregnancy. As an alternative to continuing metformin therapy, those women with increased risk of abnormal blood clotting may benefit from baby aspirin, folate supplementation and low dose heparin therapy. Pregnancy loss is a troubling concern. This information is provided to enable you work with your ob/gyn physician to make an informed decision about your care.

BIBLIOGRAPHY

1. Velazquez EM, Mendosa S, Hamer T, Sosa F, Glucck CJ. Metformin therapy in women with polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure, while facilitating menstrual regularity and pregnancy. Metabolism 1994,43:647­655.

2. Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450cl7alpha activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome. New England J Medicine 1996,335:617­623.

3. Utiger RD. Insulin and the polycystic ovary syndrome. New England J Medicine 1996,335:657­658

4. Dunaif A, Scott D, Finegood D, Quintana ma B, Whitcomb R. The insulin sensitizing agent Troglitazone improves metabolic and reproductive abnormalities in the polycystic ovary syndrome Endocrinol Metab 1996;81:3299­3306

5. Coetzee EJ, Jackson WP. The management of non-insulin-dependent diabets during pregnancy. Diabetes Res Clin Pract 1985-86;1:281-287

6. Homburg R. Polycystic ovary syndrome: induction of ovulation. Ballieres Cllinical Endocrinologys & Metabolism 1996; 10:281-292

7. Glueck CJ, Wang P, Fontaine R, Tracy T, Sieve-Smith L. Metformin-induced resumption of normal menses in 39 of 43 (91%) previously amenorrheic women with polycystic ovary syndrome. Metabolism 1999; 48:1-10.

8. Tulppala M, Stenman UH, Cacciatore B, Ylikorkala O. Polycystic ovaries and levels of gonadotropins and androgens in recurrent miscarriage: preliminary experience of 500 consecutive cases. Hum Reprod 1994;9:1328-32.

For more information on PCOS and other ovulation problems please read Miracle Babies and Other Happy Endings Online Edition

10.) Finasteride cream in hirsutism / Finasteride en crema para el hirsutismo

Source: http://www.aace.com/

 K. Jean Lucas, MD, FACP, FACE

ABSTRACT

Objective: To determine, in a preliminary study, whether women with hirsutism attributable to various causes would benefit from treatment with finasteride cream.

Methods: Finasteride cream (0.25%) and placebo cream were administered to eight women with various degrees of facial hirsutism. The two creams were used on opposite sides of the face in an area of excessive hair growth. The side chosen for the finasteride cream versus placebo was randomized and blinded. In a 1 cm2 area on each side of the face, hair counts were done every 2 months throughout the 6-month study period. Hair thickness was also measured.

Results: Hair follicles respond to testosterone by the conversion of this androgen to dihydrotestosterone through the action of 5a-reductase. Finasteride partially blocks this enzyme. Because of the easy solubility of this medication through the skin, a cream applied to the area of hair growth would be expected to decrease hirsutism locally. After a 6-month period, mean hair counts decreased significantly from 27.5 to 15.5 (P<0.05) in the finasteride-treated sites but showed no significant change from baseline in the placebo-applied sites. Moreover, the mean thickness of the measured hairs (in hundredths of millimeters) was significantly different between the placebo and finasteride-treated sites (4.33 versus 3.11, respectively; P<0.001).

Conclusion: In this study of women with facial hirsutism, topically applied finasteride significantly decreased hair growth and thickness, and no adverse effects were noted. (Endocr Pract. 2001;7:5-10)

INTRODUCTION

Finasteride, a 5a-reductase inhibitor, has been extensively studied and clinically used for treatment of prostatic hyperplasia (1,2). Currently, it is being assessed for use in prostate cancer (3). Because both the prostate and the hair follicle contain this enzyme, finasteride has also been used to treat male pattern baldness (4,5). The mechanism of action of this medication is to block the conversion of testosterone into its active metabolite dihydrotestosterone (DHT). By inhibiting 5a-reductase, the effect of testosterone on the prostate is blunted, and the growth of the prostatic tissue is diminished. By decreasing the levels of DHT and not testosterone, finasteride has not been shown to affect luteinizing hormone, follicle-stimulating hormone, or testosterone levels substantially over time. Only 4 to 5% of men have any change in potency or libido (6,7).

Stimulation of 5a-reductase in hair follicles causes male pattern hair to grow on the face and body and to be lost on the scalp. In tissue culture, the hair follicle isoenzyme was less affected by finasteride than the enzyme in the prostate tissue culture (8).

