Bienvenido a mi blog donde abordo temas de las dos pasiones de mi vida: La dermatología y la Poesía.

Junio del 2007

Estás viendo los artículos de Antonio Rondón Lugo correspondientes al mes Junio del 2007.

Androgenetic Alopecia

Androgenetic Alopecia
Last Updated: March 8, 2006 Rate this Article

Synonyms and related keywords: common baldness, familial baldness, hereditary baldness, male pattern baldness, female pattern baldness, pattern baldness, hair loss, androgenic alopecia
Author: Robert P Feinstein, MD, Associate Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons
Robert P Feinstein, MD, is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Noah Worcester Dermatological Society, and Phi Beta Kappa

Editor(s): Leonard Sperling, MD, Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences; David F Butler, MD, Professor, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; and Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center

Disclosure

INTRODUCTION Section 2 of 9

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

Background: Androgenetic alopecia is an extremely common disorder affecting both men and women. The incidence is generally considered to be greater in males than females, although some evidence suggests that the apparent differences in incidence may be a reflection of different expression in males and females.
Pathophysiology: This genetically determined disorder is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients have a reduction in the terminal-to-vellus hair ratio, normally at least 2:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical distribution of hair loss.
Frequency:
• Internationally: This is an extremely common disorder that affects roughly 50% of men and perhaps as many women older than 40 years. As many as 13% of premenopausal women reportedly have some evidence of androgenetic alopecia. However, the incidence increases greatly in women following menopause, and, according to one author, it may affect 75% of women older than 65 years.
Mortality/Morbidity: This is essentially a cosmetic disorder. Other than affecting the patient psychologically, the disorder is significant only in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. Males with androgenetic alopecia may have an increased incidence of myocardial infarction. An increase in benign prostatic hypertrophy has also been associated. If these associations are proven conclusively, this disorder will be of greater clinical significance.
Race: The incidence and the severity of androgenetic alopecia tend to be highest in white men, second highest in Asians and African Americans, and lowest in Native Americans and Eskimos.
Age: Almost all patients have an onset prior to age 40 years, although many of the patients (both male and female) show evidence of the disorder by age 30 years.

CLINICAL Section 3 of 9

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

History:
• The onset is gradual.
• Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline. For the most part, the evolution of baldness progresses according to the Norwood/Hamilton classification of frontal and vertex thinning.
• Women usually present with diffuse thinning on the crown. Bitemporal recession does occur in women but usually to a lesser degree than in men. In general, women maintain a frontal hairline.
Physical:
• In both males and females with androgenetic alopecia, the transition from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs in the involved areas is gradual. As the disorder progresses, the anagen phase shortens with the telogen phase remaining constant. As a result, more hairs are in the telogen phase, and the patient may notice an increase in hair shedding. The end result can be an area of total denudation. This area varies from patient to patient and is usually most marked at the vertex.
• Women with androgenetic alopecia generally lose hair diffusely over the crown. This produces a gradual thinning of the hair rather than an area of marked baldness. The part is widest anteriorly.
• The frontal hairline is often preserved in women with this disorder, whereas men note a gradual recession of the frontal hairline early in the process.
Causes: Androgenetic alopecia is a genetically determined condition. Androgen is necessary for progression of the disorder, as it is not found in males castrated prior to puberty. The progression of the disorder is stopped if postpubertal males are castrated. Androgenetic alopecia is postulated to be a dominantly inherited disorder with variable penetrance and expression. However, it may be of polygenic inheritance. Recently, it was noted that follicles from balding areas of persons with androgenetic alopecia are able to produce terminal hairs when implanted into immunodeficient mice. This suggests that systemic or external factors may play a role in this disorder.
DIFFERENTIALS Section 4 of 9

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

Alopecia Areata
Anagen Effluvium
Telogen Effluvium

Other Problems to be Considered:
Alopecia of senescence
Alopecia associated with virilizing disorders of women where it may be seen with hirsutism and menstrual problems
Anagen effluvium after exposure to toxic chemicals, including chemotherapeutic agents
Alopecia associated with hypothyroidism or hyperthyroidism
Telogen effluvium may accelerate androgenetic alopecia, and causes, such as iron deficiency and papulosquamous diseases of the scalp, must be considered. Quick Find
Author Information
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Bibliography

Click for related images.

Related Articles
Alopecia Areata

Anagen Effluvium

Telogen Effluvium

Continuing Education
CME available for this topic. Click here to take this CME.

Patient Education
Click here for patient education.

WORKUP Section 5 of 9

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

Lab Studies:
• The most important aspects are the history and the physical examination.
o In the case of a woman, if virilization is evident, laboratory analysis of dehydroepiandrosterone (DHEA)-sulfate and testosterone may need to be obtained. Some authors have suggested that total testosterone level alone may be adequate to screen for a virilizing tumor.
o If a thyroid disorder is suspected, obtaining a thyrotropin level is indicated.
• If telogen effluvium is present, laboratory analysis of serum iron levels or a biopsy to note an underlying papulosquamous disorder may be indicated. Telogen effluvium may accelerate the course of pattern alopecia. Iron deficiency is a common and reversible cause of telogen effluvium. A normal CBC count does not exclude iron deficiency as a cause of hair loss. While a low ferritin level is always a sign of iron deficiency, ferritin behaves as an acute phase reactant, and levels may be normal despite iron deficiency. Iron, total iron-binding capacity, and transferrin saturation are inexpensive and sensitive tests for iron deficiency.
• Diffuse alopecia areata may mimic pattern alopecia. The presence of exclamation point hairs, pitted nails, or a history of periodic regrowth or tapered fractures noted on hair counts suggests the diagnosis of diffuse alopecia areata.
Procedures:
• A biopsy is rarely necessary to make the diagnosis. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected. Some dermatopathologists recommend that if a biopsy is to be performed, a sample should be obtained from 2 sites: one for horizontal sectioning and one for vertical sectioning of the hair follicles. Other dermatopathologists point out that one may commonly obtain sufficient information from serial vertical sections to diagnose the condition.
Histologic Findings: In pattern alopecia, hairs are miniaturized. In evolving-pattern alopecia, the diameter of hair shafts varies. Fibrous tract remnants (so-called streamers) can be found below miniaturized follicles. Although androgenetic alopecia is considered a noninflammatory form of hair loss, at times, a superficial, perifollicular, inflammatory infiltrate is noted. A mildly increased telogen-to-anagen ratio is often observed.
TREATMENT Section 6 of 9

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

Medical Care: Only 2 proven, food and drug administration (FDA)-approved medications are currently available for treatment of androgenetic alopecia: minoxidil and finasteride.
• Minoxidil
o Although the method of action is essentially unknown, minoxidil appears to lengthen the duration of the anagen phase, and it may increase the blood supply to the follicle. Regrowth is more pronounced at the vertex than in the frontal areas and is not noted for at least 4 months. Continuing topical treatment with the drug is necessary indefinitely because discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern.
o Patients who respond best to this drug are those who have a recent onset of androgenetic alopecia and small areas of hair loss. The drug is marketed as a 2% or a 5% solution, with the 5% solution being somewhat more effective. A recent 48-week study compared the 2 strengths in men. Findings indicated that 45% more regrowth occurred with the 5% compared with the 2% solution. In general, women respond better to topical minoxidil than men. The increase in effectiveness of the 5% solution was not evident for women in the FDA-controlled studies. Subsequent studies have shown at best a modest advantage to the higher concentration in women. In addition, the occurrence of facial hair growth appears to be increased with the use of the higher-concentration formulation.
• Finasteride
o Finasteride is given orally and is a 5 alpha-reductase type 2 inhibitor. It is not an antiandrogen. The drug can be used only in men because it can produce ambiguous genitalia in a developing male fetus. Finasteride has been shown to diminish the progression of androgenetic alopecia in males who are treated, and, in many patients, it has stimulated new regrowth.
o Although it affects vertex balding more than frontal hair loss, the medication has been shown to increase regrowth in the frontal area as well. Finasteride must be continued indefinitely because discontinuation results in gradual progression of the disorder. A study in postmenopausal women indicated no beneficial effect of the medication in treating female androgenetic alopecia.
• Some drugs are non-FDA-approved but potentially helpful medications. In women with androgenetic alopecia, especially those with a component of hyperandrogenism, drugs that act as androgen suppressants or antagonists (eg, spironolactone, oral contraceptives) may be beneficial.
• Androgenetic alopecia is very common; therefore, not surprisingly, it may accompany other forms of hair loss. Cases of telogen effluvium often occur in patients with underlying androgenetic alopecia. Therefore, a search for treatable causes of telogen effluvium (eg, anemia, hypothyroidism), especially in patients with an abrupt onset or a rapid progression of their disease, is indicated.
Surgical Care:
• Surgical treatment of androgenetic alopecia has been successfully performed for the past 4 decades. Although the cosmetic results are often satisfactory, the main problem is covering the bald area with donor plugs (or follicles) sufficient in number to be effective. Micrografting produces a more natural appearance than the old technique of transplanting plugs. Patients with less than 40 follicular units/cm2 in their donor areas are poor candidates for the procedure. Scalp reduction has been attempted to decrease the size of the scalp to be covered by transplanted hair. However, the scars produced by the reduction technique often spread and become more noticeable with time.
• Hair weaving techniques are available, and, together with hairpieces, they offer the patient a prosthetic method of coverage.

