Role of basal sweating in maintaining skin hydration in the finger: A long-standing paradox in dry skin resolved.

A long-standing paradox in dermatology is why skin dehydration in the fingers can be triggered by repeated water exposure despite the action of water to hydrate skin tissue. Potential clues might be provided by identifying a mechanism through which water is held in the skin of the fingers. We speculated that this mechanism would be impaired after repeated water exposure. Here, we investigated whether there might be glabrous skin-specific water-holding machinery and whether this machinery might be impaired in dry skin/hand eczema. We examined this by using an impression-mould technique, allowing for an accurate quantification of sweat gland/duct activity and optical coherence tomography. Unlike in hairy skin, sweat pores were rarely detected at the folds of the finger at baseline. Surprisingly, after water exposure, sweat pores at the folds opened and those at the ridges closed in healthy controls (HCs). Sweating in the dermal folds of the hands correlated with skin hydration, and decreased in dry skin/hand eczema, suggesting that its impairment may be one of the causes of dry skin. After repeated water exposure, basal sweating response at the folds was exhausted in patients with dry skin/hand eczema as well as HCs. This exhaustion was rescued by exposing individuals to high humidity. Basal sweating defects would be a target for dry skin/hand eczema. Maintaining basal sweating responses in the finger is the best preventive measures in achieving prevention of dry skin/hand eczema.

Herpes simplex virus-induced murine dry skin model through sweating disturbance.

BACKGROUND: Given that ocular glands become infected secondarily to herpes simplex virus 1 (HSV-1) keratitis, resulting in the loss of tear production, sweat glands may also be susceptible to HSV-1 infection, resulting in sweating disturbance, which is observed frequently in atopic dermatitis. However, due to the lack of sweat glands on the hairy skin of mice, the role of sweating in the maintenance of skin hydration has not been elucidated. OBJECTIVE: To determine the relationship between HSV-1 infection of sweat glands and sweating disturbance-induced dry skin. METHODS: By using the impression mold technique, we examined the sweating response together with the detection of HSV-1 DNA in the sweat glands of footpads, the only area with sweat glands in mice, after local cutaneous HSV-1 inoculation of immunocompetent mice. RESULTS: The sweating response and skin surface hydration were significantly decreased at 7-14 days post-infection. Sweating disturbance and dry skin was markedly enhanced when HSV-1 inoculation was followed by hyperthermic stress. Both resolved spontaneously and became resistant to a second HSV-1 inoculation, associated with increased anti-HSV-IgG antibodies. HSV-1 DNA was detected in sweat glands and dorsal root ganglia. The sweating response remained decreased after subcutaneous injection with pilocarpine, correlating histologically with marked dilatation of sweat gland lumens. These findings indicate that sweating disturbance is unlikely to be the outcome of nerve damage by HSV-1 infection. CONCLUSION: Sweating disturbance could be due to HSV-induced dysfunction of sweat glands. We developed a sweating disturbance-induced dry skin mouse model by infection with HSV-1.

Varicella Zoster Virus-Associated Meningitis as a Rebound Varicella Zoster Disease after Antiviral Discontinuation.

Varicella zoster virus (VZV)-associated meningitis is usually progressive and can be fatal, and early diagnosis and aggressive treatment with intravenous antivirals such as acyclovir (ACV) are required in immunocompromised patients. Patients receiving corticosteroids and immunosuppressive therapy have a significantly higher risk of VZV-associated meningitis. In this report, we describe an unusual case of herpes zoster (HZ) in a young woman who was first diagnosed during tapering of prednisone for dermatomyositis. The skin lesions affected the left L2 and L3 dermatomes, which is unusual in VZV-associated meningitis. Despite showing a good rapid response to antivirals, she developed VZV-associated meningitis immediately after discontinuation of ACV. This phenomenon is often called rebound VZV reactivation disease and occurs after discontinuation of antivirals. This case was notable in that the affected dermatomes were distant from the cranial nerves. Thus, progression of HZ to VZV reactivation-associated meningitis can occur even in appropriately treated HZ patients. Continuation of antivirals beyond 1 week in patients on immunosuppressive therapy may be associated with a decreased risk of severe rebound VZV disease, such as VZV-associated meningitis.

Hypercalcemia Associated with Extramammary Paget's Disease.

Hypercalcemia of malignancy occurs in up to one third of patients at some point during the course of their advanced stage. The majority of them is caused by humoral hypercalcemia of malignancy due to systemic secretion of parathyroid hormone-related protein (PTHrP) by tumor cells. Extramammary Paget's disease is a slow-growing cutaneous malignancy commonly limited to the epidermis of the anogenital region, but rarely becomes invasive and metastatic to distant sites. Herein, we report a 70-year-old male patient with metastatic extramammary Paget's disease. He consulted our hospital with altered consciousness and tumor in his genital area. Physical examination revealed erythematous plaque with a tumor on the scrotum and perineum. It was diagnosed as extramammary Paget's disease (multiple liver metastases and multiple lymph node metastases by skin biopsy and image examination). Increases in serum-corrected calcium and PTHrP-intact levels (15.3 mg/dL and 66.1 pg/L, respectively) were confirmed. PTHrP immunohistochemistry showed positive staining in the tumor cells. We diagnosed humoral hypercalcemia of malignancy. We treated hypercalcemia with saline, furosemide, zoledronic acid, and elcatonin. Regarding the local control of the tumor, 30 Gy/10 Fr electron beam therapy was performed. However, treatment with zoledronic acid was only temporally effective to correct hypercalcemia, and an increased serum calcium level developed again. Concurrently, the liver metastases were rapidly enlarged, and his general condition gradually deteriorated. The patient died on day 55. When patients with extramammary Paget's disease show unconsciousness, serum calcium level should be measured and PTHrP-producing tumor distinguished.