Background: Syphilitic alopecia is not common in patients with secondary syphilis. Though the clinical and histopathological findings of syphilitic alopecia have been described, the trichoscopy features are unknown yet. Main observation:A 42-year-old Chinese man was admitted to our clinic with a complaint of hair loss. The patient presented clinically with moth-eaten alopecia over the whole scalp without any previous discomfort or skin rashes. The serology for syphilis was positive. Trichoscopy showed black dots, focal atrichia, hypopigmentation of hair shaft and yellow dots. Conclusions:On the basis of trichoscopy, along with serology testing syphilitic alopecia can be differentiated from other hair loss diseases with similar clinical presentation. (J Dermatol Case Rep. 2014; 8(3): 78-80) The clinical and trichoscopic features of syphilitic alopecia Yanting Ye, Xiaoting Zhang, Ying Zhao, Yugang Gong, Jian Yang, Huan Li, Xingqi Zhang Department of Dermatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, People's Republic of China. IntroductionSyphilis as a "great mimic" can present various manifestations indistinguishable from other diseases. Syphilitic alopecia is an uncommon clinical manifestation of secondary syphilis with an incidence of 2.9%-11.2%. 1,2The clinical manifestations and histopathological features of syphilitic alopecia have been described in detail, but the trichoscopic features of syphilitic alopecia have not been described yet. Here we present a case of syphilitic alopecia, and describe the clinical and trichoscopic features. Case reportA 42-year-old Chinese man came to our clinic with a complaint of hair loss for 2 weeks, without scalp pruritus or pain. He also complained about being under high mental stress recently. He was heterosexual and was engaging in casual sex. He denied having any skin lesions in the genital area before the hair loss, i.e., the clinical manifestations of primary syphilis. The patient had a past history of asthma and diabetes mellitus, but no history of hair loss.On physical examination of the scalp area, numerous small scattered non-scarring hairless patches with incomplete hair loss were observed. The patches were irregular in size without defined borders, ranged from 0.2cm-0.5cm in diameter, distributed over the whole scalp giving the appearance of moth-eaten alopecia (Fig. 1). The hairless areas showed no signs of inflammation or desquamation. The gentle pull test was negative. Under trichoscopy black dots, focal atrichia, hypopigmentation of hair shafts and yellow dots were observed (Fig. 2). The empty ostia of hair follicle were presented. No skin rash was found all over the body. Up till now, the primary clinical impressions include syphilitic alopecia (SA) and alopecia areata (AA).Blood tests were performed including blood count, total IgE, antinuclear autoantibodies tests, serology for HIV and syphilis. The results of serology for syphilis were positive: rapid plasma reagin test (RPR) with titer of 1:64...
Alopecia areata (AA) is a chronic inflammatory disease mediated by an array of cells and cytokines. Immunohistochemistry (IHC) of histological sections with antibodies to mast cell tryptase, CD4, CD8, CD1a and semi-quantitative real-time PCR analysis of Th1- and Th2-type cytokines were performed in 55 patients to investigate the infiltration features of mast cells (MCs), T lymphocytes and Langerhans cells (LCs) in scalp lesions of patients with AA. In AA patients, increased MCs mainly infiltrated the peri-follicular and peri-vascular areas, and correlated positively with numbers of CD8(+) T lymphocytes in deep peri-follicular areas (P = 0.04), but negatively with CD4(+) T lymphocytes in deep peri-vascular areas (P = 0.031). In patients with active hair loss, LCs in epidermis, deep dermis and peri-vascular were elevated (Ps < 0.05). Infiltration of LCs in upper peri-vascular areas and CD8(+) T cell infiltration in deep peri-follicular areas were positively correlated (R = 0.618, P = 0.011), as well as LCs in deep peri-vascular areas with CD8(+) T cells in upper peri-follicular areas (R = 0.570, P = 0.017). In patients with active hair loss, Th1-type cytokine (IL-2, IL-8, TNF-α) mRNA expression in deep dermis were higher than in upper dermis (Ps < 0.05). However, in patients with non-active hair loss, Th2-type cytokine (IL-5, IL-10) mRNA expression in deep dermis was higher than that in the upper dermis (Ps < 0.05). Positive correlations were found existing between MCs and CD8(+) T cells, as well as between LCs and CD8(+) T cells. In conclusion, findings in this study allow us to propose a close relationship between mast cells and CD8(+) T cells, as well as between LCs and CD8(+) T cells in AA, as well as allergy may interfere with infiltrating T lymphocytes in AA lesional regions. Also, Th1-type cytokine are related to disease activity of alopecia areata, whereas Th2-type cytokines may be associated with persistence of AA.