The degree of 5a-reductase activity may account for the varied severity of hirsutism found in women with the same levels of circulating androgens (9). Even though the isoenzymes of 5a-reductase in the prostate (type 2) and the hair follicles (type 1) have different structures, some cross-reactivity of finasteride on the isoenzyme in the hair follicle may occur (10,11). The areas of the scalp and body that are directly affected by male hormone would be the ones most likely to be affected by inhibition of 5a-reductase.

In women, who have much lower androgen levels than do men, one might expect finasteride to have an even greater effect on areas containing 5a-reductase. In men with inherited 5a-reductase deficiency, facial hair is sparse, and baldness does not develop (12,13). Women with excessive hair growth in male pattern predominant areas may have an increased sensitivity to male hormones in the hair follicle. Women with idiopathic hirsutism have been shown to have increased 5a-reductase activity in their genital skin (14). Gonadotropins in women have been shown to be unaffected by finasteride (15).

Three recent studies (16-18) have demonstrated the effectiveness of finasteride in idiopathic hirsutism. Finasteride has also been compared with spironolactone as a treatment for hirsutism (19,20). Because finasteride is readily soluble through the skin (package insert, Merck & Co.), a cream containing this medication might be beneficial therapy for mild facial hirsutism.

The current study was a preliminary investigation to determine whether women with hirsutism attributable to various etiologic factors and with varied levels of circulating androgens would benefit from the use of finasteride cream.

MATERIAL AND METHODS

Study Subjects

Eight consecutive patients with excessive facial hair were enrolled in the study, including one patient with non androgenic facial hair. This patient was included to ensure that the finasteride would affect only androgenic facial hair and not have a generalized effect on all types of hair. Patients with different severities and causes of hirsutism were included to assess whether the level of androgen or the cause of the excessive production of androgen determined the response to the finasteride.

Of the eight study participants, four had used low androgenic birth control pills (Demulen in two, Tri-Cyclen in one, and Desogen in one) for more than 6 months before the start of the study. Three study subjects were taking no oral contraceptives, and one postmenopausal patient was taking Estrace (Table 1). The ages of the women ranged from 31 to 51 years (mean ± standard error of the mean [SEM], 39.2 ± 2.34). The body mass index ranged from 19 to 57 kg/m2 (mean ± SEM, 36.5 ± 5.72).

Four of the subjects had polycystic ovary syndrome, two had idiopathic hirsutism, one had hypertrichosis, and one had a mild form of congenital adrenal hyperplasia. Polycystic ovary syndrome was defined clinically as a combination of irregular menstrual periods, hirsutism, and obesity. Idiopathic hirsutism was characterized by excessive hair growth in male hormone-affected areas without concomitant increases in androgen levels or other androgenic abnormalities such as abnormal menses, acne, or androgenic alopecia. Hypertrichosis was defined as excessive facial and body hair on all areas of the body, not just androgen-affected areas. Mild congenital adrenal hyperplasia was defined as an exaggerated response of 17-hydroxyprogesterone to the intravenous administration of 250 mg of cosyntropin.

The patients were informed about the previous uses of finasteride in the treatment of prostate enlargement and male pattern baldness. They were told that this medication had not been approved by the US Food and Drug Administration for use in women and that potential side effects in women were unknown. All the women were told that finasteride could affect a male fetus and that pregnancy was contraindicated during the use of this medication.

Protocol

The protocol and consent form for the study were approved by the Institutional Review Board at Northside Hospital in Atlanta, Georgia. After signing the informed consent document, the women were interviewed to obtain a medical, menstrual, and hirsutism history. The menstrual history included age at menarche, regularity of menstrual cycles, age at which male pattern hair growth had begun, previous treatment, current treatment, and whether or not male pattern baldness was developing. A physical examination was performed; in particular, items noted were the degree of hirsutism, body mass index, presence of acanthosis nigricans, evidence of virilization, cushingoid features, and male pattern baldness.

The patient's hair density was determined by counting the terminal hairs in a 1 cm2 area on either side of the patient's chin or in another area of maximal hair growth on the face. A template was made by using landmarks of the middle of the chin and the chin line. The hair counts on both sides were repeated every 2 months for the duration of the study. Four hairs from areas adjacent to the template were plucked and saved for later measurement of thickness. The thickness of the midshaft of the previously plucked hairs was blindly determined by the use of a direct measurement microscope and measured in hundredths of millimeters.

