Wen Chieh Chen

Interleukin-19 upregulates keratinocyte growth factor and is associated with psoriasis

Background  Interleukin (IL)‐19, a member of the IL‐10 family, signals through the IL‐20R1/IL‐20R2 heterodimer, which is shown to be involved in abnormal keratinocyte differentiation and proliferation. Little is known about its in vitro biological functions or its role in psoriasis.

Interleukin-20 induced cell death in renal epithelial cells and was associated with acute renal failure

Acute renal failure is an abrupt decrease in renal function. Interleukin (IL)-10 inhibits ischemic and cisplatin-induced acute renal failure. We aimed to determine whether IL-20 affects renal tubular epithelial cells and is associated with acute renal failure. We analyzed the expression of IL-20 and its receptor (R) in the kidneys of rats with HgCl2-induced acute renal failure. Reverse transcription-PCR showed upregulated IL-20, and its receptors and immunohistochemical staining showed strongly expressed IL-20 protein in proximal tubular epithelial cells. We analyzed human proximal tubular epithelial (HK-2) cells, which expressed both IL-20 and its receptors. IL-20 specifically induced mitochondria-dependent apoptosis by activating caspase 9 in HK-2 cells. IL-20 also activated c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2, the downstream signals implicated in the apoptosis of HK-2 cells. Furthermore, IL-20 upregulated the transcripts of transforming growth factor (TGF)-β1, a critical mediator of renal injury. In hypoxic HK-2 cells, IL-20 and IL-22R1 transcripts increased, and IL-20 upregulated IL-1β transcripts. In vivo study further demonstrated that anti-IL-20 antibody reduced the expression of TGF-β1 and IL-1β and the number of damaged tubular cells in the kidneys of rats with acute renal failure. We concluded that IL-20 may be involved in the injury of renal epithelial cells in acute renal failure.

Testosterone synthesized in cultured human SZ95 sebocytes derives mainly from dehydroepiandrosterone

Please cite this paper as: Testosterone synthesized in cultured human SZ95 sebocytes derives mainly from dehydroepiandrosterone. Experimental Dermatology 2010; 19: 470–472.

Late-onset alopecia areata: a retrospective study of 73 patients from Taiwan.

Background  Alopecia areata (AA) is regarded to be mediated by autoimmune process, and manifests as patchy non‐scarring hair loss with occult onset. Little is known about AA occurring later in life.

Early Intervention with High-Dose Steroid Pulse Therapy Prolongs Disease-Free Interval of Severe Alopecia Areata: A Retrospective Study

Background Spontaneous recovery of severe alopecia areata is rare and the condition is difficult to treat. Objective The aim of this study is to investigate and compare the effects and safety of steroid pulse therapy between oral and intravenous administrations between 1999 and 2010 at the Department of Dermatology, National Cheng Kung University Hospital. Methods Data were retrospectively retrieved. A satisfactory response was defined as more than 75% hair regrowth in the balding area. Results A total of 85 patients with more than 50% hair loss were identified and treated, with an overall satisfactory response rate of 51.8%. The mean follow-up time was 37.6 months, with a relapse rate of 22.7%. Patients with alopecia areata (hereafter, AA) of recent onset within one year showed higher response rates (p<0.001) and lower relapse rates compared to patients with AA persisting for more than 1 year. Further, even in patients with alopecia totalis, alopecia universalis or ophiasis type, early treatment resulted in a satisfactory response rate of 47% among the treated patients. In general, oral therapy was as effective and well-tolerated as intravenous therapy. Conclusion The response rate is determined by disease severity and time of intervention, not by the administration form of steroid pulse therapy. Oral steroid pulse therapy can be considered as the first-line treatment for patients with severe AA of recent onset within one year.

