Treatment of moderate-to-severe alopecia areata in patients over the age of 65†years with baricitinib.

Baricitinib is a Janus kinase inhibitor that has been approved by the US Food and Drugs Administration for the treatment of severe alopecia areata (AA) in adults. However, the clinical trials that demonstrated the efficacy of baricitinib in the treatment of severe AA did not include men aged > 60 years or women aged > 70 years. We retrospectively assessed the efficacy and safety of baricitinib in 14 patients aged ≥ 65 years with moderate-to-severe AA. After a mean (SD) duration of 18.5 (11.9) months, a 72% reduction in mean Severity of Alopecia Tool score from baseline was observed. Partial or complete eyebrow and eyelash hair was observed in 57% and 43% of patients, respectively. The adverse effects of baricitinib were mild. No cases of venous thromboembolism, major adverse cardiovascular events or malignancy were reported.

Treatment of alopecia areata: An Australian expert consensus statement.

Alopecia areata (AA) severity varies from a single small patch to complete loss of scalp hair, body hair, eyelashes and eyebrows. While 40% of all affected individuals only ever get one patch and will achieve a spontaneous complete durable remission within 6 months, 27% will develop additional patches but still achieve complete durable remission within 12 months and 33% will develop chronic AA. Without systemic treatment, 55% of individuals with chronic AA will have persistent multifocal relapsing and remitting disease, 30% will ultimately develop alopecia totalis and 15% will develop alopecia universalis. The unpredictable course and psychological distress attributable to AA contributes to the illness associated with AA. Numerous topical, intralesional and systemic agents are currently used to treat AA; however, there is a paucity of data evaluating their use, effectiveness and tolerability. Topical therapy, including topical glucocorticosteroids, minoxidil and immunotherapy, can be used in cases of limited disease. There are no universally agreed indications for initiating systemic treatment for AA. Possible indications for systemic treatment include rapid hair loss, extensive disease (≥50% hair loss), chronic disease, severe distress or a combination of these factors. Currently available systemic treatments include glucocorticosteroids, methotrexate, ciclosporin, azathioprine, dapsone, mycophenolate mofetil, tacrolimus and sulfasalazine. The optimal treatment algorithm has not yet been described. The purpose of this consensus statement is to outline a treatment algorithm for AA, including the indications for systemic treatment, appropriate choice of systemic treatment, satisfactory outcome measures and when to discontinue successful or unsuccessful treatment.

Tropical and exotic dermatoses and ulcers.

BACKGROUND: Tropical dermatoses and ulcers, although essentially unique to tropical and subtropical areas, are occasionally seen in Australian general practice on returning travellers and migrants from endemic countries. OBJECTIVE: This article will discuss important causes of tropical and exotic ulcers occasionally seen in Australia. DISCUSSION: As tropical ulcers may mimic many other causes of skin ulceration and nodules, a history of recent travel should arouse clinical suspicion. The time frame since exposure to the causative organism is an important feature in the diagnostic process. For example, pyodermas and cutaneous larva migrans present a few days after contact with the causative agents, whereas leishmaniasis, cutaneous tuberculosis, atypical mycobacterial diseases (swimming pool granulomas) and tropical mycosis take weeks to months to appear.

Use of spironolactone in dermatology.

Spironolactone has been used as a potassium-sparing diuretic for more than 30 years. It is a synthetic 17-lactone steroid and primarily acts as an aldosterone antagonist. Since the accidental discovery of its antiandrogenic effects, it has been used in the treatment of many dermatologic conditions in which androgen plays a role in the pathogenesis. Antiandrogenic effects of spironolactone are exerted by reducing testosterone production and inhibiting its action on the target tissues. Spironolactone is used as a primary medical treatment for hirsutism and female pattern hair loss. Continuous treatment is required to sustain the effect. It is an effective alternative treatment for acne in women. It has the benefit of a long-term safety profile. Spironolactone should not be used in pregnancy due to its teratogenic effects and is not used in men due to the risk of feminization.

Male androgenetic alopecia.

IMPORTANCE OF THE FIELD: Androgenetic alopecia affects up to 80% of males by the age of 80. The synonym 'male-pattern hair loss' highlights the fact that hair loss occurs in a defined and reproducible pattern. Hair loss results in reduced self esteem, loss of confidence and anxiety in affected men. An effective treatment for hair baldness would be desirable. AREAS COVERED IN THIS REVIEW: In androgenetic alopecia, hair follicles undergo progressive miniaturization. Genetic factors and androgens play a major role in the pathogenesis of the disease. Polymorphism of the androgen receptor gene was first identified in association with androgenetic alopecia. Identification of new susceptibility genes on chromosomes 3q26 and 20p11 suggest that non-androgen-dependent pathways also are involved. WHAT THE READER WILL GAIN: Topical monoxidil and oral finasteride are commonly in use and have FDA approval for the treatment of male androgenetic alopecia; dutasteride, a type I and II 5-alpha-reductase inhibitor, is on hold in Phase III trials. A combination of medical treatment and hair transplant surgery has shown superior efficacy. TAKE-HOME MESSAGE: Androgenetic alopecia is a progressive condition and although the current available treatments are effective in arresting the progression of the disease, they allow only partial regrowth of hair at its best. Early treatment achieves the best desirable outcome.

Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss.

Patterned hair loss in men and women, although medically benign, is a common, albeit unwelcome, event that may cause considerable anxiety and concern. Patterned hair loss is progressive and when untreated leads to baldness. The prevalence and severity of this physiologic process both increase with advancing age. Although androgens play a key role in the pathogenesis of male pattern hair loss (MPHL), the role of androgens in female pattern hair loss (FPHL) is less well established. Satisfactory treatment response to antiandrogen therapy supports the involvement of androgens in the pathogenesis of FPHL. Spironolactone has been used for 30 years as a potassium-sparing diuretic. Spironolactone is a synthetic steroid structurally related to aldosterone. Since the serendipitous discovery 20 years ago that spironolactone given to a woman for polycystic ovary syndrome (PCOS) and associated hypertension also improved hirsutism, it has been used as a primary medical treatment for hirsutism. Spironolactone both reduces adrenal androgen production and exerts competitive blockade on androgen receptors in target tissues. Spironolactone has been used off-label in FPHL for over 20 years. It has been shown to arrest hair loss progression with a long-term safety profile. A significant percentage of women also achieve partial hair regrowth. Spironolactone is not used in male androgenetic alopecia because of the risk of feminization.

Co-infection of mucosal leishmaniasis and extra pulmonary tuberculosis in a patient with inherent immune deficiency.

BACKGROUND: In Sri Lanka, cutaneous leishmaniasis is a well-established disease caused by Leishmania donovani. Only a few cases of visceral disease and mucosal localization have been reported to date. CASE REPORT: A 52-year-old man presented with severe local destruction of his upper and lower lip and total destruction of the anterior nasal septum and was diagnosed with mucosal leishmaniasis. The causative organism was confirmed to be Leishmania donovani. In addition he had tuberculous lymphadenitis and inherent immune deficiency. His previous medical history was unremarkable. The patient was successfully treated with intramuscular sodium stibogluconate. CONCLUSION: The clinical picture and satisfactory treatment response to antimony are similar to mucosal leishmaniasis caused by L. donovani reported in India and Sudan and with the absence of primary skin lesions make it different from new world mucosal leishmaniasis. Even though leishmania and tuberculous co-infection has been reported in association with HIV this has not been reported in inherent immune deficiency.