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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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viernes, 24 de octubre de 2025

THE SEBORRHEIC DERMATITIS, A REVIEW. / LA DERMATITIS SEBORREICA, REVISION


LA DERMATITIS SEBORREICA Y SUS ALTERNATIVAS TERAPÉUTICAS, ACTUALIZACIÓN.

  

THE SEBORRHEIC DERMATITIS AND THERAPEUTIC ALTERNATIVES, A REVIEW.

 


DERMATITIS SEBORREICA MEJILLAS

  

Dermatitis seborreica

PUBLICADO 2017 ACTUALIZADO 2025



 

EDITORIAL ESPAÑOL
===================
Hola amigos de la red, DERMAGIC EXPRESS de nuevo, hoy con el interesante tema: LA DERMATITIS SEBORREICA, una enfermedad no tan severa pero muy frecuente hoy en dia en la población, tanto niños como adultos, hombres y mujeres.
 
 
1.) HISTORIA:
 
La dermatitis seborreica fue descrita por primera vez en 1732 por Paul Gerson Unna,  medico Alemán, uno de los pioneros en dermatología. 
 
En 1873 el medico Italiano Giuseppe Rivalta sugirió un posible origen micótico de la DERMATITIS SEBORREICA.
 
En 1874 Louis-Charles Malassez medico oriundo de Francia, relacionó la presencia de levaduras llamadas Malassezia con la dermatitis seborreica, al identificar unas estructuras fungicas en el cuero cabelludo las cuales denomino "champignon de la pelade" ("hongo de la calvicie"), y las relaciono con la pitiriasis capitis (una afección ligada a la dermatitis seborreica). 
 
Su contribución fue importante y diriase clave al descubrir la presencia de estas levaduras en la piel, y su probable papel en algunas enfermedades dermatológicas. debido a este hecho, el género de estas levaduras fue nombrado "Malassezia" en su honor,
 
En 1952 Riccardo Galeazzi Leone medico italiano tambien,  encontró la asociación entre Pityrosporum ovale (hoy Malassezia furfur) y esta enfermedad.
 
Con respecto al hongo MALASSEZIA FURFUR, esta fue descubierta en 1846 por el médico ginecólogo y dermatólogo alemán Karl Ferdinand Eichstedt, relacionada con LA PITIRIASIS VERSICOLOR, también patología cutánea; y posteriormente también se le relaciono con la DERMATITIS SEBORREICA, como lo acabamos de mencionar.

2.) SÍNTOMAS CLÍNICOS:

La enfermedad afecta principalmente la cara, el cuero cabelludo, y también tórax anterior y posterior menos frecuentemente. 
 
Caracterizada por ser placas eritematosas y descamativas con prurito, es de evolución crónica y representa un verdadero reto su tratamiento, debido al hecho de que es frecuente su recaída, aun con las mejores opciones de tratamiento

Las areas mas afectadas del organismo son las llamadas "zonas seborréicas" que son las áreas del cuerpo con mayor concentración de glándulas sebáceas y donde suele aparecer la dermatitis seborréica, incluyen:

A - Cuero cabelludo: la línea de implantación del cabello, llamada corona seborréica, pero todo el cuero cabelludo puede estar afectado.

B - Región facial media:  cejas, surcos nasogenianos, alas de la nariz.
 
C - Región del pecho medio y zona interescapular de la espalda: entre  omóplatos.
 
D - Detrás de las orejas y conductos auditivos externos.
 
E - Pliegues axilares, submamarios e inguinales: no tan frecuente.

F   - Área periglútea: pliegue interg
lúteo.

G - Párpados y borde palpebral:  a veces afectando las pestañas, conocida con el nombre de BLEFARITIS SEBORREICA.

Estas zonas se caracterizan por presentar piel grasa, o con secreción sebácea abundante, lo cual favorece el desarrollo de la enfermedad.