Escrito por Antonio Rondon Lugo el 29 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y General y Lecturas sugeridas.

Alopecia Areata

Alopecia Areata
Last Updated: June 21, 2006 Rate this Article

Author: Chantal Bolduc, MD, FRCPC, Assistant Professor, Department of Dermatology, University of Montreal
Coauthor(s): Harvey Lui, MD, FRCPC, Professor and Chairman, Department of Dermatology and Skin Science, Vancouver General Hospital, University of British Columbia; Jerry Shapiro, MD, FRCPC, Clinical Associate Professor, Department of Medicine, Division of Dermatology, University of British Columbia, Canada
Chantal Bolduc, MD, FRCPC, is a member of the following medical societies: American Academy of Dermatology, and Canadian Dermatology Association

Editor(s): Leonard Sperling, MD, Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences; Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA; Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory; Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania; and William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

Disclosure

INTRODUCTION Section 2 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Background: Alopecia areata (AA) is a recurrent nonscarring type of hair loss that can affect any hair-bearing area. Clinically, AA can present with many different patterns. Although medically benign, AA can cause tremendous emotional and psychosocial stress in affected patients and their families.
Pathophysiology: The pathophysiology of alopecia areata remains unknown. The most widely accepted hypothesis is that AA is a T-cell mediated autoimmune condition that is most likely to occur in genetically predisposed individuals.
Autoimmunity
Much evidence supports the hypothesis that AA is an autoimmune condition. The process appears to be T-cell mediated, but antibodies directed to hair follicle structures also have been found in AA patients with increased frequency compared to control subjects. Using immunofluorescence, antibodies to anagen phase hair follicles were found in as many as 90% of patients with AA compared to fewer than 37% of control subjects. The autoantibody response is heterogeneous and targets multiple structures of the anagen phase hair follicle. The outer root sheath is the structure targeted most frequently, followed by the inner root sheath, the matrix, and the hair shaft. Whether these antibodies play a direct role in the pathogenesis or whether they are an epiphenomenon is not known yet.
Histologically, lesional biopsies of AA show a perifollicular lymphocytic infiltrate around anagen phase hair follicles. The infiltrate consists mostly of T-helper cells and, to a lesser extent, T-suppressor cells. CD4+ and CD8+ lymphocytes likely play a prominent role because the depletion of these T-cell subtypes results in complete or partial regrowth of hair in the Dundee experimental bald rat (DEBR) model of AA. The animals subsequently lose hair again once the T-cell population is replete. The fact that not all animals experience complete regrowth suggests that other mechanisms likely are involved. Total numbers of circulating T lymphocytes have been reported with both decreased and normal levels.
Recent studies in humans also reinforce the hypothesis of autoimmunity. Studies have shown that hair regrows when affected scalp is transplanted onto SCID (severe combined immunodeficiency) mice that are devoid of immune cells. Autologous T lymphocytes isolated from affected scalp were cultured with hair follicle homogenates and autologous antigen-presenting cells. Following initial regrowth, injection of the T lymphocytes into the grafts resulted in loss of regrown hairs. Injections of autologous T lymphocytes that were not cultured with follicle homogenates did not trigger hair loss.
A similar experiment on nude (congenitally athymic) mice failed to trigger hair loss in regrown patches of AA after serum from affected patients was injected intravenously into the mice. However, the same study showed that mice injected with AA serum showed an increased deposition of immunoglobulin and complement in hair follicles of both grafted and nongrafted skin compared to mice injected with control serum, which showed no deposition.
In addition, it has been shown that AA can be induced using transfer of grafts from AA-affected mice onto normal mice. Transfer of grafts from normal mice to AA-affected mice similarly resulted in hair loss in the grafts. In conclusion, certain factors within the hair follicles, and possibly, in the surrounding milieu, trigger an autoimmune reaction. Adding or subtracting immunologic factors profoundly modifies the outcome of hair growth.
Clinical evidence favoring autoimmunity suggests that AA is associated with other autoimmune conditions, the most significant of which are thyroid diseases and vitiligo (see History).
In conclusion, the beneficial effect of T-cell subtype depletion on hair growth, the detection of autoantibodies, the ability to transfer AA from affected animals to nonaffected animals, and the induction of remission by grafting affected areas onto immunosuppressed animals are evidence in favor of an autoimmune phenomenon.
Genetics
Many factors favor a genetic predisposition for AA. The frequency of positive family history for AA in affected patients has been estimated to be 10-20% compared to 1.7% in control subjects. The incidence is higher in patients with more severe disease (16-18%) compared to patients with localized AA (7-13%). Reports of AA occurring in twins also are of interest. No correlation has been found between the degree of involvement of AA and the type of AA seen in relatives.
Several genes have been studied and a large amount of research has focused on human leukocyte antigen. Two studies demonstrated that human leukocyte antigen DQ3 (DQB1*03) was found in more than 80% of patients with AA, which suggests that it can be a marker for general susceptibility to AA. The studies also found that HLA DQ7 (DQB1*0301) and human leukocyte antigen DR4 (DRB1*0401) were present significantly more in patients with alopecia totalis (AT) and alopecia universalis (AU).
Another gene of interest is the interleukin-1 receptor antagonist gene, which may correlate with disease severity. Finally, the high association of Down syndrome with AA suggests the involvement of a gene located on chromosome 21.
In summary, genetic factors are likely to play an important role in determining susceptibility and disease severity. AA is likely to be the result of polygenic defects rather than a single gene defect. The role of environmental factors in initiating or triggering the condition is yet to be determined.
Cytokines
Interleukin 1 and tumor necrosis factor were shown to be potent inhibitors of hair growth in vitro. Subsequent microscopic examination of these cultured hair follicles showed morphologic changes similar to those seen in AA.
Innervation and vasculature
Another area of interest concerns the modification of perifollicular nerves. The fact that patients with AA occasionally complain of itching or pain on affected areas raises the possibility of alterations in the peripheral nervous system. Circulating levels of the neuropeptide calcitonin gene-related peptide (CGRP) were decreased in 3 patients with AA compared to control subjects. CGRP has multiple effects on the immune system, including chemotaxis and inhibition of Langerhans cell antigen presentation and inhibition of mitogen-stimulated T-lymphocyte proliferation.
CGRP also increases vasodilatation and endothelial proliferation. Similar findings were reported in another study, in which decreased cutaneous levels of substance P and of CGRP but not of vasoactive intestinal polypeptide were found in scalp biopsies. The study also noted a lower basal blood flow and greater vasodilatation following intradermal CGRP injection in patients with AA compared to control subjects. More studies are needed to shed light on the significance of these findings.
Viral etiology
Other hypotheses have been proposed to explain the pathophysiology of AA, but more evidence is needed to support them. AA was believed to possibly have an infectious origin, but no microbial agent has been isolated consistently in patients. Many efforts have been made to isolate cytomegalovirus, but most studies have been negative.
Frequency:
• In the US: Prevalence in the general population is 0.1-0.2%. The lifetime risk of developing AA is estimated to be 1.7%. AA is responsible for 0.7-3% of patients seen by dermatologists.
• Internationally: Worldwide prevalence of AA is the same as in the US.
