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domingo, 7 de diciembre de 2025

THE ANDROGENIC ALOPECIA, A REVIEW. / LA ALOPECIA ANDROGENICA, REVISION.


 

LA ALOPECIA ANDROGÉNICA Y SUS ALTERNATIVAS TERAPÉUTICAS. !

 

 ANDROGENIC ALOPECIA AND THERAPEUTIC ALTERNATIVES. !


Androgenic Alopecia in adult man



Updated

ACTUALIZADO 2025




EDITORIAL ESPAÑOL:
 ==================
Hola amigos de la red DERMAGIC EXPRESS hoy con otro tema interesante, actualmente muy discutido y estudiado: ALOPECIA ANDROGÉNICA, Y SUS ALTERNATIVAS TERAPÉUTICAS.  
 
La ALOPECIA ANDROGENICA (AGA), el tipo más común de pérdida de cabello, se produce en 80% de los hombres y 50% de las mujeres, fundamentalmente de índole genético y hormonal. 
 
 
1.) HISTORIA: 
 
- En Egipto antiguo ( 1500 años    A.C.), ya se conocía la calvicie masculina, y en textos como el Papiro Ebers recomendaban remedios caseros como: cebolla, grasa de león, de hipopótamo y excremento de murciélagos. 
 
- Hipócrates de Cos ( 460-370 años A.C.), médico griego considerado padre de la medicina occidental de Grecia, describió la calvicie masculina y notó su ausencia en eunucos, (masculinos con extirpación de genitales INCAPACES de producir la hormona TESTOSTERONA
 
- James B. Hamilton (1909-1990): dermatólogo estadounidense de Nueva York, estableció en 1942 la relación entre la alopecia androgenica con los  andrógenos al estudiar eunucos, y estableció la primera clasificación de esta patología en 5 tipos.
 
- O'Tar T. Norwood (1920-2022): dermatólogo estadounidense de Oklahoma especializado en trasplantes capilares, modificó y amplió la escala a 7 tipos en 1975, luego de analizar 1000 (mil) casos.
 
- Erich Ludwig: dermatólogo alemán especializado en tricología y enfermedades del cabello, quien en 1977 desarrolla una escala simplificada de la calvicie en las mujeres, en 3 grados,  basado en el hecho de que la perdida de cabello en la mujer es difusa y central, a diferencia de los hombres que presentan diferentes patrones.
 
 
2.) CLASIFICACIÓN:  
 
A.) Hombres: (Escala Norwood-Hamilton, 7 tipos):

- TIPOS:
 
    I: Línea frontal normal.
    II: Retroceso leve bifrontal.
    III: Entradas profundas (±vertex).
    IV: Avance frontal + calvicie parcial vertex.
    V: Mayor pérdida, puente mínimo.
    VI: Fusión frontal-vertex.
    VII: Cabello en "U" posterior (80% de los casos).

B.) Mujeres: (Escala Ludwig, 3 grados):

    I: Rarefacción central leve.
    II: Moderada con partición ensanchada.
    III: Avanzada, posible calvicie total central.

​Esta clasificación es con fines educativos,  y de comprensión, que pueden orientar al medico tratante a escoger el método mas adecuado para tratar la patología; en mujeres predomina el PATRON DIFUSO, en masculinos el PATRON mas común es la ALOPECIA EN "U", con un 80% de los casos (areas con calvicie desde la region frontal hasta media region occipital, respetando areas laterales temporales y parietales.
 
 
2.)  ETIOLOGÍA: 
 
- Primeramente hay que explicar a la audiencia NO MEDICA, que la alopecia androgenica es la perdida del cabello producida por un aumento de los ANDRÓGENOS, (principalmente la testosterona), en nuestro cuerpo, tanto en el hombre como la mujer. específicamente su metabolito o derivado llamado: DIHIDROTESTOSTERONA.

- Este exceso de ANDRÓGENOS específicamente la DIHIDROTESTOSTERONA, se depositan en el folículo piloso y lo atrofian, provocando la caída del cabello. Este es el mecanismo principal que ocasiona LA ALOPECIA ANDROGÉNICA.

- Caracterizada por una caída del cabello progresiva, que afecta tanto hombres como mujeres post puberales, la cual puede llegar a ser severa en ambos sexos.
 
- En la mujer enfermedades como el SÍNDROME DE OVARIO POLIQUISTICO, produce aumento de los andrógenos con la subsecuente caída del cabello.

- En el hombre, la enfermedad tiene sin duda un componente genético, porque no todo el mundo está afectado, y es importante que usted sepa que, hay hombres que NUNCA SUFRIRÁN DE ALOPECIA ANDROGÉNICA, generalmente siempre hay un historial de calvicie en los afectados.
 
3.) EVOLUCIÓN:

- Aquí hay que explicar que el cabello no esta "ADHERIDO CON PEGAMENTO" al cuero cabelludo, tiene un ciclo de de "VIDA: ANAGENO, o crecimiento, dura de 1 a 7 años, CATAGENO, o de transición, que dura de 2 a 3 meses y TELOGENO o de reposo la cual dura unos 3 meses aproximadamente, luego el cabello se cae y es sustituido por uno nuevo.

- NORMALMENTE SE CAEN ENTRE 50 Y 100 CABELLOS DIARIOS.

- Es interesante que también sepas que cuando el cuerpo esta sometido a un gran ESTRÉS, y otros factores el cabello entra prematuramente en FASE TELOGENA y comienza a caerse abundantemente produciendo una notable ALOPECIA.

- De modo que factores como el ESTRÉS  y otros que alteren el CICLO del cabello contribuirán a que la ALOPECIA ANDROGÉNICA sea mayor.