En el cuero cabelludo la descamación producida por la DERMATITIS SEBORREICA es conocida con el nombre vulgar de "CASPA", quizá una de las causas mas frecuentes de la consulta dermatologica.


DERMATITIS SEBORREICA DE LA CARA

 

Dermatitis seborreica de la cara


3.) EVOLUCIÓN:

El Curso de la DERMATITIS SEBORREICA es crónico y recurrente, con períodos de remisión y exacerbación. 
 
Puede comenzar desde la infancia, y el rango mas comun esta en adultos jóvenes y mayores. 
 
Los brotes empeoran con estrés, clima frío o muy calurosoy enfermedades subyacentes (p. ej. VIH, Parkinson). En raros casos, en algunos pacientes puede generalizarse, pero suele limitarse a zonas seborreicas ya descritas.

4.)  TRATAMIENTOS:
 
A.- Decada de los años 50-60: comenzaron a utilizarce los corticosteroides topicos para disminuir la inflamacion Uso de corticosteroides tópicos, de baja potencia (HIDROCORTISONA) , la SULFACETAMIDA, y el AZUFRE, para disminuir la el prurito, eritema e inflamación, aun vigentes hoy dia.
 
B.- En la decada de los años 70-80: se introdujeron FORMALMENTE el uso de antimicoticos como KETOCONAZOL, FLUCONAZOL, BIFONAZOL, ITRACONAZOL, SERTACONAZOL, MICONAZOL, TREBINAFINA y CICLOPIROXOLAMINA, para controlar la levadura MALASSEZIA, algo tardio, pues la relacion de este hongo con la dermatitis seborreica se establecio practicamente en los años 50.
 
- En los eños 80 (1985), se introdujo ESPECIFICAMENTE el ITRACONAZOLE.
- En los alos 90 se comenzo a usar el METRONIDAZOLE en gel topico. 
 
C.- Decada de los años 90 - 2000: se introduce  el uso adicionalde queratoliticos y alquitranes (aceite de cade, urea) para mejorar la descamacion y producir la regeneracion cutanea.
 
- En los años 2000 aparecen el TACROLIMUS y PIMECROLIMUS, como alternativas terapeuticas. 
 
D.- Decadas de los años 2000 -2025: Se introduce la combinacion de los anteriores: antimicoticos topicos, con cosrtoesteroides de baja potencia, y formulas magistrales con bioasufre fluido, ciclopiroxolamina, y otros componentes,  preparadas en champu y cremas para uso topico.
 


DERMATITIS SEBORREICA SEVERA DEL CUERO CABELLUDO

 

Dermatitis seborreica cuero cabelludo

 
 
Hoy dia 2.025 les presento en esta revisión las MEJORES ALTERNATIVAS TERAPÉUTICAS que han sido descritas en el tratamiento de esta enfermedad: 

1.) CORTICOSTEROIDES TOPICOS:  CLOBETASOL,  DEXAMETASONA, MOMETASONA.
2.) UREA.
3.) ÁCIDO SALICÍLICO.
4.) PROPILENGLICOL.
5.) PIRITIONATO DE ZINC.
6.) BIOTINA.
7.) KETOCONAZOL.
8.) FLUCONAZOL.
9.) SERTACONAZOL.
10.) ITRACONAZOL.
11.) DITRANOL.
12.) SUCCINADO DE LITIO.
13.) VITAMINA-COMPLEJO B.
14.) PEROXIDO DE BENZOILO.
15.) SULFURO DE SELENIO.
16.) SULFACETAMIDA.
17.) TACROLIMUS y 18.) PIMECROLIMUS  (Hoy día 2025 estos medicamentos tienen una advertencia severa por la FDA tipo "BLACK BOX" o "CAJA NEGRA", en sus enpaques acerca de que el prolongado puede inducir malignidad)
18.) PIMECROLIMUS.
19.) METRONIDAZOL.
20.) TERBINAFINA.
21.) ALQUITRAN DE PINO.
22.) ALQUITRAN DE HULLA.
23.) GLICERINA.
24.) TACALCITOL.
25.) FOTOTERAPIA y FOTOQUIMIOTERAPIA
26.) AZUFRE.
27.) BIFONAZOL.
28.) CICLOPIROXOLAMINA.
29.) L - DOPA.
 
