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    • Notably in psoriatic patients the presentation of schizophre

    2018-11-12

    Notably, in psoriatic patients, the presentation of schizophrenia is more prevalent in women and those aged > 40-years. Generally, schizophrenia is more common in men than in women, with a ratio of 1.4:1, and women tend to experience disease onset in older age. In women, there is a peak occurrence between the ages of 20 years and 35 years, with a second smaller peak between the ages of 45 years and 49 years. Estrogen exhibits a neuroprotective role and may account for the sex difference in schizophrenia. Interestingly, it was also proposed that estrogen might improve psoriasis by inhibiting T cell response and reducing cytokine and chemokine secretion by keratinocytes. Considering the protective roles of estrogen in both schizophrenia and psoriasis, decreased estrogen levels may contribute to the onset of schizophrenia in female psoriatic patients susceptible to schizophrenia in older age. Further investigations are required to test this hypothesis. There were some limitations to this study. First, this is a cross-sectional study; therefore, the causal relationship between psoriasis and schizophrenia could not be determined. Second, the identification of patients relied upon ICD-9-CM codes from the claim database. Psoriatic patients were defined as enrollees that had been documented with a code of psoriasis one time or more during the study period. However, there may be mismatches between coding and diagnosis. For schizophrenia, the possibility of miscoding was reduced by using concomitant catastrophic illness certificates to define schizophrenia. Third, we only adjusted for age, gender, and comorbidities in the statistical analysis. Psoriasis and schizophrenia are complex diseases, and some confounding factors may not be included in our analysis. Medication use, for example, could be involved in the association between psoriasis and schizophrenia. The role of medication was not evaluated in our present study.
    Introduction Hailey–Hailey disease (HHD), which is also known as familial benign chronic pemphigus, is a rare autosomal lose your own voice hereditary blistering skin disorder, which was first described by the brothers Howard and Hugh Hailey in 1939. It is caused by heterozygous mutations in the ATP2C1 gene that encodes the secretory pathway Ca2+/Mn2+ ATP-ase protein (SPCA1) of the Golgi apparatus, leading to alterations in Ca2+-dependent intracellular signaling and resulting in the loss of cellular adhesion in the epidermis. The first onset of HHD generally occurs between 20 years and 40 years of age. HHD is clinically characterized by recurrent eruption of blisters, erythema, and erosion in the friction areas, mainly in the neck, axillae, submammary folds, groin, and perineum. However, lesions also can occur in non-skin-fold areas. HHD can be easily misdiagnosed because of its nonspecific, common symptoms, such as erythema, erosion, blisters, itching, and pain. Various triggers, including humidity, maceration, friction, trauma, and infection, are known to exacerbate dermatoses. Among these, secondary infection is the most common deuteropathy in HHD. Thus, controlling secondary infections is indispensable for treating HHD in conjunction with the use of anti-inflammatory drugs such as topical steroids. Anti-inflammatory drugs such as steroids and tacrolimus are supposed to normalize HHD skin lesions by upregulating ATP2C1 expression, although these drugs are thought to be effective only when secondary infection is prevented. To demonstrate that HHD is controllable, we report the results of a clinical investigation of 26 patients with HHD, with special reference to the importance of controlling secondary infections in these patients.
    Methods
    Results
    Discussion In this study, we demonstrated that HHD is controllable when secondary infection is prevented. Secondary infection accompanied HHD in 22 of our patients (85%), which was a high rate. The primary infectious agents were S. aureus and C. albicans; both of which are often found in skin infections. The presence of dermatitis facilitated bacterial invasion, and a humid environment was considered favorable for fungal growth. Thus, the patients\' symptoms were aggravated in the summer season. Moreover, excess body weight can favor friction and maceration. Infection with S. aureus and C. albicans can induce the production of several cytokines, including interleukin-6, from keratinocytes, and interleukin-6 can reportedly prolong the duration of lesions or exacerbate skin lesions by reducing ATP2C1 gene expression.