Potentially, elevated pre-treatment serum levels of IL-4 and IL-12 can be used as unfavorable and favorable predictors of DPCP therapeutic effect, respectively. In addition, pre-treatment elevated serum total IgE may predict increased risk for severe adverse side-effects to DPCP application. Whether serum cytokine expression levels can be used as predictors of response to other forms of treatment is unknown, but it may warrant investigation in the development of personalized treatments for AA.
BackgroundThe pathogenesis of Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is not fully understood. Our previous study reported that chemokine CCL27 was overexpressed in serum of SJS/TEN patients. The objective of this study was to investigate the levels of CCL27 and TNF-α in serum and blister fluid from patients with SJS/TEN during the acute stage or resolution phase.MethodsA total of 27 patients with SJS/TEN and 39 healthy donors were recruited to the study. Serum and vesicular levels of CCL27 and TNF-α were determined by enzyme-linked immunosorbent assays.ResultsSerum levels of CCL27 and TNF-α were significantly elevated in patients with SJS/TEN during the acute stage as compared to the resolution phase and also compared with levels observed in normal controls (P = 0.001/< 0.001; P = 0.012/< 0.001). Serum TNF-α levels were significantly higher in patients with SJS/TEN during the resolution phase compared with normal controls (P < 0.001). Serum CCL27 levels were positively correlated with TNF-α levels during the acute stage (rs = 0.660; P < 0.001). Blister fluid exhibited much lower CCL27 levels than serum did during the acute stage (P = 0.008). TNF-α levels were much higher in vesicles in contrast to serum from acute stage (P = 0.040) as well as serum from resolution phase (P = 0.029).ConclusionsOur study demonstrated roles of CCL27 and TNF-α in promoting the course of SJS/TEN. CCL27 may act early in the course of disease, via the circulation, whereas TNF-α acts throughout the course of disease, in skin lesions.
BACKGROUND Endoplasmic reticulum (ER) stress is an important mechanism in the progression of chronic and acute liver diseases, especially in the progression and recovery of liver fibrosis. Excessive and long-term ER stress induces apoptosis. ER stress-induced apoptosis is considered to be an important pathway in the development of liver fibrosis. Cyclooxygenase-2 (COX-2) induction is also closely related to ER stress. In our previous studies, we showed that celecoxib, a COX-2 inhibitor, improves liver fibrosis and portal hypertension. However, the role and mechanism of celecoxib in alleviating liver fibrosis remain unclear. AIM To investigate whether celecoxib alleviates liver fibrosis by inhibiting hepatocyte apoptosis via the ER stress response. METHODS Cirrhosis was induced by intraperitoneal injections of thioacetamide (TAA) for 16 wk (injection dose is 200 mg/kg per 3 d for the first 8 wk and 100 mg /kg per 3 d after 8 wk). Thirty-six male Sprague-Dawley rats were randomly divided into three groups, namely, control group, TAA group, and TAA + celecoxib group. In the last 8 wk, TAA-induced cirrhotic rats received celecoxib (20 mg/kg/day) or the vehicle by gastric gavage. After 16 wk, the rats were sacrificed, and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB) were detected. The hepatic fibrosis areas were evaluated by Sirius red staining and the degree of fibrosis was assessed by measuring the level of hydroxyproline. ER stress levels were evaluated by detecting the marker proteins glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP), PKR-like ER protein kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 alpha (IRE1α). Apoptosis levels were evaluated by detecting caspase-12 and caspase-3. RESULTS The serum ALT and AST levels in the liver were significantly reduced by celecoxib; however, the serum ALB had no significant changes. Celecoxib significantly reduced the degree of liver fibrosis and the levels of hydroxyproline (-38% and -25.7%, respectively, P < 0.01). Celecoxib ameliorated ER stress by reducing the level of GRP78 compared to the TAA group ( P < 0.05). Consistently, after celecoxib administration, the upregulation of TAA-induced hepatic apoptosis markers (caspase-12 and caspase-3) and CHOP were significantly inhibited. In addition, after celecoxib treatment, the expression of key molecules associated with ER stress (PERK, ATF6, and IRE1) was decreased ( P < 0.05). CONCLUSION Therapeutic administration of celecoxib effectively reduces hepatic apoptosis in TAA-induced cirrhotic rats. The mechanism of action may be attributed to the suppression of CHOP expression, which subsequently inhibits ER stress.
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