30.) SULFATO o GLUCONATO DE ZINC.

Probablemente existan  otras mas, de modo que el tratamiento de la DERMATITIS SEBORREICA hoy dia, constituye un RETO para todo dermatólogo, pues el indice de RECAÍDAS o BROTES es muy FRECUENTE.

5.) NUEVOS TRATAMIENTOS:

- ROFLUMILAST: es un inhibidor de la fosfodiesterasa-4 (PDE4) cuyo mecanismo de accion es reducir la inflamación cutánea. 
 
- Se trata de una espuma tópica  al 0,3% la cual fue aprobada el 16 de diciembre de 2023 por la FDA para el tratamiento de la DERMATITIS SEBORREICA, en adultos y niños mayores de 9 años de edad.
 
- Es el primer medicamento aprobado en más de dos décadas, quiere decir esto desde los años 80, para tratar esta patología; su principal efecto: controlar el enrojecimiento y la y la inflamación cutaea.

De resto se siguen utilizando las ya conocidas, cremas y champu comerciales, quedando como GRANDES opciones LAS FORMULACIONES MAGISTRALES para estos casos, como champús preparados a base de azufre, ácido salicílico y lociones capilares también preparadas, INTERCALADAS con productos ya conocidos.

La dermatitis seborreica en muchos casos es recalcitrante, difícil de tratar pues recaen mucho los pacientes una vez presentan mejoría, el exceso de grasa en la cara y el estrés son GRANDES factores desencadenantes y de recaídas.

Saludos a todos. 

Dr. José Lapenta.
Dr.  José M. Lapenta.
 
 
 
  
EDITORIAL ENGLISH
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Hello friends of the network, DERMAGIC EXPRESS is back again, today with the interesting topic: SEBORRHEIC DERMATITIS, a disease that is not very severe but very common nowadays in the population, affecting both children and adults, men and women.

1.) HISTORY:


SEBORRHEIC DERMATITIS was first described in 1732 by Paul Gerson Unna, a German physician and one of the pioneers in dermatology.

In 1873, the Italian physician Giuseppe Rivalta suggested a possible fungal origin for SEBORRHEIC DERMATITIS.

In 1874, Louis-Charles Malassez, a physician from France, linked the presence of yeasts called Malassezia to seborrheic dermatitis. He identified fungal structures on the scalp, which he called "champignon de la pelade" ("baldness fungus"), and associated them with pityriasis capitis (a condition linked to seborrheic dermatitis).

His contribution was significant and arguably key in discovering the presence of these yeasts on the skin and their probable role in some dermatological diseases. Because of this, the genus of these yeasts was named "Malassezia" in his honor.

In 1952, Riccardo Galeazzi Leone, also an Italian physician, discovered the association between PITYROSPORUM OVALE (now MALASSEZIA FURFUR) and this disease.

Regarding the fungus MALASSEZIA FURFUR, it was discovered in 1846 by the German gynecologist and dermatologist Karl Ferdinand Eichstedt, and was associated with PITYRIASIS VERSICOLOR, also a skin condition; and later it was also linked to SEBORRHEIC DERMATITIS, as we just mentioned.

2.) CLINICAL SYMPTOMS:

The disease primarily affects the face and scalp, and less frequently the anterior and posterior chest.

Characterized by itchy, scaly, erythematous plaques, seborrheic dermatitis is a chronic condition that presents a significant treatment challenge due to its frequent relapse, even with the best treatment options.

The most affected areas of the body are the so-called "seborrheic zones," which are areas with the highest concentration of sebaceous glands and where seborrheic dermatitis typically appears. These include:

A - Scalp: the hairline, called the seborrheic corona, but the entire scalp can be affected.