- Otro factor que que empeora LA ALOPECIA ANDROGÉNICA ES LA DERMATITIS SEBORREICA del cuero cabelludo, comúnmente denominada "AUMENTO DE LA GRASA EN EL CABELLO, de modo que mientras mas uses un champú anti caspa, MENOS SEBORREA habrá, por lo tanto menos caída del cabello.
 
4.) TRATAMIENTOS: 

Tratamientos para LA ALOPECIA ANDROGÉNICA hay variados, y te resalto los mas utilizados hoy dia:

1.) MINOXIDIL, TÓPICO (ANTIHIPERTENSIVO).
2.) FINASTERIDE (INHIBIDOR DE LA 5-ALFA REDUCTASA).
3.) DUTASTERIDE (INHIBIDOR DE LA 5-ALFA REDUCTASA).
4.) FLUTAMIDA (INHIBIDOR DE LA 5-ALFA REDUCTASA).
5.) CYPROTERONA ACETATO (ANTICONCEPTIVO ORAL).
6.) ESPIRONOLACTONA (ANTIDIURETICO ORAL).
7.) SERENOA REPENS O PALMETTO SAW (NATURISTA, ANTI-ANDROGENO).
8.) CYPERUS ROTUNDUS (NATURISTA).
9.) ESTEROIDES TÓPICOS.
10.) CHAMPU ANTI-CASPA. (KETOCONAZOL, PIRITIONATO DE ZINC, BIFONAZOL)
11.) DROSPIRENONA (ANTICONCEPTIVO ORAL).

 
5.) NUEVOS TRATAMIENTOS: 
 
A.- TÓPICOS: 
 
- FINASTERIDE TOPICO al 0.25%: Salio al mercado en Noviembre del 2024 con el nombre de FINASTOPIC, del laboratorio ISDIN de España. Esta alternativa se venia buscando desde los años 2000, y tiene la ventaja sobre el FINASTERIDE en pastillas, de minimizar los efectos secundarios.
 
- CLASCOTERONE 5%: con los nobres comerciales de Breezula y Winlevi: Antagonista tópico del receptor androgénico (AR), bloquea la DIHIDROTESTOSTERONA localmente sin efectos sistémicos; el producto NO ESTA APROBADO; se encuentra en  fase III.
 
B.- NO TOPICOS: 
 
- PRP optimizado (iPRF): Plasma rico en fibrina con células madre; 4-6 sesiones anuales, para aumentar el grosor capilar.
 
- Minoxidil oral microdosis (0.25-5mg) + dutasterida tópica. 
 
- Mesoterapia capilar: Microinyecciones de vitaminas, péptidos, ácido hialurónico y minoxidil. 
 
- Laser LLLT: Terapia de laser de baja intensidad, aprobado por la FDA para el tratamiento de la alopecia androgenica, año 2007, considerado un dispositivo seguro y efectivo. Los dispositivos de este tipo disponibles son:
 
- cHairMax® LaserComb (Lexington International): Primer dispositivo aprobado (2007).  Es un peine láser de diodo rojo (655 nm) para uso doméstico.

iRestore® Laser Growth System: Aprobado en 2016; se trata de un casco con 21 diodos y 30 LEDS infrarrojos.

- Capillus® / LaserCap® / Theradome®:
Aprobados entre 2012 y 2018, se trata de laser tipo cascos gorras con frecuencia de 272-560 nm.

 
Los trasplantes capilares NO SON NUEVOS, comenzaron a usarse desde la década de 1930, cuando el medico japones Dr. Shoji Okuda desarrolló la técnica de injertos "punch" o "sacabocado" para restaurar cabello en quemados y alopésicos.
 
 - En la década de los 1950 el medico Americano Dr. Norman Orentreich (EE.UU.) realizó el primer trasplante moderno para calvicie en 1952, procedimiento tipo "punch"
 
- EVOLUCIÓN DE LA TÉCNICA HASTA 2025: 
 
- 1950s-70s: Punch grafts grandes (4-5mm), antiestéticos ("muñeco").

- 1980s-90s: Microinjertos (1-4 folículos) por Dr. Bobby Limmer (FUT).

- 2000s: FUE:
(2002, Dr. Rassman/FUE Research Committee).
 
La técnica más utilizada hoy dia 2025, es la FUE (Follicular Unit Extraction): Extrae folículos individuales (0.8-1mm) con punch motorizado/robótico, no se extrae tira lineal de piel, tampoco deja cicatriz visible, con un porcentaje del 80 90% de utilización global, con rápida recuperación.
 
6.) CONCLUSIONES: 

Existe en nuestro cuerpo una enzima denominada 5 alpha reductasa que es la encargada de convertir la TESTOSTERONA EN DIHIDROTESTOSTERONA. Al aumentar este metabolito, mayor sera la caída del cabello.

Por lo tanto una de las estrategias para evitar la ALOPECIA ANDROGENICA es inhibir la enzima 5 alfa-reductasa, y para ello ya se han inventado y descubierto medicinas farmacológicas y naturistas, estas son las ya mencionadas:
 
- DUTASTERIDE.
- FLUTAMIDA.
- SERENOA REPENS O SAW PALMETTO (NATURISTA, ANTI-ANDROGENO).
CYPERUS ROTUNDUS (NATURISTA). 
 
Todas estas medicinas tienen sus VENTAJAS y sus EFECTOS ADVERSOS, pero si nos ubicamos en la realidad, la ciencia ha avanzado notablemente en este campo, hace muchos años se decía popularmente: 

" ...A LA CAÍDA DEL CABELLO SOLO LA DETIENE EL PISO O SUELO.."

Hoy dia este viejo adagio no es cierto, por la aparición de medicamentos principalmente como DUTASTERIDE, FINASTERIDE Y FLUTAMIDA, los cuales inhiben la enzima 5 alfa-reductasa, principal causante del aumento de los ANDRÓGENOS en nuestro cuerpo.
 