Mortality/Morbidity: AA is a benign condition and most patients are asymptomatic; however, it can cause emotional and psychosocial stress in affected individuals. Self-consciousness concerning personal appearance can become important. Openly addressing these issues with patients is important in helping them cope with the condition.
Race: All races are affected equally by AA; no increase in prevalence has been found in a particular ethnic group.
Sex: Data concerning the sex ratio for AA vary slightly in the literature. In one study including 736 patients, a male-to-female ratio of 1:1 was seen. In another study on a smaller number of patients, a slight female preponderance was seen.
Age: AA can occur at any age from birth to the late decades of life. Congenital cases have been reported. Peak incidence appears to occur from age 15-29 years. As many as 44% of people with AA have onset at younger than 20 years. Onset in patients older than 40 years is seen in fewer than 30% of patients with AA.
History: The natural history of AA is unpredictable. Extreme variations in duration and extent of the disease occur from patient to patient.
• AA most often is asymptomatic, but some patients (14%) experience a burning sensation or pruritus in the affected area.
• The condition usually is localized when it first appears. Of patients with AA, 80% have only a single patch, 12.5% have 2 patches, and 7.7% have multiple patches. No correlation exists between the number of patches at onset and subsequent severity.
• AA most often affects the scalp (66.8-95%); however, it can affect any hair-bearing area. The beard is affected in 28% (males; see Image 1), eyebrows in 3.8%, and extremities in 1.3% of patients (see Image 2). More than one area can be affected at once.
• Localized AA: Episodes of localized (<50% involvement) patchy AA usually are self-limited; spontaneous regrowth occurs in most patients within a few months, with or without treatment.
• Extensive AA: Extensive (>50% involvement) forms of AA are less common. AT or AU were reported to occur at some point in 7% of patients; AA involving more than 40% hair loss is seen in 11%. The proportion of patients with AT appears to decrease with every decade of life.
o In 30% of patients with AT, complete hair loss occurred within 6 months after onset of disease. Sharma reported a mean progression period to AT of 4 months after onset. The natural evolution of AT is unpredictable, but recurrences of AA (not necessarily AT) are expected.
o In a study involving 736 patients, the relapse rate was 90% over 5 years. One percent of children and 10% of adults can experience long-lasting regrowth. Forty-four percent of children and 34% of adults experience a significant period of normal or near-normal hair growth. Twenty-two percent of children and 34% of adults do not experience regrowth.
• Associated conditions: Because some of the entities associated with AA occur uncommonly in the general population, a large number of patients with AA need to be examined to confirm whether an increased prevalence of these conditions exists among patients with AA. Unfortunately, most studies are performed on small groups; therefore, the data should be interpreted carefully.
o Atopic dermatitis is seen in 9-26% of patients with AA. In the general population, the prevalence of atopic dermatitis in children in temperate developed countries varies from 5-20%. In adults, the prevalence decreases to 2-10%. Some authors have found atopy to be a poor prognostic factor for AA.
o Vitiligo is seen with an incidence varying from 1.8-3% compared to 0.3% in control subjects.
o Thyroid disease: Clinically evident thyroid disease was found in 0.85% of 1700 patients with AA. The prevalence of thyroid disease determined on a clinical or laboratory basis varies among studies from 0.85-14.7%. The incidence of thyroid disease in control subjects is estimated to be 0.17-2%.
o The presence of microsomal antibodies is found in 3.3-16% of patients. Antibodies can be found with or without signs or symptoms of thyroid disease, but patients with positive autoantibodies have a higher incidence of functional abnormalities found on thyroid-releasing hormone tests (26% vs 2.8%). The incidence of thyroid microsomal and thyroglobulin antibodies in control subjects is 7%. Other studies have not supported these results. A study in 100 patients with AA failed to find an increased incidence of circulating autoantibodies including mitochondrial and thyroglobulin antibodies.
o Collagen vascular diseases have been found in 0.6-2% of patients with AA, while the incidence in control subjects was 0.17%. The incidence of AA in 39 patients with lupus erythematous was 10% in a study by Werth et al, in contrast to 0.42% of general dermatologic patients.
o Diabetes mellitus was found to be more common in control subjects (1.4%) than in patients with AA (0.4%). The occurrence of AA may protect against the appearance of insulin-dependent diabetes mellitus. However, the incidence of type I diabetes mellitus was significantly higher in relatives of patients with AA compared to the general population.
o Down syndrome: AA is seen in 6-8.8% of patients with Down syndrome, but only 0.1% of patients with AA have Down syndrome. The high frequency of AA in patients with Down syndrome suggests that a genetic linkage for AA may exist on chromosome 21.
o Emotional stress and psychiatric disease: Anxiety, personality disorders, depression, and paranoid disorders are seen with increased incidence varying from 17-22% of patients, and the lifetime prevalence of psychiatric disorders was estimated to be 74% in patients with AA. Psychiatric problems are seen in both children and adults. No association has been made between the severity of the psychiatric disorder and that of AA.
o Stressful life events within the 6-month period preceding episodes of AA were significantly higher in patients with AA compared to patients with androgenetic alopecia or tinea capitis. Major stress factors (eg, death in family) were reported in 12% of patients.
o Others associations: Pernicious anemia, myasthenia gravis, ulcerative colitis, lichen planus, and Candida endocrinopathy syndrome also have been associated with AA in some studies.
• Precipitating factors: A precipitating factor can be found in 15.1% of patients with AA. Major life events, febrile illnesses, drugs, pregnancy, trauma, and many other events have been reported, but no clear conclusions can be drawn. Despite these findings, most patients with AA fail to report a triggering factor preceding episodes of hair loss.
Physical:
• Presence of smooth slightly erythematous (peach color) or normal-colored alopecic patches is characteristic.
• Presence of exclamation point hairs (ie, hairs tapered near proximal end) is pathognomonic but is not always found.
• Positive pull test at the periphery of a plaque usually indicates that the disease is active, and further hair loss can be expected.
• Hair loss on other hair-bearing areas also favors the diagnosis.
• The most common presentation is the appearance of 1 or many round-to-oval denuded patches.
• No epidermal changes are associated with the hair loss.
• AA can be classified according to its pattern.
o Hair loss most often is localized and patchy (see Image 3).
o Reticular pattern occurs when hair loss is more extensive and the patches coalesce.
o Ophiasis pattern occurs when the hair loss is localized to the sides and lower back of the scalp (see Image 4).
o Conversely, sisaipho (ophiasis spelled backwards) pattern occurs when hair loss spares the sides and back of the head (see Image 5).
o AT occurs with 100% hair loss on the scalp (see Image 6).
o AU occurs with complete loss of hair on all hair-bearing areas.
o AA usually is focal; however, it can be diffuse, thereby mimicking telogen effluvium (TE) or the type of androgenetic alopecia seen in women (see Image 7).
• Nail involvement is as follows:
o Nail involvement is found in 6.8-49.4% of patients and most commonly is seen in patients with severe forms of AA.
o Pitting is the most common finding.
o Several other abnormalities have been reported (eg, trachyonychia, Beau lines, onychorrhexis, onychomadesis, koilonychia, leukonychia, red lunulae).
o Fingernails predominantly are affected.
Causes: The true cause of AA remains unknown. The exact role of possible factors needs to be clarified (see Pathophysiology).
• No known risk factors exist for AA, except positive family history.
• The exact role of stressful events remains unclear, but they most likely trigger a condition already present in susceptible individuals, rather than acting as the true primary cause.
Other Problems to be Considered:
Trichotillomania: Alopecic patches have unusual shapes and sizes and show broken hairs; no inflammation or epidermal change occurs. A scalp biopsy can be helpful if the diagnosis is difficult clinically.