B - Midface: eyebrows, nasolabial folds, and sides of the nose.

C - Mid-chest and interscapular region of the back: between the shoulder blades.

D - Behind the ears and external auditory canals.

E - Axillary, inframammary, and inguinal folds: less common.

F - Perigluteal area: intergluteal fold.

G - Eyelids and eyelid margins: sometimes affecting the eyelashes, known as SEBORRHEIC BLEPHARITIS.

These areas are characterized by oily skin, or abundant sebum secretion, which favors the development of the disease.

On the scalp, the flaking caused by SEBORRHEIC DERMATITIS is commonly known as "DANDRUFF", perhaps one of the most frequent reasons for dermatological consultations.
 
3.) EVOLUTION:

The course of seborrheic dermatitis is chronic and recurrent, with periods of remission and exacerbation.

It can begin in childhood, and it is most common in young adults and older adults.

Outbreaks worsen with stress, cold or very hot weather, and underlying diseases (e.g., HIV, Parkinson's). In rare cases, it can become generalized in some patients, but it is usually limited to the seborrheic areas already described.

4.) TREATMENTS:

A.- 1950s-1960s: Topical corticosteroids began to be used to reduce inflammation. The use of low-potency topical corticosteroids (hydrocortisone), sulfacetamide, and sulfur to reduce itching, erythema, and inflammation is still current.

B. In the 1970s and 80s: the use of antifungals such as KETOCONAZOLE, FLUCONAZOLE, BIFONAZOLE, ITRACONAZOLE, SERTACONAZOLE, MICONAZOLE, TERBINAFINE and CYCLOPRIROXOLAMINE was FORMALLY introduced to control the MALASSEZIA yeast. This was somewhat late, as the relationship between this fungus and seborrheic dermatitis was practically established in the 1950s.

- In the 1980s (1985), ITRACONAZOLE was specifically introduced.

- In the 1990s, METRONIDAZOLE began to be used in topical gel form.

C.- From the 1990s to 2000: the additional use of keratolytic agents and tars (cade oil, urea) was introduced to improve scaling and promote skin regeneration.

- In the 2000s, TACROLIMUS  and PIMECROLIMUS emerged as therapeutic alternatives.

D.- 2000-2025: Combinations of the above were introduced: topical antifungals with low-potency corticosteroids, and MAGISTRAL FORMULATIONS with fluid biosulfur, ciclopiroxolamine, and other components, prepared as shampoos and creams for topical use. 


soborrheic dermatitis of the scalp
 
 
Today, in 2025, I present in this review the BEST THERAPEUTIC ALTERNATIVES that have been described in the treatment of this disease:
 
1.) TOPICAL CORTICOSTEROIDS: CLOBETASOL, DEXAMETASONE, MOMETASONE.
2.) UREA.
3.) SALIYLIC ACID.
4.) PROPYLENE-GLYCOL.
5.) PYRITHIONE ZINC.
6.) BIOTIN.
7.) KETOCONAZOLE.
8.) FLUCONAZOLE.
9.) SERTACONAZOLE.
10.) ITRACONAZOLE.
11.) DITHRANOL.
12.) LITHIUM SUCCINATE.
13.) VITAMIN-COMPLEX B.
14.) BENZOYL PEROXIDE.
15.) SELENIUM SULFIDE.
16.) SULFACETAMIDE.
17.) TACROLIMUS. 18.) PIMECROLIMUS, (Today 2023 these drugs TACROLIMUS AND PIMECROLIMUS have a severe warning from the FDA that their prolonged use can induce cancer)
18.) PIMECROLIMUS.
19.) METRONIDAZOLE.
20.) TERBINAFINE.
21.) PINE TAR.
22.) COALTAR.
23.) GLYCERINE.
24.) TACALCITOL.
25.) PHOTOTHERAPY.
26.) SULFUR.
27.) BIFONAZOLE.
28.) CYCLOPYROXOLAMINE.
29.) L-DOPA.
30.)  ZINC SULFATE OR ZINC GLUCONATE.
 