Expression of Sex-Determining Genes in the Scalp of Men with Androgenetic Alopecia

Background: The regulation of the cutaneous steroidogenesis in patients with androgenetic alopecia remains largely unclear. Objective: The purpose of this study was to quantify the expression of the sex-determining genes in different scalp areas. Methods: Paired scalp specimens from frontal and occipital scalp areas of 10 patients were examined by real-time RT-PCR for mRNA expression and of 40 patients (mean age 34.9 years, range 22–58) by Western blotting for protein analysis. Results: The SOX-9 mRNA was most abundant in the skin, while SF-1 mRNA was sparsely detected. The protein levels of DAX-1, SRY and WT-1 were significantly higher in the bald scalp (p = 0.003, 0.004 and 0.03, respectively). Only the SRY expression showed a positive correlation with the baldness severity in Norwood-Hamilton classification (p = 0.024). There was no association between patient’s age and the protein levels. Immunostaining of SOX-9 was detected in the outer root sheath keratinocytes of hair follicles but not in the dermal papillae. Conclusion: Further study on a larger population, including normal subjects and female patients, is needed to confirm the pathogenic role of sex-determining genes in androgenetic alopecia.

Case of co‐morbidity of alopecia areata and pityriasis lichenoides in a five year old boy for two years

Dear Editor, A 5-year-old Indo-Taiwanese mixed boy was brought to us with concurrence of multifocal alopecia areata (AA) and pityriasis lichenoides (PL) of 1 year. On examination, there were several circumscribed bald patches over his scalp without erythematous or scaly changes (Fig. 1). Additionally, 20–30 papulonecrotic lesions were scattered mainly over the trunk and proximal extremities (Fig. 2a), and showed typical features of PL characterized histopathologically by a superficial and deep dermal lymphohistiocytic infiltrate, confluent parakeratosis, vacuolar change at the dermoepidermal junction, ballooning of keratinocytes with intraepidermal vesiculation and necrosis of keratinocytes (Fig. 2b). According to his mother, he first became ill with malaise, sore throat, arthralgia and fever of up to 39°C during travel in India, followed by the first attack of cutaneous lichenoid papules in 2 weeks. Soon thereafter, several foci of alopecia areata developed with involvement of eyebrows and trunk. Family history of atopic diathesis with allergic rhinitis was identified in the boy and his mother. Virology study showed negative findings of infection with Epstein–Barr virus (EB-VCA immunoglobulin [Ig]A, EB-VCA IgG, EB-VCA IgM, EBEA, EBNA), cytomegalovirus (CMV IgG, CMV IgM) and Toxoplasma gondii (T. gondii IgG, T. gondii IgM). Treatment with systemic antibiotics and corticosteroids was attempted without significant modification of the disease course. In the ensuing 2-year follow up, the two kinds of skin lesions seemed to wax and wane in parallel, with PL usually preceding the activity of AA. Alopecia areata is a common form of non-scarring hair loss of unclear etiology. Both genetic predisposition and environmental factors have been proposed for its etiopathogenesis. Common associated diseases include atopic syndrome, vitiligo, thyroid diseases, diabetes mellitus and Down’s syndrome. Association with various other immunological disorders have been observed and there is strong evidence demonstrating AA to be an organ-specific autoimmune disease mediated by T cells directed to the hair follicle. Results of study in monozygotic twins showed only a 55% concordance rate of AA occurring in families, suggesting that, in addition to a genetic component, some unknown environmental triggers possibly exist. CMV infection has been correlated with various autoimmune disorders. Using molecular biology techniques, DNA sequences of CMV have been reported in paraffin sections of AA lesions and reactivation of the CMV infection has been postulated as one of the pathogenic mechanisms in AA. Other studies using different techniques examining mRNA from tissue samples of patients with active patchy AA, however, did not find any correlation between AA and infection of CMV or other β-herpes viridae.

The Acne Genes

Acne is one of the most common skin diseases. Many epidemiologic studies and twin studies have provided substantial evidence about the genetic influence in the development of acne [1–5], at least in certain stages of acne such as neonatal acne, teenage acne [6], adult persistent acne, or in special forms of acne such as acne comedonica, acne inversa [7, 8], acne fulminans [9], or in acne severity [10] and therapeutic resistance [11]. Acne is very likely mediated by polygenic inheritance or multifactorial inheritance attributed to the interplay between multiple genes and the environment, especially the sex hormones. It is unknown if each candidate “acne gene” contributes equally or additively to the disease phenotype, or whether there exists a master gene that presides or leads the disease development. All the candidate genes may influence each other and perpetuate the disease process. The problem in many of the existing epidemiologic studies may include (1) a small sample size with single or few families examined without matched control; (2) lack of standardization in the disease definition or severity classification; (3) variability of age onset, duration, course, and psychosocial influence.