Childhood Alopecia Areata: An Overview of Treatment and Recent Patents.

BACKGROUND: Alopecia Areata (AA) is a systemic autoimmune condition that usually starts in childhood. OBJECTIVE: This article aims to review genetics, therapy, prognosis, and recent patents for AA. METHODS: We used clinical queries and keywords "alopecia areata" AND "childhood" as a search engine. Patents were searched using the key term "alopecia areata" in Patents.google.com and freepatentsonline. com. RESULTS: Due to an immune-mediated damage to the hair follicles, hair is lost from the scalp and other areas of the body temporarily or even permanently. Children with AA are generally healthy. Evidence of genetic association and increased predisposition for AA was found by studying families with affected members. Pathophysiologically, T- lymphocytes attack hair follicles and cause inflammation and destruction of the hair follicles and hair loss. In mild cases, there would be well-demarcated round patchy scalp hair loss. The pathognomonic "exclamation mark hairs" may be seen at the lesion periphery. In more severe cases, the hair loss may affect the whole scalp and even the whole body. The clinical course is also variable, which may range from transient episodes of recurrent patchy hair loss to an indolent gradually deteriorating severe hair loss. The treatment of AA depends on factors including patients' age, the extent of the hair loss, duration of disease, psychological impact, availability and side effect profile of the treatments. For localized patchy alopecia, topical application of corticosteroids and/or intralesional corticosteroids are the treatment of choice. Other topical treatments include minoxidil, anthralin, coal tar and immunotherapy. In severe resistant cases, systemic immunosuppressants may be considered. Although herbal medicine, acupuncture, complementary and alternative medicine may be tried on children in some Asian communities, the evidence to support these practices is lacking. To date, only a few recent patents exist in topical treatments, including Il-31, laser and herbal medications. Clinical efficacy is pending for these treatment modalities. CONCLUSION: None of the established therapeutic options are curative. However, newer treatment modalities, including excimer laser, interleukin-31 antibodies and biologics, are evolving so that there may be significant advances in treatment in the near future. AA can be psychosocially devastating. It is important to assess the quality of life, degree of anxiety, social phobia and mood of the patients and their families. Psychological support is imperative for those who are adversely affected psychosocially.

Hyper IgE in Childhood Eczema and Risk of Asthma in Chinese Children.

BACKGROUND: Atopic eczema is a common childhood disease associated with high IgE and eosinophilia. We characterized the clinical features associated with hyper-IgE (defined as IgE > 2000 IU/L) in eczema. METHODS: Nottingham Eczema Severity Score (NESS), family and personal history of atopy, skin prick test (SPT) for common food and aeroallergens, highest serum IgE ever and eosinophil counts were evaluated in 330 children eczema patients. Childhood-NESS (NESS performed at <10 years of age) and adolescent-NESS (NESS performed at >10 years of age) were further analyzed. RESULTS: IgE correlated with NESS (spearman coefficient 0.35, p < 0.001) and eosinophil percentage (spearman coefficient 0.56, p = 0.001). Compared with IgE ≤ 2000IU/L (n = 167), patients with hyper-IgE (n = 163) were associated with male gender (p = 0.002); paternal atopy (p = 0.026); personal history of atopic rhinitis (p = 0.016); asthma (p < 0.001); dietary avoidance (p < 0.001); use of wet wrap (p < 0.001); traditional Chinese medicine use (TCM, p < 0.001); immunomodulant use (azathioprine or cyclosporine, p < 0.001); skin prick sensitization by dust mites (p < 0.001), cats (p = 0.012), dogs (p = 0.018), food (p = 0.002); eosinophilia (p < 0.001); more severe disease during childhood (p < 0.0001) and during adolescence (p < 0.0001), but not onset age of eczema or maternal atopy. Logistic regression showed that hyper-IgE was associated with personal history of asthma (exp(B) = 5.12, p = 0.002) and eczema severity during childhood and adolescence (p < 0.001). For patients <10 years of age, dust mite sensitization (p = 0.008) was associated with hyper-IgE. For patients >10years of age, food allergen sensitization was associated with hyper-IgE (p = 0.008). CONCLUSIONS: Hyper-IgE is independently associated with asthma, more severe atopy and more severe eczema during childhood and adolescence. IgE > 2000 IU/L may be a tool to aid prognostication of this chronic relapsing dermatologic disease and its progression to asthma.

Clinical features and Staphylococcus aureus colonization/infection in childhood atopic dermatitis.

INTRODUCTION: Staphylococcus aureus (SA) colonization/infection is important in the pathophysiology of childhood atopic dermatitis (AD). This study evaluated which clinical features may predict presence of SA colonization/infection and reviewed antimicrobial sensitivity of SA in patients with AD. METHODS: The associations between bacteriologic culture results of skin swabs (taken at the most severely affected area and at the antecubital fossa) and SCORing-Atopic-Dermatitis (SCORAD), skin hydration, transepidermal water loss (TEWL), and quality of life were evaluated. RESULTS: Moderate-to-heavy growth of SA was present in 31% of the swabs of the most severe area and in 16% of the flexural (antecubital fossae) areas of 95 AD patients (12.5 ± 4.8 years). Binomial logistic regression showed moderate-to-heavy growth of SA in the severe area were associated with objective SCORAD (p = 0.004) and lesion intensity [erythema (p = 0.022) and lichenification (p = 0.035)]; and excoriation (p = 0.024) and TEWL (p = 0.009) in the antecubital fossa. The relative risk of isolating moderate-to-heavy growth of SA in the most affected area in patients with severe disease (objective SCORAD >40) is 2.73 (1.43-5.21, p = 0.001). Any growth of SA in either swab sites was associated with objective SCORAD and lesion intensity (p = 0.001-0.019). SA had no association with quality of life and other clinical parameters. All specimens of methicillin-sensitive SA were sensitive to cloxacillin. All methicillin-resistant SA (MRSA) (5.7%) was sensitive to co-trimoxazole and fusidic acid. CONCLUSIONS: Clinical features, especially severity and lesion intensity, are useful in "predicting" moderate-to-heavy SA colonization/infection in AD patients. Cloxacillin has a favorable sensitivity profile for MSSA, and co-trimoxazole and fusidic acid for MRSA. As colonization and infection are ambiguous and potentially overlapping clinical states, we recommend to abandon these terms and propose to describe quantitatively/semi-quantitatively SA isolation as none, mild, scanty, moderate or heavy growth instead in clinical trials.