The pharmacokinetics of finasteride was analyzed to calculate the appropriate concentration of the medication in the cream. Fifteen tablets of finasteride (5 mg each) were triturated (ground into a fine powder) and then wetted with 2 mL of propylene glycol. The mixture was incorporated into Dermabase (Paddock Laboratories, Inc.) by levigation (that is, mixed evenly by high-speed mixer and gradually incorporated). The final cream contained 0.25% finasteride. The weight of the tablets was 2.3 g. The weight of the Dermabase was 25.7 g. The 30-g mixture was put into a tube. For 6 tubes, the contents were as follows: 90 tablets (weighing 13.8 g), 12 mL of propylene glycol, and 154.2 g of Dermabase.

The placebo cream consisted of the Dermabase alone in the same size and type of tube. No difference in color or texture was evident between the placebo and the drug-containing cream. Patients applied a thin layer of cream to the areas of the excessive hair growth twice per day. The patients were instructed to use the cream labeled "R" on the right side of their face and the cream labeled "L" on the left side of the face. The women and the researcher were blinded to the identity of the cream in each of the tubes. Randomization was accomplished by the numbering of the cream and placebo tubes in pairs. As each woman was enrolled in the study, she was given the next consecutive pair of numbers. The original numbering of the tubes was done by a person not involved with the examination of the patients or the recording of the data. The women in the study who had been taking oral contraceptives or estrogen replacement therapy had done so for at least 6 months before the beginning of the study. Each patient's hair growth had stabilized before the study. Stabilization was confirmed by the frequency of hair-removal techniques used by the study subjects. The study participants received no other medication for hirsutism during the study and for at least 2 months before the beginning of the study.

The finasteride cream, placebo cream, and previous doses of oral contraceptives or estrogens were continued for the entire study. After the 6-month study period, the patients were given the option of continuing the finasteride treatment indefinitely or changing back to their previous medication.

The patients were seen in consultation at 2-month intervals. Questions were asked about side effects, menstrual abnormalities, missed menstrual periods, and changes in libido. The subjective view of the effect of the medication on the rate of hair growth was ascertained by questioning about the number of times per week the patients had shaved or clipped hairs. Patients' perceptions about differences in the two sides of the face were also noted at each visit. They were asked whether they noted any differences between the two sides and whether they thought that they knew which cream contained the medication. Inquiries about hair-removal techniques were made at each visit. The women had consented to only clipping or shaving of the hairs during the study. They were told to avoid clipping or shaving for at least 24 hours before each scheduled visit. Electrolysis, waxing, and plucking were not permitted during the study.

Biochemical Evaluation

Women who were premenopausal had serum pregnancy tests every 2 months while the medication was being used. The basic hirsutism evaluation (measurement of testosterone, dehydroepiandrosterone sulfate, prolactin, and thyroid-stimulating hormone) was completed on each patient and was repeated at the end of the 6-month interval. Biochemical profiles and complete blood cell counts were also done at the beginning and end of the study. All blood specimens except for the serum pregnancy tests were submitted to commercial laboratories (National Health Laboratory and SmithKline Laboratory). Evaluation of ovulation was not performed for this study.

Statistical Analysis

All data are expressed as mean values ± SEM. Data from the study included hair numbers and hair thickness for two groups: placebo versus medication (finasteride). These data were compared with paired t tests. Significant differences were defined as P values less than 0.05.

RESULTS

Tolerability and Safety

None of the women reported any problems with irregularity of menstrual periods, changes in libido, changes in energy level, nausea, vomiting, diarrhea, abdominal pain, or headache. No patient became pregnant during the study. No study participant had any allergic reaction to the medication or skin eruption in the areas to which the creams were applied. All serum chemistry studies and blood cell counts remained essentially the same from the beginning until the conclusion of the study.

Clinical Effects

By subjective evaluation, six of the eight patients noted a considerably diminished rate of hair growth and decrease in the thickness of hairs on one side of the face versus the other. These six women correctly guessed the side on which the medication had been used. Five of these women continued use of the finasteride cream after the study and have continued to show decreased facial hirsutism.

Two study participants had no difference in their hair counts throughout the study. One of these patients had facial hypertrichosis. This condition would not have been expected to improve because the cause of this disorder does not involve increased sensitivity to androgens. The other patient had been treated with multiple combinations of medications for hirsutism during the years before the study and had shown no major response to any of these therapies.