Tinea capitis: The diagnosis is suggested by erythema, scaling, and crusting locally on the scalp.

Scarring alopecia and posttraumatic alopecia: These can be differentiated by the absence of follicular ostia or some degree of atrophy.

Syphilis: Syphilis rarely is seen but should be suspected in patients at high risk or with other signs or symptoms.

Telogen effluvium (TE) and androgenetic alopecia: Exclude these when hair loss is diffuse. In androgenetic alopecia, hair loss is patterned and usually is slowly progressive rather than acute. Differentiating TE from diffuse AA is difficult in absence of an obvious precipitating factor that can result in TE. Hair loss on other hair-bearing areas can be helpful and favors a diagnosis of AA.
Procedures:
• Diagnosis usually can be made on clinical grounds; a scalp biopsy seldom is needed, but can be helpful when clinical diagnosis is less certain.
Histologic Findings: A histologic diagnosis of AA can be made when characteristic features are present. Horizontal sections usually are preferred to vertical sections, since they allow examination of multiple hair follicles at different levels.
The most characteristic feature is a peribulbar lymphocytic infiltrate, which is described as appearing similar to a swarm of bees. The infiltrate often is sparse and usually involves only a few of the affected hairs in a biopsy specimen. Occasionally, no inflammation is found, which can result in diagnostic difficulties. A significant decrease in terminal hairs is associated with an increase in vellus hairs, with a ratio of 1.1:1 (normal is 7:1). Other helpful findings include pigment incontinence in the hair bulb and follicular stellae.
A shift occurs in the anagen-telogen ratio, which is not specific. The normal ratio is approximately 90% anagen phase to 10% telogen phase hair follicles; in AA, 73% of hairs were found to be in the anagen phase and 27% in the telogen phase. In long-standing cases of AA, the percentage of telogen phase hairs can approach 100%. Degenerative changes of the hair matrix can be found but are uncommon. Eosinophils may be present in fibrous tracts and near hair bulbs.
Tratamientos
Medical Care: Treatment is not mandatory because the condition is benign, and spontaneous remissions and recurrences are common. Treatments used are believed to stimulate hair growth, but no evidence exists that they influence the ultimate natural course of the disease. Treatment modalities usually are considered first according to the extent of hair loss and the patient's age.
Assessment of the efficacy of a treatment must be considered with care, since the condition is highly unpredictable in presentation, evolution, and response to treatment. Little data exist regarding the natural evolution of the condition. For example, in patients with less than 40% scalp involvement, a study showed no benefit with treatment (minoxidil 1% and topical immunotherapy) over placebo. The high spontaneous remission rate makes it difficult to assess clearly the true efficacy of a therapy unless appropriate controls with placebo treatment are studied.
For patients with extensive AA (>40% hair loss), little data exist on the natural evolution. The rate of spontaneous remission appears to be less than in patients with less than 40% involvement. Vestey and Savin reviewed 50 patients with extensive AA. Of the 50 patients, 24% experienced spontaneous complete or nearly complete regrowth at some stage during the observation period of 3-3.5 years. The relapse rate is high in patients with severe forms of AA.
Patients with AT/AU usually have a poorer prognosis, and treatment failure is seen in most patients with any therapy.
Since AA is believed to be an autoimmune condition, different immunomodulators have been used to treat this condition. Additional treatment options for AA include minoxidil and other treatment modalities.
• Corticosteroids
o Intralesional steroids: Few studies are available regarding the efficacy of intralesional steroids, but they are used widely in the treatment of AA.
 Intralesional steroids are the first-line treatment in localized conditions.
 In a study including 84 patients, regrowth on treated areas was present in 92% of patients with patchy AA and 61% of patients with AT. Regrowth persisted 3 months after treatment in 71% of patients with patchy AA and 28% of patients with AT. Regrowth usually is seen within 4-6 weeks in responsive patients. Patients with rapidly progressive, extensive, or long-standing AA responded poorly.
 Another study showed regrowth in most patients (480) treated with intralesional steroids, except in 2 patients with AU.
 Hair growth may persist for 6-9 months after a single injection.
 Injections are administered intradermally using a 3-mL syringe and a 30-gauge needle.
 Triamcinolone acetonide (Kenalog) is used most commonly; concentrations vary from 2.5-10 mL.
 Less than 0.1 mL is injected per site, and injections are spread out to cover the affected areas (approximately 1 cm between injection sites; see Image 8).
 Adverse effects mostly include pain during injection and minimal transient atrophy (10%). The atrophy rarely can be severe and permanent.
 Injections are administered every 4-6 weeks.
 Avoid reinjecting areas of denting, which usually is sufficient to allow atrophy to revert.
o Topical steroids: Few studies have been performed regarding the efficacy of topical steroids in the treatment of AA, and their usefulness remains under debate.
 Fluocinolone acetonide cream 0.2% (Synalar HP) twice per day induced a satisfactory-to-excellent response in 61% of patients, which was maintained in 71% of patients. Children younger than 10 years responded better, as did patients with a duration of hair loss of less than 1 year.
 Betamethasone dipropionate cream 0.05% (Diprosone) showed similar efficacy.
 A 2005 study by Tosti et al in patients with AT/AU showed that the use of 2.5 g of clobetasol propionate under occlusion with a plastic film 6 d/wk for 6 months induced regrowth in 8 (28.5%) of 28 patients. Regrowth was seen 6-14 weeks after the onset of therapy. Regrowth was maintained for at least 6 months after cessation of therapy in 5 (62.5%) of 8 patients. Even though only 17.8% of patients showed long-term benefits from that treatment, keep in mind that the study was performed in a subgroup of patients that is usually refractory to treatment.
 Treatment must be continued for a minimum of 3 months before regrowth can be expected, and maintenance therapy often is necessary.
 Despite these data, the authors do not believe that monotherapy with a topical steroid has been of great benefit in the authors' practice.
 The most common adverse effect is local folliculitis, which appears after a few weeks of treatment. Telangiectasias and local atrophy also have been reported. No systemic adverse effects have been reported.
o Prednisone: The use of systemic steroids for the treatment of AA is under much debate. Some authors support a beneficial role of systemic steroids in halting the progression of AA, but many others have had poor results with this form of therapy.
 Rate of regrowth varies greatly (27-89%), and many dose regimens have been used in these studies.
 Although the initial regrowth appears promising, the prednisone dose necessary to maintain cosmetic growth usually must be high enough that adverse effects are inevitable, and most patients relapse after therapy is discontinued.
 Some benefit was shown using minoxidil 2% solution applied twice per day following a 6-week taper of prednisone, but the relapse rate remained at a minimum of 50% at 4 months in the treated group.
 Adverse effects from systemic therapy were common in these reports and included diabetes, weight gain, hypertension, psychological changes, osteoporosis, suppression of the adrenocorticotropic axes, striae, acne, hypertrichosis, and purpura.
 Systemic steroids most likely are effective via their immunosuppressive effects.
 An initial benefit may occur by using systemic prednisone in some patients, but the relapse rate is high, and it does not appear to alter the course of the condition.
 Systemic prednisone is not an agent of choice for AA because of the adverse effects associated with both short-term and long-term treatment.
• Topical immunotherapy: Topical immunotherapy is defined as the induction and periodic elicitation of an allergic contact dermatitis by topical application of potent contact allergens.
o Commonly used agents for immunotherapy include squaric acid dibutylester (SADBE) and diphencyprone (DPCP). These 2 sensitizers are not present in the natural or industrial environment. Dinitrochlorobenzene (DNCB) has become less popular as a result of reports that it is mutagenic in the Ames assay (a bacterial assay).
o No rigorous toxicologic and pharmacologic studies on humans exist with the use of these agents.
o Although DPCP and SADBE have not been found mutagenic in the Ames assay, neither is approved by the Food and Drug Administration, and unknowns still exist concerning their safety profiles.
o No contaminants have been found in SADBE. Acetone solutions and alcohol solutions of SADBE are equally stable for 2 months under storage conditions.
o DPCP occasionally can contain mutagenic contaminants; therefore, it should be screened periodically to ensure purity. No formal data are available on DPCP regarding its longevity in solution.
o Cosmetically acceptable regrowth with topical immunotherapy rates in patients with severe AA (>50% involvement) varies from 22-68%. Most studies have a success rate of 30-50%. Wiseman et al retrospectively reported the results of a large cohort of 148 consecutive patients treated with diphencyprone.
 Their analysis showed that the cumulative patient response at 32 months was 77.9%.
 The response rate varied with the extent of the alopecia. Cosmetically acceptable regrowth was seen in 17.4% of patients with AT/AU, 60.3% in patients with 75-99% hair loss, 88.1% in patients with 50-74% hair loss, and 100% regrowth in those with 25-49% hair loss.
 Age at onset was also a significant variable, with older age at onset leading to a better prognosis. A lag period of 3 months was usually present between the onset of therapy and the presence of regrowth.
 The median time to achieve significant regrowth was 12.2 months. Some patients showed regrowth on the treated side after 18 months of therapy.
 No benefit is achieved with continuing therapy after 24 months in the absence of regrowth.
 The relapse rate after reaching significant regrowth was 62.6%.
o The type of AA before treatment, duration of the disease, and presence of nail changes were found to predict a lower response to treatment. Age at onset and sex of the patient do not appear to influence the prognosis. Controversy exists concerning whether atopy is an adverse prognosis factor.
o Topical immunotherapy has been used for almost 20 years; no serious adverse effects have been reported.
o The most common side effect, which is desired, is a mild contact dermatitis (redness, scaling, itching).
o Adverse effects include cervical lymphadenopathy and pigment changes. Vitiligo has developed on the application site in 6.7-7.5% of patients. Transient leucoderma on a distant untreated area has been reported. Of patients who develop vitiligo, 31% (4 of 13) had a history of vitiligo. Only 0.75% of patients developed hyperpigmentation. Confetti-type dyschromia (ie, hyperpigmentation, hypopigmentation) has been described as an adverse effect of DPCP and occurred in 1.6% of 243 patients treated. Less common adverse effects include erythema multiforme-like eruptions and urticaria, which were reported in 3 patients treated with DPCP.
o The mechanism of action of topical immunotherapy is unknown. Antigenic competition was hypothesized, ie, the introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify the preexisting infiltrate and allow regrowth.
o Since topical immunotherapy involves the production of contact sensitivity in a previously naive patient, it is best to seek approval for the treatment by the ethics review board and to have the patient sign an informed consent.