Ademas de ello la modernización de la TÉCNICA del micro injerto, donde se trasplanta una unidad de cabello, con un micro punch electrónico, mas la aparición de los nuevos tópicos (FINASTOPIC), ha demostrado el avance de la ciencia en el tratamiento de esta patología.


Te dejo 70 referencias bibliográficas sobre el tema y en el adjunto fotos de ALOPECIA ANDROGÉNICA en HOMBRE y MUJER.

Saludos a todos.

Dr. Jose Lapenta.
Dr. Jose M. Lapenta. 
 
 
 EDITORIAL ENGLISH
===================

Hello friends of the DERMAGIC EXPRESS network today with another interesting topic, currently much discussed and studied: ANDROGENIC ALOPECIA, AND THEIR THERAPEUTIC ALTERNATIVES.
 
Androgenetic alopecia (AGA), the most common type of hair loss, occurs in 80% of men and 50% of women, primarily due to genetic and hormonal factors.

1.) HISTORY:


- In ancient Egypt (1500 BC), male pattern baldness was already known, and texts such as the Ebers Papyrus recommended home remedies such as onions, lion fat, hippopotamus fat, and bat guano.


- Hippocrates of Kos (460-370 BC), a Greek physician considered the father of Western medicine, described male pattern baldness and noted its absence in eunuchs (males whose genitals had been removed and who were therefore unable to produce the hormone testosterone).

- James B. Hamilton (1909-1990): an American dermatologist from New York, established the relationship between androgenic alopecia and androgens in 1942 while studying eunuchs, and created the first classification of this condition into 5 types.

- O'Tar T. Norwood (1920-2022): an American dermatologist from Oklahoma specializing in hair transplants, modified and expanded the scale to 7 types in 1975, after analyzing 1,000 cases.

- Erich Ludwig: a German dermatologist specializing in trichology and hair diseases, who in 1977 developed A simplified scale of FEMALE PATTERN baldness, in 3 grades, is based on the fact that hair loss in women is diffuse and central, unlike in men who present different patterns.

2.) CLASSIFICATION:

A.) MEN: (Norwood-Hamilton Scale, 7 types):

- TYPES:

I: Normal frontal hairline.
II: Mild bifrontal receding hairline.
III: Deep receding hairline (±vertex).
IV: Frontal hairline advancement + partial vertex baldness.
V: Greater hair loss, minimal hairline.
VI: Frontal-vertex fusion.
VII: Posterior "U" hairline (80% of cases).

B.) WOMEN: (Ludwig Scale, 3 grades):

I: Mild central thinning.
II: Moderate with widened parting.
III: Advanced, possible total central baldness.

This classification is for educational and comprehension purposes, which can guide the treating physician in choosing the most appropriate method to treat the condition. In women, the DIFFUSE PATTERN predominates, while in men, the most common PATTERN is U-SHAPED ALOPECIA, accounting for 80% of cases (areas of baldness from the frontal region to the mid-occipital region, sparing lateral temporal and parietal areas).

2.) ETIOLOGY:


- First, it is important to explain to the NON-MEDICAL audience that androgenic alopecia is hair loss caused by an increase in ANDROGENS (mainly testosterone) in the body, in both men and women. Specifically, it is caused by its metabolite or derivative called DIHYDROTESTOSTERONE.

- This excess of ANDROGENS, specifically DIHYDROTESTOSTERONE, is deposited in the hair follicle and causes it to atrophy, resulting in hair loss. This is the main mechanism that causes androgenetic alopecia.

- Characterized by progressive hair loss, it affects both post-pubertal men and women, and can be severe in both sexes.

- In women, conditions such as polycystic ovary syndrome (PCOS) cause an increase in androgens, leading to hair loss.

- In men, the condition undoubtedly has a GENETIC component, as not everyone is affected. It's important to know that some men will never experience androgenetic alopecia, although there is usually a history of baldness in those affected.

3.) EVOLUTION:

It's important to explain  to explain that the hair is not "ADHERED WITH GLUE" to the scalp, it has a cycle of "LIFE: ANAGEN, or growth, lasts from 1 to 7 years, CATAGEN, or transición, that lasts from 2 to 3 months and TELOGEN or resting which lasts about 3 months, then the hair falls and is replaced by a new one.
 
USUALLY 50 TO 100 HAIRS FALL EVERY DAY.
 
It is interesting that you also know that when the body is submitted to a great STRESS, and other factors the hair enters prematurely in the TELOGEN PHASE and the hair begins to fall abundantly producing a remarkable ALOPECIA.
 
So factors such as the STRESS and others that alter the hair CYCLE will contribute to the ANDROGENIC ALOPECIA be worse.
 
Another factor that worsens ANDROGENIC ALOPECIA is the SEBORRHEIC DERMATITIS  of the scalp, commonly called "INCREASE OF THE GREASE IN THE HAIR, so that the more you use an anti-dandruff shampoo, there will be less SEBORRHEA therefore less hair loss.
 
 4.) TREATMENTS:
 
Treatments for ALOPECIA ANDROGENIC are varied, and I highlight the most used today:
 
 1.) MINOXIDIL, TOPICAL (ANTIHYPERTENSIVE).
 2.) FINASTERIDE (5-ALPHA REDUCTASE INHIBITOR).
 3.) DUTASTERIDE (5-ALPHA REDUCTASE INHIBITOR).
 4.) FLUTAMIDE (5-ALPHA REDUCTASE INHIBITOR).
 5.) CYPROTERONE ACETAT. (ORAL ANTICONCEPTIVE)
 6.) SPIRONOLACTONE. (ORAL ANTIDIURETIC).
 7.) SERENOA REPENS OR SAW PALMETTO (NATURIST, ANTI-ANDROGEN).
 8.) CYPERUS ROTUNDUS (NATURIST).
 9.) TOPICAL STEROIDS.
10.) ANTI-DANDRUFF SHAMPOO (KETOCONAZOLE, ZINC PIRYTHIONE, BIFONAZOLE)
 11.) DROSPIRENONE (ORAL ANTICONCEPTIVE).
 