In comparison with baseline, hair counts in the finasteride-treated sites decreased significantly over the duration of the study (Fig. 1). Mean (and SEM) hair counts decreased from 27.5 ± 13.0 to 15.5 ± 7.3 (P<0.05). The placebo sites showed no significant change in hair counts during the study. By the end of the study, the thickness of the hairs (mean ± SEM, in hundredths of millimeters) differed significantly between the placebo sites (4.33 ± 0.07) and the finasteride sites (3.11 ± 0.05) (Fig. 2).

Levels of male hormones did not change significantly during the study. The effect on the hair counts, on hair thickness, or on hair growth was not related to the level of androgens in any patient. Likewise, blood pressure and body mass index did not change significantly throughout the study.

DISCUSSION

Hirsutism, a devastating problem for many women, may lead to psychologic abnormalities, including low self-esteem, withdrawal from social interaction, isolation, and depression (10,21). Affected women may be ridiculed or pitied by others throughout their lives. They become extremely self-conscious about their appearance. Because the most conspicuous unwanted hair is that on the face, women may resort to plucking, waxing, bleaching, or shaving in attempts to eliminate this embarrassing trait. With the rapidity of hair growth seen in some women, these hair-removing procedures achieve the desired result for only a brief period. No drug had been approved by the US Food and Drug Administration for this condition until recently, when eflornithine hydrochloride (Vaniqa) cream (Bristol-Myers Squibb) was approved for inhibiting the growth of unwanted facial hair. Spironolactone (Aldactone) (10,19,21), the most commonly used medication for this condition, is effective but may have major side effects, including irregular menstrual periods, gastrointestinal disturbances, fatigue, and dizziness; it also may not result in loss of excess hair or improvement in male pattern hair loss. Flutamide (22,23) and ketoconazole (24,25) have also been successfully used to treat hirsutism; however, these drugs can cause serious side effects, including liver toxicity.

The use of finasteride for treatment of hirsutism is logical because of its specific effect on 5a-reductase, the enzyme responsible for sensitizing the hair to testosterone. In previous studies, orally administered finasteride has been successfully used in the treatment of hirsutism (26-28). Contraindications to its use in women include the effect on the developing male fetus. Early inhibition of this enzyme would be detrimental to the development of normal male genitalia.

In this study, all the women of reproductive age were required to use some form of contraception for the duration of the study. The only postmenopausal study participant was receiving estrogen replacement therapy before and for the duration of the study.

A previous study (16) assessed the use of finasteride in 17 women of reproductive age who had idiopathic hirsutism. Only five of these women were taking oral contraceptives; the others were using barrier methods of birth control. Another report (19) described the use of finasteride in 14 women with hirsutism, none of whom was taking oral contraceptives. Many medications are contraindicated during pregnancy, and their use must be discontinued before pregnancy. Finasteride can be used safely until a woman wants to have children. Women using this medication must be aware of the danger to a male fetus should they become pregnant.

The current investigation was a preliminary study designed to observe the clinical effects of topically applied finasteride cream on facial hirsutism, regardless of the cause of the excessive hair growth or the level of circulating androgens. Hair thickness and hair counts showed significant improvements in the area treated by the finasteride cream. The degree of hyperandrogenism did not make a difference in the response of the patient to the cream. Part of the response to the placebo cream may be attributable to the small area of the chin; a crossover effect of the finasteride cream onto the other side of the chin may have occurred. Thus, the separation of the two study sites may have been suboptimal. In future studies, this problem may be eliminated by using the placebo cream and the finasteride cream sequentially.

The long-term side effects of treatment with finasteride cream in women (except for pregnancy concerns) are unknown; however, the specific nature of the medication makes it unlikely to cause substantial problems. Only long-term studies in such a setting will provide answers to this question. Nevertheless, the use of a 0.25% topical preparation of finasteride would be expected to be considerably safer and less expensive than the systemic medication.

CONCLUSION

Finasteride tablets and topical finasteride cream have been shown to be effective treatments for hirsutism in women. Future studies should be undertaken to assess long-term side effects, optimal treatment regimens, combination therapies with spironolactone, and the effect on androgenic alopecia in women.

ACKNOWLEDGMENT

Keith Ahlfinger, PharmD, prepared the finasteride cream for this study. I appreciate the assistance of my endocrinology colleagues in providing patients for this study. I thank Jessica Tapia and Tabitha Sapp, who diligently organized and helped with the details of the study, as well as the local Merck & Co. representative for the idea for this study.

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DATA-MÉDICOS/DERMAGIC JOURNAL APRIL 2003-2004/ DR. JOSE LAPENTA R. 

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Venezuela 1.998-2.024

Producido por Dr. José Lapenta R. Dermatólogo Venezuela 1.998-2.0024

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