o Both SADBE and DPCP appear to be effective equally. Acetone-based solutions usually are preferred because they evaporate quickly, allowing patients to wear a hat or wig immediately after treatment. Quick drying also decreases the chances of dissemination to other body parts by contact.
 Treatment is provided weekly.
 The patient first is sensitized directly on the scalp with a 2% concentration on a small area (2 cm).
 The following week, a low concentration (0.0001%) is applied.
 The concentration is increased slowly every week as needed until a mild tolerable allergic contact dermatitis is elicited. Many concentrations are available that achieve this goal.
 Treating only one half of the head allows the physician to use the untreated half as a control. Once regrowth occurs on the treated half, treatment can be applied to the entire scalp. If regrowth initially occurs on both sides, spontaneous remission is likely, although treatment cannot be excluded as the cause.
 Avoid severe contact dermatitis. Patients are advised to avoid light exposure on the scalp for 48 hours, since light degrades the chemical. Patients also are advised not to wash the scalp for 48 hours.
o Initial regrowth may be seen at weeks 12-24. Once cosmetically acceptable regrowth is achieved, the treatment can be tapered gradually. Almost all patients relapse if the treatment is discontinued, and maintenance treatment is needed.
• Anthralin: The efficacy of anthralin was assessed in 3 studies, which unfortunately were uncontrolled.
o Both short-contact and overnight treatments have been used. Anthralin concentrations varied from 0.2-1%.
o A 2004 study by Tang et al showed no benefit in using anthralin. Other studies showed a response rate of 20-75%, respectively, for patchy AA and a 25% response rate for AT. The mean time to response was 11 weeks, and the mean time to cosmetic response was 23 weeks. Anthralin was used by Tang et al in balding C3H/HeJ mice, which is one animal model for AA. Half the body was treated with anthralin 0.2%, while the other side was treated with the vehicle ointment. Regrowth was seen on the treated side in 64% of mice after 10 weeks. Four mice had almost complete regrowth. The untreated side showed either no regrowth or continued hair loss. Cytokine studies performed with an RNase protection assay showed that tumor necrosis factor-alpha and beta were inhibited in mice that responded to treatment.
o Most patients experienced irritant contact dermatitis. Whether the dermatitis is necessary for efficacy remains under debate.
o Cosmetically acceptable regrowth was maintained during therapy in 71% of responders. No correlation exists between duration of the current episode and response to treatment.
o Adverse effects include pruritus, erythema, scaling folliculitis, local pyoderma, and regional lymphadenopathy. Withholding treatment for a few days results in rapid disappearance of adverse effects. Treatment then can be reinstituted, but anthralin should be left on for shorter periods. Staining of clothes and skin can be a concern.
o The mechanism of action of anthralin is unknown. Most likely, it creates inflammation by generating free radicals, which have antiproliferative and immunosuppressive actions.
• Psoralen plus UV-A: Many studies have been performed regarding the efficacy of psoralen plus UV-A (PUVA) in the treatment of AA, and the initial response rate varies from 20-73%. The relapse rate unfortunately is high (50-88%). Most patients relapse within a few months (mean 4-8 mo) after treatment is stopped.
o Both systemic and topical PUVA therapies have been used.
o The number of treatments required for regrowth varies, but 20-40 treatments usually are sufficient in most cases.
o A younger age at onset, a longer duration of disease, and the presence of AT or AU appear to indicate a poorer outcome.
 Taylor and Hawk published 10 years of experience with PUVA. The initial response rate (>90% regrowth) was comparable to other studies and was 43.8% for partial AA and 50% for AT and AU. However, after excluding patients with of vellus hair regrowth and patients who relapsed rapidly in the follow-up period (approximately 4 mo), they found the success rate to be at best 6.3% for partial AA and 12.5% for AT and AU. They concluded that PUVA generally is not an effective long-term treatment for AA.
 PUVA is a relatively safe treatment modality; adverse effects include burning and, possibly, an increased risk of skin cancer.
o Cyclosporine: Cyclosporine has been used both topically and systemically in the treatment of AA.
 Topical cyclosporine has not proven to be effective in severe AA, since no patient (0 of 10) showed benefit with application of a 10% cyclosporin A (CsA) solution twice per day for 12 months.
 Another study of 14 patients using a 5% solution of cyclosporine twice per day for 4-6 months resulted in vellus growth in 3 of 14 patients and normal hair growth in 3 patients with patchy AA. No regrowth was seen in 8 of the patients.
 Neither study showed systemic absorption of CsA, and routine blood examination showed only transient increase of hepatic enzymes in 1 patient.
 Oral cyclosporine was effective in the DEBR model for AA. All rats had a full pelage by 5 weeks of treatment with 10 mg/kg/day, 5 days per week for 7 weeks. Studies in humans also have proven efficacy with doses of 6 mg/kg daily for 3 months in 6 patients. All patients experienced regrowth, and cosmetically acceptable regrowth was seen in 3 of 6 patients. Unfortunately, all patients relapsed within 3 months of discontinuation of cyclosporine. No evidence exists that CsA can prevent hair loss during an active episode, since reports exist of patients on CsA who developed AA while they were under treatment for unrelated conditions.
 The mechanism of action of cyclosporine remains unclear. It may act through its immunosuppressive effect, since in patients who regrew hair, clearance of immune cells from the hair follicles and alteration in the balance of regulatory lymphocytes occurred (ie, decrease of the CD4/CD8 ratio). Cyclosporine causes hypertrichosis in patients treated for conditions unrelated to hair loss. The mechanism by which cyclosporine stimulates hair growth remains unknown.
 In conclusion, topical cyclosporine has shown limited efficacy. Although systemic CsA appears to be effective in AA, the adverse effect profile, the recurrence rate after treatment discontinuation, and thus, the inability to produce long-term remissions make CsA unattractive for the treatment of AA.
o Tacrolimus: Regrowth was shown on the application site of topical tacrolimus in 2 studies using the DEBR model. Oral tacrolimus was ineffective. No benefit was shown in the use of topical tacrolimus for AA in a small 2005 study by Price et al that included 11 patients.
o Interferon: A study of 11 patients with AA ranging from patchy AA to AU showed no benefit using intralesional interferon alfa-2 (1.5 million IU, 3 times per wk for 3 wk).
o Dapsone: Dapsone 50 mg twice per day was used in a 6-month, double-blind, placebo-controlled study. Of patients in the study, 54% (7 of 13) withdrew from the dapsone group because of adverse effects such as malaise. Of the remaining 6 patients, 3 experienced generalized growth of terminal hair compared to 4 (4 of 13) patients in the placebo group who experienced only sparse patchy regrowth of vellus hair. The authors concluded that although dapsone showed some efficacy, the high incidence of adverse effects rendered it unacceptable. Another study showed a rate of success comparable to the occurrence of spontaneous regrowth reported in the literature.
• Minoxidil: Minoxidil appears to be effective in the treatment of AA in patients with extensive disease (50-99% hair loss). Response rates in that group vary from 8-45%. Minoxidil was of little benefit in patients with AT/AU.
o The 5% solution appears to be more effective.
o No more than 25 drops are applied twice per day regardless of the extent of the affected area.
o Initial regrowth can be seen within 12 weeks, but continued application is needed to achieve cosmetically acceptable regrowth.
o Minoxidil usually is well tolerated. Adverse effects include distant hypertrichosis (5%) and irritation (7%).
o The exact mechanism of action of minoxidil remains unclear. Minoxidil does not appear to have either a hormonal or immunosuppressant effect. Minoxidil most likely has a direct mitogenic effect on epidermal cells, both in vitro and in vivo. Anagen phase hair bulbs plucked from men applying minoxidil showed a significant increase in proliferation index as measured by DNA flow cytometry. Minoxidil also was shown to prolong the survival time of keratinocytes in vitro. Finally, minoxidil may oppose intracellular calcium entry. Calcium influx normally enhances epidermal growth factors to inhibit hair growth. Minoxidil is converted to minoxidil sulfate, which is a potassium channel agonist and enhances potassium ion permeability, thus opposing the entry of calcium into cells. Local vasodilatation does not appear to play a primary role in hair growth associated with minoxidil.
• Other treatment modalities: Many other modalities have been reported to have variable response rates in small studies. These include latanoprost (Ross, 2005), nitrogen mustard, massage and relaxation, isoprinosine, acupuncture, and aromatherapy among others. The efficacy of these treatments needs to be demonstrated in larger placebo-controlled trials before they can be recommended.
• Nonpharmacologic methods: Cosmetic treatments for patients with AA include the following:
o Dermatography has been used to camouflage the eyebrows of patients with AA. Follow-up visits at 4 years showed that 30 of 39 of patients demonstrated excellent cosmetic results, and 3 had good results. On average, 2-3 sessions lasting 1 hour each were required for each patient. No adverse effects were reported.
o Hairpieces are useful for patients with extensive disease and allow them to carry on their usual social life. Reassure patients about the natural look provided by hairpieces.
Therapies most commonly include corticosteroid injections, corticosteroid creams, minoxidil, anthralin, topical immunotherapy, and phototherapy. The choice of one agent over the others depends on patient age (children do not always tolerate adverse effects), extent of condition (localized vs extensive), and the patient's personal preference. The University of California (San Francisco) and University of British Columbia have devised a treatment algorithm that can guide the physician in the treatment of AA (see Image 9).
For patients younger than 10 years, options include corticosteroid creams, minoxidil, and anthralin. For adults with less than 50% scalp involvement, the first option usually is an intralesional corticosteroid, followed by corticosteroid cream, minoxidil, and anthralin. For adults with greater than 50% scalp involvement, topical immunotherapy and phototherapy are additional options.
Drug Category: Immunomodulators — Since AA is believed to be an autoimmune condition, different immunomodulators have been used to treat the condition. Exact mechanism of action of topical immunotherapy is unknown. Antigenic competition was hypothesized (ie, introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify preexisting infiltrate and allow regrowth).
Commonly used agents for immunotherapy include SADBE and DPCP.
Drug Name Squaric acid dibutylester and diphencyprone — May modulate key factors of the immune system.
Adult Dose First, sensitize patient directly on scalp using 2% concentration on small area (2 cm); the following wk, apply lowest concentration (0.0001%); slowly increase concentration each wk thereafter as needed until mild tolerable allergic contact dermatitis is elicited
Pediatric Dose <12 years: Not established
>12 years: Apply as in adults
Contraindications Documented hypersensitivity, documented anaphylaxis, pregnancy, breast-feeding
Interactions None reported
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Most common side effect, also desired, is contact dermatitis; adverse effects include cervical lymphadenopathy and pigment changes; less common adverse effects include erythema multiforme-like eruptions and urticaria