5.) NEW TREATMENTS:

A.- TOPICAL:

- TOPICAL FINASTERIDE 0.25%: Launched in November 2024 under the name FINASTOPIC, by the Spanish laboratory ISDIN. This alternative had been sought since the 2000s and has the advantage over oral FINASTERIDE of minimizing side effects.

- CLASCOTERONE 5%: with the trade names Breezula and Winlevi: A topical androgen receptor (AR) antagonist, it blocks DIHYDROTESTOSTERONE locally without systemic effects; the product IS NOT APPROVED; it is in Phase III trials.

B.- NON-TOPICAL:

- Optimized PRP (iPRF): Fibrin-rich plasma with stem cells; 4-6 sessions per year to increase hair thickness.

- Oral minoxidil microdose (0.25-5 mg) + topical dutasteride.

- Hair mesotherapy:
Microinjections of vitamins, peptides, hyaluronic acid and minoxidil.

- LLLT Laser: Low-level laser therapy, approved by the FDA in 2007 for the treatment of androgenetic alopecia, considered a safe and effective device. The available devices of this type are:

- cHairMax® LaserComb (Lexington International): The first device approved (2007). It is a red diode laser comb (655 nm) for home use.

iRestore® Laser Growth System: Approved in 2016; it is a helmet with 21 diodes and 30 infrared LEDs.

- Capillus® / LaserCap® / Theradome®: Approved between 2012 and 2018, these are cap-type lasers with a frequency of 272-560 nm.

C. HAIR TRANSPLANTATION:


Hair transplants are NOT NEW. They began to be used in the 1930s, when the Japanese physician Dr. Shoji Okuda developed the "punch" grafting technique to restore hair in burn victims and those with alopecia.

- In the 1950s, the American physician Dr. Norman Orentreich (USA) performed the first modern transplant for baldness in 1952, a "punch" type procedure.

- EVOLUTION OF THE TECHNIQUE UNTIL 2025:


- 1950s-70s: Large punch grafts (4-5mm), unattractive ("doll-like").

- 1980s-90s: Micrografts (1-4 follicles) by Dr. Bobby Limmer (FUT).

- 2000s: FUE:
(2002, Dr. Rassman/FUE Research Committee).

The most widely used technique today (2025) is FUE (Follicular Unit Extraction): It extracts individual follicles (0.8-1 mm) with a motorized/robotic punch. No linear strip of skin is removed, and it leaves no visible scar. It has an 80-90% global utilization rate and offers rapid recovery.
 
6.) CONCLUSIONS:

There is in our body an ezyme called 5-alpha reductase that is responsible for converting TESTOSTERONE IN DIHYDROTESTOSTERONE. By increasing this metabolite, the greater the fall of hair.

Therefore, one of the strategies to avoid ANDROGENIC ALOPECIA is to inhibit the enzyme 5-alpha reductase, and for that already have been invented and discovered pharmacological and natural medicines: These are the ones already mentioned:
 
- DUTASTERIDE.
- FLUTAMIDA.
- SERENOA REPENS O SAW PALMETTO (NATURIST, ANTI-ANDROGEN).
CYPERUS ROTUNDUS (NATURIST).
 
 
All these medicines have their ADVANTAGES and their ADVERSE EFFECTS, but if we place ourselves in reality, science has advanced remarkably in this field, many years ago it was popularly said:
 
  "...TO THE FALL OF THE HAIR ONLY STOPS THE FLOOR OR SOIL .."
 
 Today this old adage is not true, mainly due to the appearance of drugs like DUTASTERIDE, FINASTERIDE and FLUTAMIDE, which inhibit the enzyme 5 alpha reductase, the main cause of the increase of ANDROGENS in our body.
 
In addition, the modernization of the micro-grafting technique, where a hair unit is transplanted with an electronic micro-punch, plus the emergence of new topical treatments (FINASTOPIC), has demonstrated the advancement of science in the treatment of this pathology. 
 
I leave you 70 bibliographical references on this theme and in the attached photos of ANDROGENIC ALOPECIA in MEN and WOMEN.
 


Alopecia androgenica difusa mujer adulta


Greetings.

Dr. Jose Lapenta.

Dr. Jose M. Lapenta.