 
 
Seborrheic dermatitis of the face


There are probably other causes as well, so treating seborrheic dermatitis today presents a challenge for every dermatologist, as the rate of relapses or flare-ups is very frequent.

5.) NEW TREATMENTS:

- ROFLUMILAST: is a phosphodiesterase-4 (PDE4) inhibitor whose mechanism of action is to reduce skin inflammation.

- It is a 0.3% topical foam which was approved on December 16, 2023, by the FDA for the treatment of seborrheic dermatitis in adults and children over 9 years of age.

- It is the first medication approved in more than two decades, meaning since the 1980s, to treat this condition; its main effect is to control redness and skin inflammation.

Otherwise, the well-known commercial creams and shampoos continue to be used, with MAGISTRAL FORMULATIONS remaining excellent options for these cases, such as shampoos prepared with sulfur, salicylic acid, and hair lotions, interspersed with other commonly used products.

Seborrheic dermatitis is often recalcitrant and difficult to treat, as many patients relapse after showing improvement. Excess oil on the face and stress are major triggers and causes of relapse.

Greetings to all.

Dr. Jose Lapenta.
Dr. Jose M. Lapenta.


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REFRENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES
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1.) Topical metronidazole in seborrheic dermatitis - a double-blind study.
2.) Treatment of seborrheic dermatitis: comparison of sertaconazole 2 % cream versus pimecrolimus 1 % cream.
3.) Single-blind, randomized controlled trial evaluating the treatment of facial seborrheic dermatitis with hydrocortisone 1% ointment compared with tacrolimus 0.1% ointment in adults.
4.) New strategies in dandruff treatment: growth control of Malassezia ovalis.
5.) Narrow-band ultraviolet B (ATL-01) phototherapy is an effective and safe treatment option for patients with severe seborrhoeic dermatitis.
6.) Four cases of sebopsoriasis or seborrheic dermatitis of the face and scalp successfully treated with 1a-24 (R)-dihydroxycholecalciferol (tacalcitol) cream.
7.) High prevalence of seborrhoeic dermatitis on the face and scalp in mountain guides.
8.) The antifungal action of dandruff shampoos.
9.) Treatment of scalp seborrheic dermatitis and psoriasis with an ointment of 40% urea and 1% bifonazole.
10.) [Effect of anti-seborrhea substances against Pityrosporum ovale in vitro].
11.) Facial seborrheic dermatitis treated with fluconazole 2% shampoo.
12.) Pityrosporum ovale and skin diseases.
13.)[Therapy of seborrheic eczema with an antifungal agent with an antiphlogistic effect].
14.) [A case of seborrhoeic blepharitis].
15.) Treatment of sebopsoriasis with itraconazole.
16.) Treatment of seborrheic dermatitis.
17.) Pityrosporum ovale (Malassezia furfur) as the causative agent of seborrhoeic dermatitis: new treatment options.
18.) Relation Between Skin Temperature and Location of Facial Lesions in Seborrheic Dermatitis
19.) Insulin Quantification in Patients With Seborrheic Dermatitis
20.) Humoral immunity to Malassezia furfur serovars A, B and C in patients with pityriasis versicolor, seborrheic dermatitis and controls.
21.) Management of common superficial fungal infections in patients with AIDS.
22.) Pityrosporum infections.
23.) Seborrheic dermatitis as a revealing feature of HIV infection in Bamako, Mali [letter]
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25.) The efficacy of 1% metronidazole gel in facial seborrheic dermatitis: a double blind study.
26.) A double blind study of the effectiveness of sertaconazole 2% cream vs. metronidazole 1% gel in the treatment of seborrheic dermatitis.
27.) Pimecrolimus 1% cream, methylprednisolone aceponate 0.1% cream and metronidazole 0.75% gel in the treatment of seborrhoeic dermatitis: a randomized clinical study.