Drug Name Cyclosporine (Sandimmune, Neoral) — Used both topically and systemically for the treatment of AA. Topical cyclosporine showed limited efficacy so far. Although systemic CsA appears to be effective in AA, the adverse effect profile, recurrence rate after treatment discontinuation, and inability to produce long-term remissions make CsA unattractive for the treatment of AA.
Mechanism by which cyclosporine stimulates hair growth remains unknown. May act through its immunosuppressive effect, since patients who regrew hair had clearance of immune cells from the hair follicles and alteration in the balance of regulatory lymphocytes (ie, decreased CD4/CD8 ratio). Causes hypertrichosis in patients treated for conditions unrelated to hair loss.
Adult Dose Topical cyclosporine: Apply 5-10% formulations bid
Systemic cyclosporine: 1-6 mg/kg/d PO in 2 divided doses
Pediatric Dose Not established
Contraindications Documented hypersensitivity, uncontrolled hypertension or malignancies, do not administer concomitantly with PUVA or UV-B radiation in psoriasis, since it may increase risk of cancer
Interactions Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease cyclosporine concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase cyclosporine toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzymes; may increase risk of infection and lymphoma; reserve IV use for patients who cannot take PO
Drug Name Methoxsalen (8-MOP, Oxsoralen) — Inhibits mitosis by binding covalently to pyrimidine bases in DNA when photoactivated by UV-A.
Adult Dose 0.6-0.8 mg/kg PO, 1-2 h prior to UV-A exposure; can be administered topically (cream, lotion, soak)
Pediatric Dose Not established
Contraindications Documented hypersensitivity, history of melanoma or squamous cell carcinoma, photosensitive conditions (eg, lupus, porphyria), intolerance to heat, or claustrophobia, ingestion of photosensitizing drugs, hepatitic disease, arsenic therapy
Interactions Toxicity increases with phenothiazines, griseofulvin, nalidixic acid, tetracyclines, thiazides, sulfanilamides; bacteriostatic soaps and organic staining dyes
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Severe burns may occur from sunlight or UV-A if dose or treatment frequency exceeded; use only if response to other forms of therapy is inadequate; long-term use may increase risk of skin cancer
Drug Name Anthralin (Anthra-Derm, Drithocreme, Micanol) — Synthetic derivative of a tree bark extract. Mechanism of action in AA is unknown. Most likely creates inflammation by generating free radicals, which have antiproliferative and immunosuppressive actions. Both short-contact and overnight treatments have been used. High concentration (1-3%) is used for short-contact treatments. Lower concentrations (0.1-0.4%) are used for overnight treatments. Applications in excessive amounts may stain clothing.
Adult Dose Apply sparingly to affected areas; usually, short-contact treatments last a few h (depending on level of cutaneous irritation), then wash off with soap and water; overnight treatments apply hs and wash off in am
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity, acutely or actively swollen psoriatic lesions
Interactions Long-term corticosteroid treatment withdrawal may cause complications of rebound phenomenon (allow 1-wk interval between discontinuation of corticosteroids and initiation of anthralin therapy)
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Caution in renal disease; avoid eye contact; if redness develops, discontinue application; adverse effects include pruritus, erythema, scaling folliculitis, local pyoderma, and regional lymphadenopathy; caution on irritated skin, since most likely aggravates preexisting condition; may discolor skin to brown-orange color (temporary)
Drug Category: Glucocorticoids — Have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
Topical corticosteroids (including intralesional corticosteroids) are safe and easy to use. They are acceptable cosmetically and allow patients to wear hats or wigs shortly after application. They also are relatively inexpensive. While the usefulness of high-potency topical corticosteroids is under debate, they remain a good (painless) option in children.
Intralesional steroids are first-line treatment in localized conditions.
Oral prednisone usually is reserved for patients with rapidly progressive AA. The relapse rate is high, and the potential for multiple severe adverse effects when used long term limits its usefulness.
Drug Name Clobetasol propionate (Temovate) — Class I superpotent topical steroid. Suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Treatment should continue until cosmetically acceptable regrowth is achieved or for a minimum of 3-4 mo.
Adult Dose Apply bid for up to 2 wk; not to exceed 50 g/wk
Pediatric Dose Not established
Contraindications Documented hypersensitivity; viral or fungal skin infections
Interactions None reported
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions May suppress adrenal function in prolonged therapy; most common adverse effect is local folliculitis, which appears after few wk of treatment; telangiectasias and local atrophy have been reported; dryness, burning, itching, and local irritation may occur; secondary infection is rare; no systemic adverse effects have been reported
Drug Name Prednisone (Deltasone, Meticorten, Sterapred) — Immunosuppressant occasionally used in rapidly progressive AA in an attempt to halt condition, but relapse rate is high. Use of systemic steroids for treatment of AA is under much debate. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production.
Many drug doses and regimens have been used in treatment of AA, but no formal recommendation exists.
Adult Dose <60 kg: Not established
>60 kg: 40 mg PO for 1 wk, 35 mg PO for 1 wk, 30 mg PO for 1 wk, 25 mg PO for 1 wk, 20 mg PO for 3 d, 15 mg PO for 3 d, 10 mg PO for 3 d, and 5 mg PO for 3 d
Pediatric Dose 4-5 mg/m2/d PO or 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve
Contraindications Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease
Interactions Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy B – Usually safe but benefits must outweigh the risks.
Precautions Abrupt discontinuation of glucocorticoids may cause adrenal crisis; adverse effects from systemic therapy are common and include diabetes, weight gain, hypertension, electrolyte and fluid imbalance, psychological changes, osteoporosis, suppression of adrenocorticotropic axes, striae, acne, hypertrichosis, and purpura; ocular or GI complaints, renal function impairment, immunosuppression, and avascular necrosis may occur
Drug Name Triamcinolone (Aristospan Intra-articular) — In AA, intralesional triamcinolone is believed to suppress the immune system locally and thereby allow hair to regrow. Injections are administered with 3-mL syringe and 30-gauge needle intralesionally.
Pediatric patients generally are less tolerant of intralesional injections because of local discomfort.
Adult Dose 2.5-5 mg/mL concentrations typically administered, injected intralesionally, spread out to cover affected areas (approximately 1 cm between injection sites)
2.5-40 mg (10 mg/mL or 40 mg/mL formulations; intraarticular, intrasynovial); repeat prn
Alternatively, 60 mg IM followed by additional doses of 20-100 mg when symptoms recur
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; fungal, viral, and bacterial skin infections
Interactions Coadministration with barbiturates, phenytoin, and rifampin decreases effects of triamcinolone
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Adverse effects include pain during injection and minimal transient atrophy (10%); rarely, atrophy is severe and permanent (avoid reinjecting area of denting to allow atrophy to revert); if large volume is injected per session, suppression of HPA axis may occur
Drug Name Betamethasone (Celestone) — For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Adult Dose Apply thin film bid until response
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; paronychia, cellulitis, impetigo, angular cheilitis, erythrasma, erysipelas, rosacea, perioral dermatitis, and acne
Interactions Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions Not for use in skin with decreased circulation; can cause atrophy of groin, face, and axillae; if infection unresponsive to antibiotic treatment develops, discontinue until infection is controlled; do not use as monotherapy to treat widespread plaque psoriasis
Drug Category: Vasodilators — Relax arteriolar smooth muscle, causing vasodilation; hair growth effects are secondary to vasodilation.
Drug Name Minoxidil (Rogaine) — Stimulates hair growth in general and is effective in many types of hair loss. Exact mechanism of action remains unclear, but does not appear to have either hormonal or immunosuppressant effects. The 5% solution appears to be more effective.
Adult Dose Apply <25 gtt bid regardless of extent of affected area
Pediatric Dose Not established
Contraindications Documented hypersensitivity, pheochromocytoma, coronary artery disease, cardiac dysrhythmias, congestive heart failure, or valvular heart disease, pregnancy, breast-feeding
Interactions Concurrent use with guanethidine, diuretics, or hypotensive agents may result in additive hypotension
Pregnancy C – Safety for use during pregnancy has not been established.
Precautions May exacerbate angina pectoris; caution in pulmonary hypertension, congestive heart failure, coronary artery disease, and significant renal failure
FOLLOW-UP
Deterrence/Prevention:
• AA is highly unpredictable. No treatment is effective in preventing or halting progression of the condition. No trigger can be found to explain disease exacerbation in most patients.
Prognosis:
• The natural history of AA is unpredictable. Most patients have only a few focal areas of alopecia, and spontaneous regrowth usually occurs within 1 year.
• Probably, less than 10% of patients experience extensive alopecia, and less than 1% have AU.
• Patients with extensive long-standing conditions are less likely to experience significant long-lasting regrowth.
• Adverse prognosis factors include nail abnormalities, atopy, onset at a young age, and severe forms of AA.
Patient Education:
• Patient education is a key factor in AA. Inform patients of the chronic relapsing nature of AA. Reassure patients that the condition is benign and does not threaten their general health.
• Most patients try to find an explanation about why this is happening to them. Reassure these patients that they have done nothing wrong and that it is not their fault.
• Inform patients that expectations regarding therapy should be realistic.
• Support groups are available in many cities; it is strongly recommended that patients be urged to contact the National Alopecia Areata Foundation at 710 C St, Suite 11, San Rafael, CA 94901 or view the web site.
• Many patients are reluctant to use hairpieces or take part in support groups, since at first, these often are perceived as last-resort options. Take the time to discuss the options with patients, since they are of great benefit.
MISCELLANEOUS Section 9 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Medical/Legal Pitfalls:
• Failure to discuss at length realistic treatment expectations and treatments that have serious adverse effects or are not approved by the Food and Drug Administration (ie, topical immunotherapy)
PICTURES Section 10 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Caption: Picture 1. Alopecia areata affecting the beard.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 2. Alopecia areata affecting the arms.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 3. Patchy alopecia areata.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 4. Ophiasis pattern of alopecia areata.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 5. Sisaipho pattern of alopecia areata.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 6. Alopecia totalis.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 7. Diffuse alopecia areata.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 8. Corticosteroid injection.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Photo
Caption: Picture 9. Treatment algorithm for alopecia areata.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: Graph
BIBLIOGRAPHY Section 11 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