 =============================================================
 REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES
 ============================================================= 
 =============================================================
1.) Increased scalp skin and serum 5 alpha-reductase reduced androgens in a man relevant to the acquired progressive kinky hair disorder and developing androgenetic alopecia.
2.) Androgen metabolism as it affects hair growth in androgenetic alopecia.
3.) [Finasteride: a new drug for the treatment of male hirsutism and androgenetic alopecia?] [La finasteride: un nuovo farmaco nel trattamento dell'irsutismo e dell' alopecia androgenica maschile?]
4.) Alterations in androgen conjugate levels in women and men with alopecia.
5.) Hormonal basis of male and female androgenic alopecia: clinical relevance.
6.) [Current treatment of androgenetic male and female alopecia(with the exception of hormone treatment)] [Traitements actuels des alopecies androgenetiques masculines et feminines (traitements hormonaux exceptes).]
7.) Androgenetic alopecia: an autosomal dominant disorder.
8.) [Hair growth promoters in androgenetic alopecia. Expectations and reality] [Haarwuchsmittel bei androgenetischer Alopezie. Anspruch und Realitat.]
9.) Effects of ozonized autohaemotherapy on human hair cycle.
10.) Estrogen and progesterone receptors in androgenic alopecia versus alopecia areata.
11.) Androgens and women's health.
12.) Female androgenetic alopecia: an update.
13.) A prospective study of the prevalence of clear-cut endocrine disorders and polycystic ovaries in 350 patients presenting with hirsutism or androgenic alopecia.
14.) Ketoconazole shampoo: effect of long-term use in androgenic alopecia. 
15.) Anagen hairs may fail to replace telogen hairs in early androgenic female alopecia. 
16.) Different levels of 5alpha-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia. 
17.) Safety surveillance of esterified estrogens-methyltestosterone
 (Estratest and Estratest HS) replacement therapy in the United States. 
18.) Balding hair follicle dermal papilla cells contain higher levels ofandrogen receptors than those from non-balding scalp.  
19.) A comparison of the culture and growth of dermal papilla cells from hair follicles from non-balding and balding (androgenetic alopecia) scalp. 
20.) Messenger RNA expression of steroidogenesis enzyme subtypes in thehuman pilosebaceous unit. 
21.) Treatment of androgen excess in females: yesterday, today and tomorrow. 
22.) Association of benign prostatic hyperplasia with male pattern baldness. 
23.) Hair regrowth. Therapeutic agents. 
24.) Androgenic effects of oral contraceptives: implications for patient compliance. 
25.) Diffuse hypertrichosis during treatment with 5% topical minoxidil.
26.) Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells. 
27.) Biphasic effects of minoxidil on the proliferation and differentiation of normal human keratinocytes. 
28.) Alopecia and mood stabilizer therapy. 
29.) Improvement in androgenetic alopecia (stage V) using topical minoxidil in a retinoid vehicle and oral finasteride [see comments] 
30.) Clinical significance of testosterone and dihydrotestosteronemetabolism in women] 
31.) The 5 alpha-reductase system and its inhibitors. Recent development
 and its perspective in treating androgen-dependent skin disorders. 
32.) Finasteride: a clinical review. 
33.) 19-nor-10-azasteroids: a novel class of inhibitors for human steroid 5alpha-reductases 1 and 2. 
34.) Genetic analysis of male pattern baldness and the 5alpha-reductase genes. 
35.) Effects of topically applied spironolactone on androgen stimulated sebaceous glands in the hamster pinna. 
36.) Androgens affect the activity of human sebocytes in culture in a manner dependent on the localization of the sebaceous glands and their effect is antagonized by spironolactone. 
37.) Antiandrogen treatment with spironolactone and linestrenol decreases bone mineral density in eumenorrhoeic women with androgen excess. 
38.) [Serum hormones before and during therapy with cyproterone acetate and spironolactone in patients with androgenization] 
39.) The insulin resistance in women with hyperandrogenism is partially reversed by antiandrogen treatment: evidence that androgens impair insulin action in women. 
40.) Topical spironolactone reduces sebum secretion rates in young adults. 
41.) Other antiandrogens. 
42.) Mechanism of action and pure antiandrogenic properties of flutamide. 
43.) Drospirenone: a novel progestogen with antimineralocorticoid and antiandrogenic activity.  
44.) Cutaneous Manifestations of Polycystic Ovary Syndrome: A Cross-Sectional Clinical Study.
45.) A Retrospective Review of Treatment Results for Patients With Central Centrifugal Cicatrical Alopecia.
46.) The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis.
47.) Dutasteride in androgenetic alopecia: An update.
48.) A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia.
49.) New Treatments for Hair Loss.
50.) Efficacy and safety of 5% minoxidil topical foam in male pattern hair loss treatment and patient satisfaction.
51.) Post-Finasteride Adverse Effects in Male Androgenic Alopecia: A Case Report of Vitiligo.
52.) Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review.
53.) Atypical post-finasteride syndrome: A pharmacological riddle.
54.) Emotional Consequences of Finasteride: Fool's Gold.
55.) The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride.
56.) Interventions for female pattern hair loss.
57.) Antiandrogenic Therapy with Ciproterone Acetate in Female Patients Who Suffer from Both Androgenetic Alopecia and Acne Vulgaris.
58.) Treatment of female pattern hair loss.
59.) [Spironolactone in dermatological treatment. On and off label indications].
60.) Treatment of male androgenetic alopecia with topical products containing Serenoa repens extract.
61.) Comparitive effectiveness of finasteride vs Serenoa repens in male androgenetic alopecia: a two-year study.
  =======================================================================

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lunes, 11 de agosto de 2025

FINASTERIDE 5 MG AND 1 MG IN ANDROGENIC ALOPECIA. / FINASTERIDE 5 MG Y 1 MG EN ALOPECIA ANDROGENICA.


 Finasteride 5 Mgr vs 1 Mgr in Androgenic Alopecia. !


Finasteride 5 Mgr vs 1 Mgr en Alopecia Androgénica. !


Finasteride y alopecia androgenica


 

 EDITORIAL ENGLISH
 =================== 
Hello friends of the DERMAGIC network, back with a very hot topic: FINASTERIDE 5 MG VS FINASTERIDE 1 MG IN ANDROGENIC ALOPECIA.

The first article I found on this drug dates back to 1993, and others from 1994 discussed 
FINASTERIDE as a promising drug for various conditions such as acne, HIRSUTISM, PROSTATE CANCER and BENIGN PROSTATIC HYPERPLASIA (BPH).

Later, it was discovered that finasteride was and is useful in the treatment of androgenetic alopecia.

But at that time, only the 5 MG version (PROSCAR) was available, and many people began using it twice a week: they would break the original pill into 4 parts, taking 1/4 of a pill daily. This motivated the company to market the 1 mg dosage form for exclusive use in ANDROGENIC ALOPECIA, under the name PROPECIA.

There are studies in which patients were given 5 mg 
FINASTERIDE daily for 2 years without side effects. Furthermore, the first report from 1993 showed that daily doses of 80 mg FINASTERIDE for 3 months caused no side effects.