28.) Treatment with bifonazole shampoo for seborrhea and seborrheic dermatitis: a randomized, double-blind study.
29.) Quantitative skin cultures of Pityrosporum yeasts in patients seropositive for the human immunodeficiency virus with and without seborrheic dermatitis.
30.) A double-blind, placebo-controlled, multicenter trial of lithium succinate ointment in the treatment of seborrheic dermatitis. Efalith Multicenter Trial Group.
31.) Ketoconazole 2% emulsion in the treatment of seborrheic dermatitis.
32.) Seborrheic dermatitis in acquired immunodeficiency syndrome.
33.) Blood levels of vitamin E, polyunsaturated fatty acids of phospholipids, lipoperoxides and glutathione peroxidase in patients affected with seborrheic dermatitis.
34.) Skin surface lipids in HIV sero-positive and HIV sero-negative patients affected with seborrheic dermatitis.
35.) Seborrheic dermatitis and daylight [see comments]
36.) [Seborrheic dermatitis and cancer of the upper
respiratory and digestive tracts]
37.) The role of Pityrosporum ovale in seborrheic dermatitis.
38.) Correlation of Pityosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique.
39.) Immune reactions to Pityrosporum ovale in adult
patients with atopic and seborrheic dermatitis.
40.) [Treatment of seborrheic dermatitis with benzoyl peroxide]
41.)[The significance of yeasts in seborrheic eczema]
42.) Association of Pityrosporum orbiculare (Malassezia furfur) with seborrheic dermatitis in patients with acquired immunodeficiency syndrome (AIDS).
43.) Pityrosporum ovale in infantile seborrheic dermatitis.
44.)Infantile seborrheic dermatitis: seven-year follow-up and some prognostic criteria.
45.) Ketoconazole 2% cream versus hydrocortisone 1% cream in the treatment of seborrheic dermatitis. A double-blind comparative study.
46.) T-cell subset assay. A useful differentiating marker of atopic and seborrheic eczema in infancy?
47.) Propylene glycol in the treatment of seborrheic dermatitis of the scalp: a double-blind study.
48.) Seborrheic dermatitis and malignancy. An investigation of the skin flora.
49.) Efficacy of topical application of glucocorticosteroids compared with eosin in infants with seborrheic dermatitis.
50.) Erythema with features of seborrheic dermatitis and lupus erythematosus associated with systemic 5-fluorouracil.
51.)[Treatment of seborrheic dermatitis with low-dosage dithranol]
52.) Double-blind treatment of seborrheic dermatitis with 2% ketoconazole cream.
53.) Seborrheic dermatitis in neuroleptic-induced parkinsonism.
54.) Successful treatment and prophylaxis of scalp seborrhoeic dermatitis and dandruff with 2% ketoconazole shampoo: results of a multicentre, double-blind, placebo-controlled trial.
55.) Adherence of Malassezia furfur to human stratum corneum cells in vitro: a study of healthy individuals and patients with seborrhoeic dermatitis.
56.) Seborrhoeic dermatitis: treatment with anti-mycotic agents.
57.)Analyses of skin surface lipid in patients with microbially associated skin disease.
58.) Borage oil, an effective new treatment for infantile seborrhoeic dermatitis [letter]
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60.) [Skin lipids in seborrhea- and sebostasis-associated skin diseases]
61.) Use of topical lithium succinate in the treatment of seborrhoeic dermatitis [letter; comment]
62.) A dose-response study of irritant reactions to sodium lauryl sulphate in patients with seborrhoeic dermatitis and atopic eczema.
63.) Seborrhoeic dermatitis of the scalp--a manifestation of Hailey-Hailey disease in a predisposed individual?
64.) Use of topical lithium succinate in the treatment of seborrhoeic dermatitis [see comments]
65.) Erythema multiforme and dermatitis seborrhoides infantum as concomitant id-reactions to widespread candidosis in a suckling.