• Colombe BW, Lou CD, Price VH: The genetic basis of alopecia areata: HLA associations with patchy alopecia areata versus alopecia totalis and alopecia universalis. J Investig Dermatol Symp Proc 1999 Dec; 4(3): 216-9[Medline].
• Colombe BW, Price VH, Khoury EL, et al: HLA class II antigen associations help to define two types of alopecia areata. J Am Acad Dermatol 1995 Nov; 33(5 Pt 1): 757-64[Medline].
• Fiedler VC: Alopecia areata. A review of therapy, efficacy, safety, and mechanism. Arch Dermatol 1992 Nov; 128(11): 1519-29[Medline].
• Fiedler VC, Alaiti S: Treatment of alopecia areata. Dermatol Clin 1996 Oct; 14(4): 733-7[Medline].
• Hoffmann R, Happle R: Topical immunotherapy in alopecia areata. What, how, and why? Dermatol Clin 1996 Oct; 14(4): 739-44[Medline].
• Jackow C, Puffer N, Hordinsky M, et al: Alopecia areata and cytomegalovirus infection in twins: genes versus environment? J Am Acad Dermatol 1998 Mar; 38(3): 418-25[Medline].
• MacDonald N: Alopecia areata: identification and current treatment approaches. Dermatol Nurs 1999 Oct; 11(5): 356-9, 363-6[Medline].
• Madani S, Shapiro J: Alopecia areata update. J Am Acad Dermatol 2000 Apr; 42(4): 549-66; quiz 567-70[Medline].
• McDonagh AJ, Messenger AG: The pathogenesis of alopecia areata. Dermatol Clin 1996 Oct; 14(4): 661-70[Medline].
• McElwee KJ, Tobin DJ, Bystryn JC, et al: Alopecia areata: an autoimmune disease? Exp Dermatol 1999 Oct; 8(5): 371-9[Medline].
• Muller SA, Winkelmann RK: Alopecia areata. An evaluation of 736 patients. Arch Dermatol 1963 Sep; 88: 290-7[Medline].
• Perini GI, Veller Fornasa C, Cipriani R, et al: Life events and alopecia areata. Psychother Psychosom 1984; 41(1): 48-52[Medline].
• Price VH, Colombe BW: Heritable factors distinguish two types of alopecia areata. Dermatol Clin 1996 Oct; 14(4): 679-89[Medline].
• Price VH: Treatment of hair loss. N Engl J Med 1999 Sep 23; 341(13): 964-73[Medline].
• Price VH, Willey A, Chen BK: Topical tacrolimus in alopecia areata. J Am Acad Dermatol 2005 Jan; 52(1): 138-9[Medline].
• Puavilai S, Puavilai G, Charuwichitratana S, et al: Prevalence of thyroid diseases in patients with alopecia areata. Int J Dermatol 1994 Sep; 33(9): 632-3[Medline].
• Rokhsar CK, Shupack JL, Vafai JJ, Washenik K: Efficacy of topical sensitizers in the treatment of alopecia areata. J Am Acad Dermatol 1998 Nov; 39(5 Pt 1): 751-61[Medline].
• Ross EK, Bolduc C, Lui H, Shapiro J: Lack of efficacy of topical latanoprost in the treatment of eyebrow alopecia areata. J Am Acad Dermatol 2005 Dec; 53(6): 1095-6[Medline].
• Safavi K: Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey. Arch Dermatol 1992 May; 128(5): 702[Medline].
• Safavi KH, Muller SA, Suman VJ, et al: Incidence of alopecia areata in Olmsted County, Minnesota, 1975 through 1989. Mayo Clin Proc 1995 Jul; 70(7): 628-33[Medline].
• Shapiro J, Price VH: Hair regrowth. Therapeutic agents. Dermatol Clin 1998 Apr; 16(2): 341-56[Medline].
• Sharma VK: Pulsed administration of corticosteroids in the treatment of alopecia areata. Int J Dermatol 1996 Feb; 35(2): 133-6[Medline].
• Sharma VK, Dawn G, Kumar B: Profile of alopecia areata in Northern India. Int J Dermatol 1996 Jan; 35(1): 22-7[Medline].
• Shellow WV, Edwards JE, Koo JY: Profile of alopecia areata: a questionnaire analysis of patient and family. Int J Dermatol 1992 Mar; 31(3): 186-9[Medline].
• Tang L, Cao L, Sundberg JP, et al: Restoration of hair growth in mice with an alopecia areata-like disease using topical anthralin. Exp Dermatol 2004 Jan; 13(1): 5-10[Medline].
• Taylor CR, Hawk JL: PUVA treatment of alopecia areata partialis, totalis and universalis: audit of 10 years' experience at St John's Institute of Dermatology. Br J Dermatol 1995 Dec; 133(6): 914-8[Medline].
• Tosti A, De Padova MP, Minghetti G, Veronesi S: Therapies versus placebo in the treatment of patchy alopecia areata. J Am Acad Dermatol 1986 Aug; 15(2 Pt 1): 209-10[Medline].
• Tosti A, Piraccini BM, Pazzaglia M, Vincenzi C: Clobetasol propionate 0.05% under occlusion in the treatment of alopecia totalis/universalis. J Am Acad Dermatol 2003 Jul; 49(1): 96-8[Medline].
• van der Steen P, Traupe H, Happle R, et al: The genetic risk for alopecia areata in first degree relatives of severely affected patients. An estimate. Acta Derm Venereol 1992 Sep; 72(5): 373-5[Medline].
• Vestey JP, Savin JA: Natural history of severe alopecia areata. Br J Dermatol 1987 Oct; 117(4): 531[Medline].
• Wang SJ, Shohat T, Vadheim C, et al: Increased risk for type I (insulin-dependent) diabetes in relatives of patients with alopecia areata (AA). Am J Med Genet 1994 Jul 1; 51(3): 234-9[Medline].
• Werth VP, White WL, Sanchez MR, Franks AG: Incidence of alopecia areata in lupus erythematosus. Arch Dermatol 1992 Mar; 128(3): 368-71[Medline].
• Whiting D: Dermatopathology of common hair problems. J Cutan Med Surg 1999 Nov; 3 Suppl 3: S3-13[Medline].