However, subsequent studies showed that at doses of 1 mg, 
FINASTERIDE (PROPECIA), like all medications, has its side effects, mainly erectile dysfunction, mood swings, decreased semen volume, and in some cases, gynecomastia  and adenomas.

These reports appeared during the decade from 2010 to 2012, describing the so-called
POST-FINASTERIDE SYNDROME (PFS): which is still being discussed today, with symptoms that appear after prolonged treatment with this medication. I describe them as follows:

Symptoms included:

- Decreased libido.
- Erectile dysfunction.
- Changes in penile tissue.
- Loss of enjoyment or desire for sexual intercourse.
- Decreased sperm count.
- Gynecomastia, adenomas.
- Skin changes.
- Cognitive impairment: loss of memory and concentration.
- Fatigue.
- Anxiety, panic attacks.
- Depression.
- Suicidal ideation.
- Loss of muscle mass.
- Metabolic disorders.

MECHANISM PRODUCING THIS SYNDROME:

1.) FINASTERIDE inhibits the enzyme 5-alpha reductase type 2, blocking the conversion of testosterone to dihydrotestosterone (DHT), which is its main effect. This would cause an alteration in the levels of neuroactive steroids that regulate neurotransmitters such as GABA and serotonin in the brain.

2.) Alterations in hippocampal neurogenesis and changes in the gut microbiota that could influence symptoms have been detected.

3.) Genetic susceptibility and changes in androgen receptors and enzymes could be involved in the clinical manifestations.

Although this POST FINASTERIDE SYNDROME is documented and recognized by patients, it remains a topic of debate in the medical community today.

Among cases of female pattern baldness, 
FINASTERIDE was significantly more common with fetal damage and uterine disorders. Furthermore, drug-gene network analysis indicated that finasteride could profoundly alter pathways related to sex hormone signaling and oocyte maturation.

It was later discovered that 
FINASTERIDE is not useful in FEMALE pattern baldness, but is useful in HIRSUTISM.

HISTORICAL ACCOUNT:

Since it became known in the scientific world that 
FINASTERIDE produced hair growth, FINASTERIDE 5 mg (PROSCAR) began to be used, as I mentioned before, because FINASTERIDE 1 mg (PROPECIA) had not yet been marketed. The dosage: 10 mg weekly in 2 doses, Tuesdays and Thursdays, with good results.

Once FINASTERIDE 1 MG (PROPECIA) was released, the company began an
AGGRESSIVE CAMPAIGN, stating that the dose had to be 1 MG daily for 7 days a week, which would be 7 MG total, versus the 10 MG twice weekly doses of FINASTERIDE 5 MG (PROSCAR).

The TRUTH is that
FINASTERIDE 5 MG twice weekly is as good as or equal to FINASTERIDE 1 MG daily, and it's much cheaper, safer, and has fewer risks. A box of 30 tablets lasts 15 weeks (3 months and 3 weeks).

Perhaps one of the advantages that can be attributed to this regimen is that your body "rests" from the drug because you only take it twice a week, compared to taking 
FINASTERIDE 1 mg (PROPECIA) daily, from which your body doesn't rest; you always have the medicine "inside."

I went for the scientific route and used 
FINASTERIDE 5 mg in patients with androgenetic alopecia with the aforementioned regimen: 5 mg twice a week. After the fourth month, I observed significant improvement in the patients. See the attached photos.

CONCLUSIONS:

1.) 
FINASTERIDE is a wonderful product.

2.) 
FINASTERIDE5 mg twice a week is better than or equal to finasteride 1 mg daily.

3.) Merck S.D. launched PROPECIA for commercial and marketing purposes.

4.) FINASTERIDE IMPROVES BENIGN PROSTATIC HYPERPLASIA (BPH), AND PRODUCES notable improvement in ANDROGENIC ALOPECIA...!!!

5.)
TOPICAL FINASTERIDE, under the name FINASTOPIC, was be marketed by ISDIN in 2024. This has been talked about since 2000; the topical formulation most likely has fewer side effects than the oral formulation. In some presentations it comes combined with the popular MINOXIDIL, which is also useful in hair loss.

Finally, FINASTERIDE has recently been used in the treatment of
HIDRADENITIS SUPURATIVA, in both men and women, with good results. Its use as a hormonal agent is also proposed for the treatment of acne.

And its competition also emerged: DUTASTERIDE, which, in addition to being an oral formulation, comes in ampoules for local injection into the scalp. This formulation is the most commonly used, as the oral formulation is not officially approved for the treatment of this condition and is used off-label, given the beneficial clinical effects obtained.

Here is the link to the update on SERENOA REPENS or SAW PALMETTO versus FINASTERIDE for ANDROGENIC ALOPECIA.

In these references, you will learn about FINASTERIDE, its uses, and some of its adverse effects.

Greetings to all.

Dr, José Lapenta. 
Dr, José M.  Lapenta.  


Finasteride 5 Mg en Alopecia Androgenica



























 EDITORIAL ESPAÑOL
===================
Hola amigos de la red DERMAGIC, de nuevo con ustedes con un tema bien caliente: FINASTERIDE 5 MG VS FINASTERIDE 1 MG EN ALOPECIA ANDROGENICA.
 
 El primer trabajo que encontré sobre esta droga data del año 1.993 y otros mas de 1.994 donde se hablaba del FINASTERIDE COMO UNA DROGA promisoria en algunas PATOLOGÍAS COMO Acné, Hirsutismo, Cáncer de Próstata e  Hiperplasia prostatica benigna (BHP). 

Posteriormente se descubrió que el FINASTERIDE era y es útil en el tratamiento de  la ALOPECIA ANDROGÉNICA.
 