66.) The evaluation of various methods and antigens for the detection of antibodies against Pityrosporum ovale in patients with seborrhoeic dermatitis.
67.) Enhanced phagocytosis and intracellular killing of Pityrosporum ovale by human neutrophils after exposure to ketoconazole is correlated to changes of the yeast cell surface.
68.) [Therapy of seborrheic eczema with an antifungal agent with an antiphlogistic effect]
69.) Neutrophil zinc levels in psoriasis and seborrhoeic dermatitis.
70.) Skin surface electron microscopy in Pityrosporum folliculitis. The role of follicular occlusion in disease and the response to oral ketoconazole.
71.) Studies on the yeast flora in patients suffering from psoriasis capillitii or seborrhoic dermatitis of the scalp.
72.) [Histological differential diagnosis of psoriasis vulgaris and seborrheic eczema of the scalp]
73.) Tinea versicolor with regard to seborrheic dermatitis. An epidemiological investigation.
74.)Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis.
75.) Treatment of seborrheic dermatitis with biotin and vitamin B complex.
76.) L-dopa for seborrheic dermatitis.
77.) Seborrheic dermatitis of infants: treatment with biotin injections for the nursing mother.
78.) Photochemotherapy in erythrodermic seborrhoic dermatitis [letter]
79.) Old drug--in a new system--revisited.
80.) Oral use of biotin in seborrhoeic dermatitis of infancy: a controlled trial.
81.) Generalized seborrhoeic dermatitis. Clinical and therapeutic data of 25 patients.
82.)The effect of betamethasone valerate on seborrhoeic dermatitis of the scalp. A clinical, histopathological cell kinetic study.
83.) Topical glycerin in seborrhoeic dermatitis.
84.)[Therapeutic aspects of seborrhea oleosa and pityriasis simplex capillitii]
85.) Tinea versicolor and Pityrosporum orbiculare: mycological investigations, experimental infections and epidemiological surveys.
86.)[Some atypical forms of eczema in children (author's transl)]
87.) Efficacy and safety of a low molecular weight hyaluronic Acid topical gel in the treatment of facial seborrheic dermatitis final report.
88.) Treatment of seborrheic dermatitis: the efficiency of sertaconazole 2% cream vs. tacrolimus 0.03% cream.
89.) Comparison the efficacy of fluconazole and terbinafine in patients with moderate to severe seborrheic dermatitis.
90.) Efficiency of terbinafine 1% cream in comparison with ketoconazole 2% cream and placebo in patients with facial seborrheic dermatitis.
91.) A novel cosmetic antifungal/anti-inflammatory topical gel for the treatment of mild to moderate seborrheic dermatitis of the face: a open-label trial utilizing clinical evaluation and erythemadirected digital photography.
92.) Treatment of moderate to severe facial seborrheic dermatitis with itraconazole: an open non-comparative study.
93.) Role of antifungal agents in the treatment of seborrheic dermatitis.
94.) Investigations of seborrheic dermatitis. Part II. Influence of itraconazole on the clinical condition and the level of selected cytokines in seborrheic dermatitis.
95.) Efficacy and Safety of Cream Containing Climbazole/Piroctone Olamine for Facial Seborrheic Dermatitis: A Single-Center, Open-Label Split-Face Clinical Study.
96.) Topical Treatment of Facial Seborrheic Dermatitis: A Systematic Review.
97.) Low-dose oral isotretinoin for moderate to severe seborrhea and seborrheic dermatitis: a
randomized comparative trial.
98.) Effect of itraconazole on the quality of life in patients with moderate to severe seborrheic dermatitis: a randomized, placebo-controlled trial.
99.) Zinc Pyrithione: A Topical Antimicrobial With Complex Pharmaceutics.
100.) Topical pine tar: History, properties and use as a treatment for common skin conditions.
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