Escrito por Antonio Rondon Lugo el 29 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y General y Lecturas sugeridas.

 

ERISIPELA

Mi amigo  Adolfo   , de Monteria   siempre  buen  dermatólogo y Poeta , nos  regala esto  sobre

la erisipela.Montería, 22 de junio de 2007

ERISIPELA

A SAN ANTONIO DEBEMOS
CONOCER ESTA INFECCION
QUE SE PRESENTA EN LA DERMIS
CON LINFATICA AFECCION
MUJERES, NIÑOS, ANCIANOS
PRESENTAN LA ALTERACION
Y ESTAFILO O ESTREPTOCOCO
CAUSAN SIEMPRE LA INFECCION
CON SUS BORDES DIFINIDOS
SIEMPRE AFECTABA LA CARA
Y ENCONTRARLO EN LAS PIERNAS
HOY DIA NO ES COSA RARA
DE DOS A CINCO LOS DIAS
EL PERIODO DE INCUBACION
FIEBRE, NAUSEAS, ESCALOFRIOS
SON DE BRUSCA APARICION
MUY URENTE Y DOLOROSA
REACCIONA A LA PALPACION
Y SE LE SUMAN LOS GANGLIOS
DE FACIL OBSERVACION
PENICILINA ES LA DROGA
PARA TRATAR DE ELECCION
Y EN SOLO CATORCE DIAS
ACABAMOS LA INFECCION
Adolfo Gómez Agamez.
Mpontería, Colombia

Escrito por Antonio Rondon Lugo el 29 de Junio de 2007 con 3 comentarios
Lee más artículos sobre General y Poesías.

LA MUERTE

Poema  de   mi  amigo  Adolfo Gómez.

LA MUERTE

In memoriam de Romulo Bitar

NADIE CORRE HACIA LA MUERTE
SOLO HUYE DEL SUCESO DE NACER
PORQUE EL MIEDO A ESE INSTANTE
NOS REMONTA EL PRIMERO DEL SER

NOS REPUGNA ES VERDAD
CONSIDERAR LA MUERTE UNA CALAMIDAD
PUEDE SER UN SUPREMO BIEN
O LO PEOR SITUADO AL FINAL

SIN EMBARGO EL MAL
EL VERDADERO MAL ESTA DETRÁS
Y NO DELANTE DE NOSOTROS
CON QUIEN NOS OBLIGAN LUCHAR

ASI CUANDO ALGUIEN SE VA
PORQUE LA MUERTE LO LLEVA
LE HACEMOS LA DESPEDIDA

QUEDANDOSE CON NOSOTROS
LO QUE LA MUERTE SEMBRÓ
ANTES DE SU PARTIDA

Adolfo Gomez Agámez.

Montería, 27 de junio de 2007

Escrito por Antonio Rondon Lugo el 28 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre General y Poesías.

LA VIDA ES UNA ANTORCHA ESPLNDIDA

La  vida  es  la  antorcha   que  nos  hace  vivir  y pensar.  Magnífico artículo  que  me  envia mi  amiga Adelita Vargas  de  Colombia.

FERNANDOARA�JOLAVIDAESUNAANTORCHAESPLENDIDA.pdf

Escrito por Antonio Rondon Lugo el 27 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Varios y General y Informática y Lecturas sugeridas.

CODIGO DE BIOTICA Y BIOSEGURIDAD

Codigo de Bioética del Ministerio de Ciencia y Tecnología.

bioetica.pdf

Escrito por Antonio Rondon Lugo el 25 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y Artículos Varios y General y Informática y Lecturas sugeridas.

ANIMAL HEALTH AND PROTECTION ACT

A&11-1-2.pdfImportante  artículo de Bioética en animales

Escrito por Antonio Rondon Lugo el 25 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y Artículos Varios y General y Lecturas sugeridas.

Requirements for medications commonly used in the treatment

Bousquet Allergy 2003.pdf

Escrito por Antonio Rondon Lugo el 24 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y Artículos Varios y General.

AMOR CONYUGAL

Magnífico  poema  e  nuestro bardo  amigo

Antonio  Guzmán

AMOR CONYUGAL A  Elisa, Estela, Juanita, Natilse y Raquel 

Sabes mis pensamientos,

e intuyes mis deseos,

de juntos tanto tiempo,

en tu mirar me leo.

 

Eres diáfano espejo,

que muestra mis defectos.

y cuando en él me veo,

se quiebran mis afectos.

 

Conoces mis virtudes,

y mis limitaciones,

que en las vicisitudes.

me brindas mil perdones.

 

No se el modo de amarte,

no se si aprenderé,

solo puedo decirte,

que siempre te querré

 

Unidos para siempre,

en pobreza o fortuna.

lo digo yo y la gente

¿que como tú?: ninguna

 

Solo puedo ofrecerte,

sencillamente…. eso:

El no dejar de amarte

y en tu silencio: un beso

  

Antonio Guzmán

Granada – España, 18 de junio de 2007

Escrito por Antonio Rondon Lugo el 24 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre General y Poesías.

La microbiologa en enfermedades emergentes y Re emergentes

Microbiologia II.pdfSegunda  publicación  de  los  Drs  Andrade  y Marcano.  en CAIBCO

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y General y Lecturas sugeridas.

La Microbiologa en enfermedades emergentes y Re emergentes

microbiologia I.pdf  Magnífico  artículo  de  Los Drs  Ramón Eliel Andrade Pineda y Marcel Jesús Marcano  publicado en la revista digital CAIBCO, la  cual  recomendamos  su lectura.Nota exisate un  link  en  este  blog.

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre General.

Einsten y el fundamentalismo

Recomendamos su lectura , comentarios  y meditación

ARL

Einsten.pdf

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre General y Informática y Lecturas sugeridas.

Tratamiento de la Urticaria Crnica

urticaria.pdf

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y General y Lecturas sugeridas.

guideline: definition, classification and diagnosis of Urticaria

Zuberbier Allergy 2006.pdfZuberbier Allergy 2006.pdfThis guideline is the result of a consensus reached during a panel discussion at
the 2nd International Consensus Meeting on Urticaria, Urticaria 2004, a joint
initiative of the European Academy of Allergology and Clinical Immunology
Dermatology Section and the European Union (EU)-funded network of excellence,
GA2LEN. It covers the definition and classification of urticaria, taking
into account the recent progress in identifying causes, eliciting factors and
pathomechanisms of this disease. We have outlined useful diagnostic approaches
for different subtypes of urticaria. This guideline was, in addition, accepted by
the European Dermatology Forum (EDF) and was formally approved by the
European Union of Medical Specialists (UEMS).

Zuberbier Allergy 2006.pdf

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y General y Lecturas sugeridas.

management of urticaria

Zuberbier Alllergy 2006.pdfZuberbier Alllergy 2006.pdfMagnífico  ariculo  de  consenso  sobre  el manejo  de  la Urticaria

Escrito por Antonio Rondon Lugo el 21 de Junio de 2007 con comentarios no permitidos
Lee más artículos sobre Artículos Científicos y Artículos Varios y General y Lecturas sugeridas.