Pero para esa fecha solo existía la presentación de 5 MG, (PROSCAR), y mucha gente lo comenzó a usar 2 VECES por semana:  picaba la pastilla original en 4 PARTES, para tomar 1/ 4 de pastilla diaria. Esto motivo al laboratorio a sacar al mercado la presentación de 1 MG para su uso exclusivo en la ALOPECIA ANDROGÉNICA, con el nombre de PROPECIA.

EXISTEN estudios donde a pacientes se les dio FINASTERIDE 5 MGRS DIA POR 2 AÑOS SIN EFECTOS COLATERALES, MAS AUN,, en el primer reporte de 1.993 se DEMOSTRÓ que dosis diarias de 80 MGR /dia de FINASTERIDE por 3 meses NO OCASIONABAN EFECTOS SECUNDARIOS.
 
Pero en estudios posteriores se comprobó que a dosis de 1 MG, el FINASTERIDE, (PROPECIA), como todo medicamento tiene sus efectos secundarios principalmente LA DISFUNCIÓN ERÉCTIL, cambios en el humor, disminución del volumen del semen, y en algunos casos GINECOMASTIA Y ADENOMAS. 
 
Estos reportes aparecieron para la decada del 2010 al 2012 describiéndose el llamado SÍNDROME POST FINASTERIDE (SPF): el cual es discutido hoy en dia, con síntomas que se presentan luego de tratamientos prolongados con este medicamentos y te describo: 
 
Los síntomas incluyeron:
 
- Disminución de la libido.
- Disfunción eréctil.
- Cambios en el tejido del pene. 
- Perdida del disfrute o deseo por la relación sexual.
- Disminución del recuento de espermatozoides.
- Ginecomastia, adenomas.
- Cambios en la piel.
- Deterioro cognitivo: perdida de la memoria y concentración. 
- Fatiga.
- Ansiedad, ataques de pánico. 
- Depresión.
- Ideación suicida. 
- Perdida de masa muscular.
- Trastornos metabólicos. 
 
MECANISMO PRODUCTOR DE ESTE SÍNDROME: 
 
1.) El FINASTERIDE inhibe la enzima 5-alfa reductasa tipo 2, bloqueando la conversión de testosterona a dihidrotestosterona (DHT), ese es su principal EFECTO, esto provocaría una alteración de los niveles de esteroides neuroactivos que regulan neurotransmisores como GABA y serotonina en el cerebro.
 
2.) Se ha detectado alteración en la neuro génesis del hipocampo y cambios en la microbiota intestinal que podrían influir en los síntomas.
 
3.) La susceptibilidad genética y cambios, en receptores androgénicos y enzimas, pudieran estar implicados en las manifestaciones clínicas..

A pesar de que este
SÍNDROME POST FINASTERIDE esta documentado y reconocido por pacientes, hoy dia sigue siendo un tema de debate en la comunidad medica.
 
Entre los casos de alopecia femenina, EL FINASTERIDE fue significativamente más concurrente con el daño al feto y el trastorno del útero. Además, el análisis de la red de fármacos-genes indicó que el FINASTERIDE podría alterar profundamente las vías relacionadas con la señalización de las hormonas sexuales y la maduración de los ovocitos. 
 
Posteriormente se descubrió que el FINASTERIDE no es ÚTIL en la ALOPECIA ANDROGÉNICA femenina, pero si en el HIRSUTISMO.

RECUENTO HISTÓRICO:

Desde que se conoció en el mundo científico QUE EL FINASTERIDE producía crecimiento del cabello, comenzó a usarse el FINASTERIDE 5 MG (PROSCAR), como antes les mencione, porque el FINASTERIDE 1 MG (PROPECIA) no había salido al mercado. La dosis: 10 MG SEMANALES en 2 dosis, martes y jueves con BUEN RESULTADO. 

Una vez que salio al mercado el FINASTERIDE 1 MG, (PROPECIA), el laboratorio comenzó una CAMPAÑA AGRESIVA, diciendo que la dosis tenia que ser un 1 MG dia por 7 días a la semana, que serian 7 MG en total, versus los 10 MG en las 2 tomas semanales del FINASTERIDE 5 MG (PROSCAR). 

La VERDAD es que FINASTERIDE 5 MG 2 VECES SEMANAL es tan bueno o igual al FINASTERIDE 1 MG DIARIO, y el costo es muchísimo menor, mas seguro, menos riesgos. Una caja de 30 Tabs dura 15 semanas, (3 meses y 3 semanas). 
 
 Quizá una de las ventajas que puede atribuirsele a este esquema es que tu organismo ¨descansa¨ de la droga pues solo la tomas 2 veces semanal, en relación al FINASTERIDE 1 MG (PROPECIA) diario, del cual tu organismo no descansa, siempre tienes la medicina ¨adentro¨. 

Yo me fui por el lado científico y utilice el producto FINASTERIDE 5 MG       en pacientes con Alopecia Androgénica con el esquema antes dicho 5 MG 2 veces semanal y al 4to mes observe mejoría notable de los pacientes, vean las fotos del attach.

CONCLUSIONES:

1.) EL FINASTERIDE ES UN producto maravilloso. 

2.) EL FINASTERIDE 5 MG 2 veces semanal, es MEJOR o IGUAL que el FINASTERIDE 1 MG  DIARIO. 

3.) EL LABORATORIO MERCK.S.D LANZO la PROPECIA con fines COMERCIALES Y DE MERCADEO. 

4.)  EL FINASTERIDE MEJORA LA HIPERPLASIA PROSTÁTICA BENIGNA (HPB), Y PRODUCE mejoría notable en la ALOPECIA ANDROGÉNICA.. !!! 

5.) PARA el año 2024, salio al mercado el
FINASTERIDE TÓPICO, con el nombre de FINASTOPIC, por el laboratorio ISDIN. De esto se venia hablando desde el año 2000, muy probablemente la presentación tópica tiene menos efectos secundarios que la presentación oral; en algunas presentaciones viene combinado con el popular MINOXIDIL, el cual también es útil en la caída del cabello.
  
