The flare of psoriasis often occurs in lower humidity

The flare of psoriasis often occurs in lower humidity seasons and regions. The prevalence of psoriasis is 100 times higher in lower humidity regions than higher humidity regions. Studies have shown that stratum corneum hydration is lower while basal transepidermal water loss rates and skin surface pH are higher during winter than during summer. Low stratum corneum hydration alone has substantial impact on cutaneous function, including induction of pruritus (independent of mast cells), stimulation of epidermal proliferation and cutaneous inflammation. Scratching resulting from low humidity-induced pruritus can cause further damage to the epidermal permeability barrier. Moreover, during low humidity seasons, mechanical trauma, i.e., scratching and abrasion, induced barrier damage would be repaired more slowly due to the higher stratum corneum pH. A defective permeability barrier not only further increases stratum corneum pH, but also stimulates epidermal proliferation, cytokine production, inflammatory infiltration, as well as epidermal vascular endothelial growth factor production, leading to dermal capillary proliferation, all of which are prominent features of psoriasis. Furthermore, barrier disruption decreases expression levels of filaggrin and cornified envelope protein, which will also delay barrier repair. Based on the above evidence, the putative pathogenesis of psoriasis, in large part, can be postulated as a result of the skin\'s inability to overcome epidermal functional challenges from external stressors (). In normal individuals, the negative impact of exogenous stressors on epidermal function can be readily overcome or minimized. However, in patients bearing psoriasis susceptibility genes, alterations of epidermal function induced by exogenous stressors can not be repaired rapidly, due to those genetic defects. A sustained barrier defect provokes excess keratinocyte proliferation and inflammation, leading to the development of psoriasis. Thus, psoriasis could be possibly prevented by intervening with the exogenous stressors on epidermal function, including enhancing barrier function and stratum corneum hydration, acidifying stratum corneum, as well as reduction of psychological stress.
A 69-year-old woman with underlying buy Torin1 and chronic hepatitis B suffered from multiple indurated erythematous plaques on the trunk and extremities for 3 years (A and B). The plaques, initially noted on the bilateral thigh with progression to trunk and upper arms, were asymptomatic. She had also lost weight during the past year. Physical examination revealed enlarged lymph nodes at the bilateral axillae. We obtained a skin biopsy from the thigh. The histopathological examination showed mild atrophic epidermis with focal epidermotropism and dense infiltrate of small- to medium-sized atypical lymphocytes in the dermis (A–D). Nodular pattern infiltration with granulomatous reaction and multinucleated giant cells were found in the dermis (B). No caseous necrosis or foreign body was noted in the granuloma area. Acid-fast stain, periodic acid–Schiff stain, and Grocott–Gomori methenamine silver stain showed negative findings. Immunohistochemical studies revealed that atypical small- to medium-sized lymphocytes expressed CD3+ and CD4+ (E) with CD7 loss. The atypical lymphocytes did not express CD8, CD20, or CD30. The diagnosis of CD4-positive granulomatous mycosis fungoides (GMF) was made on the basis of clinical and histological findings. Laboratory examination revealed anemia (hemoglobin, 10.6 g/dL), thrombocytopenia (platelets, 120 × 10/L), and normal white blood cell counts (4.7 × 10/L). Elevated blood lactate dehydrogenase level (303 U/L) was also noted. Human T-lymphotrophic virus-1 antibody was negative. The peripheral smear reported normocytic erythrocytes, normochromic white blood cells, and adequate platelets. Bone marrow study reported no abnormal lymphoid cell infiltration. The whole-body computed tomography showed multiple enlarged axillary, mediastinal, and inguinal lymph nodes without extralymphatic organ involvement. Positron emission scanning also showed hypermetabolic nodes in bilateral thighs, bilateral inguinal, bilateral iliac, and bilateral axillary areas. Ill-defined areas with increased flourodeoxyglucose uptake in the soft tissue of bilateral lower legs and left upper arm were also seen. The final diagnosis was MF T2N1M0 Stage IIA. Although no tumor was found clinically, because the histopathology revealed tumor-like deeper infiltration rather than plaque-type MF, the oncologist suggested treating this case aggressively as stage IIB (T3N1M0) disease.