Para finalizar el FINASTERIDE a sido utilizado últimamente en el tratamiento de la HIDRADENITIS SUPURATIVA, tanto en hombres como mujeres con buen resultado. También se propone su uso como agente hormonal en el tratamiento del Acné.
 
Y también le salio su competencia: EL DUTASTERIDE,  el cual ademas de presentación oral, viene en ampollas para inyección local en el cuero cabelludo, siendo esta presentación la mas utilizada, pues la PRESENTACIÓN ORAL NO ESTA APROBADA OFICIALMENTE  para el tratamiento de esta patología, mas se usa off label, dado los efectos clínicos beneficiosos obtenidos.
 
Aquí te dejo el enlace a la actualización de la SERENOA REPENS o SAW PALMETTO versus el FINASTERIDE en la ALOPECIA ANDROGÉNICA. 

En estas referencias conocerás el FINASTERIDE , sus usos y algunos de sus efectos adversos. 

Saludos a todos ! 

Dr. José Lapenta.. 
Dr. José M. Lapenta.. 


================================================================== 
REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES 
================================================================== 

 F.- Relative safety and efficacy of finasteride for treatment of hirsutism (2004).
====================================================================         
1.) Five-year follow-up of patients with benign prostatic hyperplasia treated with  finasteride. 
2.) Therapeutic effects of finasteride in benign prostatic hyperplasia: a randomized  double-blind controlled trial. 
3.) The effect of finasteride on prostate volume, urinary flow rate and symptom score in  men with benign prostatic hyperplasia. 
4.) [5-alpha-reductase inhibitors]. 
5.) Benign prostatic hyperplasia. 
6.) The potential for hormonal prevention trials. 
7.) 5 alpha-reductase inhibition by finasteride (Proscar) in epithelium and stroma of human  benign prostatic hyperplasia. 
8.) Pharmacological treatment of benign prostatic hyperplasia with finasteride: a clinical  review. 
9.) Medical therapy for benign prostatic hyperplasia: A review of the literature. 
10.) Pretreatment with finasteride decreases perioperative bleeding associated with  transurethral resection of the prostate. 
11.) Urinary retention in patients with BPH treated with finasteride or placebo over 4  years. Characterization of patients and ultimate outcomes.The PLESS Study Group. 
12.) Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign  prostatic hyperplasia. 
13.) Chronic treatment with finasteride daily does not affect spermatogenesis or semen  production in young men. 
14.) Management of androgenetic alopecia. 
15.) Finasteride in the treatment of men with frontal male pattern hair loss. 
16.) Androgenetic alopecia in men: the scale of the problem and prospects for treatment. 
17.) [Androgenetic alopecia, hirsutism and hypertrichosis]. 
18.) Medical treatments for balding in men. 
19.) Understanding and managing common baldness. 
20.) Finasteride: a review of its use in male pattern hair loss. 
21.) Finasteride in the treatment of men with androgenetic alopecia. Finasteride Male  Pattern Hair Loss Study Group. 
22.) Genetic analysis of male pattern baldness and the 5alpha-reductase genes. 
23.) Effect of finasteride on human testicular steroidogenesis. 
24.) [Finasteride: a new drug for the treatment of male hirsutism and  androgenetic  alopecia]? 
25.) The 5 alpha-reductase system and its inhibitors. Recent development and its  perspective in treating androgen-dependent skin disorders. 
26.) Finasteride: a clinical review. 
27.) The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and  dihydrotestosterone concentrations in patients with male pattern baldness. 
28.) Finasteride: the first 5 alpha-reductase inhibitor. 
29.) Cytologic atypia in a 53-year-old man with finasteride-induced gynecomastia. 
30.) Reversible painful gynaecomastia induced by low dose finasteride (1 mg/day). 
31.) Measuring reversal of hair miniaturization in androgenetic alopecia by follicular counts 
in horizontal sections of serial scalp biopsies: results of finasteride 1 mg treatment of men  and postmenopausal women. 
32.) Improvement in androgenetic alopecia in 53-76-year-old men using oral finasteride. 
33.) New topical antiandrogenic formulations can stimulate hair growth in human bald  scalp grafted onto mice. 
34.) Current management of androgenetic alopecia in men. 
35.) Immunohistochemical localization of types 1 and 2 5alpha-reductase in human scalp. 
36.) The psychosocial consequences of androgenetic alopecia: a review of the research  literature. 
37.) Clinical dose ranging studies with finasteride, a type 2 5alpha-reductase inhibitor, in  men with male pattern hair loss. 
38.) The effects of finasteride on scalp skin and serum androgen levels in men with  androgenetic alopecia. 
39.) Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review.
40.) Interventions for Female Pattern Hair Loss.
41.) Differences in reproductive toxicology between alopecia drugs: an analysis on adverse events among female and male cases.
42.) Finasteride in Hidradenitis Suppurativa: A "Male" Therapy for a Predominantly "Female" Disease.
43.) Hidradenitis suppurativa treated with finasteride.
44.) The use of hormonal agents in the treatment of acne.
45.) Risk of gynecomastia and breast cancer associated with the use of 5-alpha reductase inhibitors for benign prostatic hyperplasia.
46.) Investigation of the Plausibility of 5-Alpha-Reductase Inhibitor Syndrome.
47.) Post-Finasteride Adverse Effects in Male Androgenic Alopecia: A Case Report of Vitiligo.
48.) Side Effects Related to 5 α-Reductase Inhibitor Treatment of Hair Loss in Women: A Review.
49.) 5 mg/day finasteride treatment for normoandrogenic Asian women with female pattern hair loss.
50.) Adverse effects of 5α-reductase inhibitors: What do we know, don't know, and need to know?
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