Uñas de pies en «salto de esquí» / Ski-Jump Toenails

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Effects of adalimumab on T-helper-17 lymphocyte- and neutrophil-related inflammatory serum markers in patients with moderate-to-severe hidradenitis suppurativa.

BACKGROUND: T-helper (Th)-17 lymphocytes and neutrophils are the main sources of the proinflammatory cytokines involved in the pathogenesis of hidradenitis suppurativa (HS). OBJECTIVES: This study aims to evaluate the improvement of the inflammatory serum markers (ISM) levels in patients with moderate-to-severe HS who receive adalimumab. METHODS: Nineteen moderate-to-severe HS patients were prospectively recruited. Each of the patients received 40 mg of adalimumab weekly. The ISM levels and modified Hidradenitis Suppurativa Score (mHSS) scores were assessed at baseline and at week 36. Nineteen healthy volunteers (HC) constituted the control group. RESULTS: Before adalimumab treatment, the HS patients showed significantly increased levels of interleukin (IL)-6, IL-8, IL-10, IL-17A, soluble TNF receptor II (sTNF-RII), and C-reactive protein (CRP) as well as an increased erythrocyte sedimentation rate (ESR) (all P < .01). At week 36, the circulating levels of IL-1ß, IL-6, IL-8, IL-10, IL-17A, soluble TNF receptor I (sTNF-RI), sTNF-RII, and CRP, as well as the ESR (all P < .05), decreased significantly in the HS patients who received adalimumab. The decrease in levels of IL-6 (r = 0.65, P = .003), IL-8 (r = 0.52, P = .024), sTNF-RI (r = 0.55, P = .015), and CRP (r = 0.47, P < .040) and the ESR (r = 0.60, P < .006) were significantly well correlated with clinical improvements according to the mHSS. CONCLUSIONS: Adalimumab improves the ISM-based systemic inflammatory burden in patients with moderate-to-severe HS. IL-6, IL-8, sTNF-RI and CRP and the ESR may serve as novel biomarkers for a therapeutic response.

The Clinical Significance of Increased Serum Proinflammatory Cytokines, C-Reactive Protein, and Erythrocyte Sedimentation Rate in Patients with Hidradenitis Suppurativa.

OBJECTIVES: To assess inflammatory serum markers including serum proinflammatory cytokines, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) according to the clinical inflammatory activity of patients with hidradenitis suppurativa (HS). PATIENTS AND METHODS: Seventy-four patients with HS were studied based on the Hidradenitis Suppurativa-Physician Global Assessment (HS-PGA) score and Hurley staging system. Proinflammatory cytokines were measured using a multiplex cytokine assay. Twenty-two healthy volunteers were recruited. RESULTS: Serum interleukin- (IL-) 6, IL-23, soluble tumour necrosis factor alpha (TNF-α) receptor I (sTNF-RI), CRP, and ESR were different in the patients with HS compared with those in the healthy controls (P < 0.05). The levels of IL-1ß, IL-6, IL-8, IL-10, IL-12p70, IL-17A, sTNF-RII, CRP, and ESR were significantly elevated according to inflammatory activity based on HS-PGA scores (r > 0.25, P < 0.05). The levels of IL-6 (r = 0.53, P < 0.001), CRP (r = 0.54, P < 0.001), and ESR (r = 0.60, P < 0.001) were especially well correlated with clinical inflammatory activity based on HS-PGA scores. The levels of IL-6, IL-8, sTNF-RI, sTNF-RII, CRP, and ESR were significantly elevated according to Hurley staging system. CONCLUSIONS: Serum proinflammatory cytokines, CRP, and ESR are increased in relation to the clinical inflammatory activity of patients with HS compared with healthy controls. Serum IL-6, CRP, and ESR are effective biomarkers for evaluating the severity of HS.

Vesiculobullous variant of erythema elevatum diutinum.

The vesiculobullous variant of erythema elevatum diutinum (EED) is a very rare variant of EED. We describe a 16-year-old boy who presented with symmetrical nodular lesions accompanied by vesicles on the dorsa of his hands. Biopsy findings were consistent with EED. The histopathological presence of IgA and neutrophils in the vesicles indicates that the joint action of both is responsible for formation of these subepidermic vesicles. We hypothesize that absence of human leucocyte antigen related to dermatitis herpetiformis (DH) in our patient might have influenced the location and distribution of the lesions, so that they were not typical of DH. We report the second case of the vesiculobullous variant of EED with IgA deposits in the dermoepidermal membrane. To our knowledge, there are only 14 previously reported cases of the vesiculobullous variant of EED.

Tratamiento multimodal de la calcifilaxis con tiosulfato sódico, alprostadil y oxigenoterapia hiperbárica / Multimodal treatment of calciphylaxis with sodium thiosulfate, alprostadil, and hyperbaric oxygen therapy

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Calcifilaxis tratada con tiosulfato sódico intralesional / Intralesional Sodium Thiosulfate to Treat Calciphylaxis

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Calcinosis cutis y calcifilaxis / Calcinosis Cutis and Calciphylaxis

La calcinosis cutis (CC) se define como el depósito de sales de calcio en la piel. Esta entidad se clasifica en 5 tipos que incluyen la CC distrófica, metastásica, idiopática, iatrogénica y calcifilaxis. La calcificación distrófica constituye el tipo más frecuente y aparece principalmente en enfermedades autoinmunes. El tratamiento de la CC incluye la extirpación quirúrgica o el uso de fármacos como diltiazem, bifosfonatos, warfarina, ceftriaxona, probenecid, minociclina e hidróxido de aluminio. La calcifilaxis se define como la calcificación de la capa media de vasos de pequeño y mediano tamaño de la dermis y tejido celular subcutáneo. Clínicamente se manifiesta como un síndrome de livedo racemosa que progresa a púrpura retiforme y necrosis cutánea. La primera línea de tratamiento es el tiosulfato sódico. El objetivo de esta revisión es proporcionar un análisis de los diferentes trastornos de calcificación cutánea enfocada en su diagnóstico y tratamiento

Calcinosis cutis (CC) is defined as the deposition of calcium salts in the skin. The condition is divided into 5 types: calciphylaxis and dystrophic, metastatic, idiopathic, and iatrogenic CC. Dystrophic CC is the most common form and usually occurs in association with autoimmune diseases. CC can be treated surgically or with the use of drugs such as diltiazem, bisphosphonates, warfarin, ceftriaxone, probenecid, minocycline, or aluminum hydroxide. Calciphylaxis is defined as calcification of the media of small- and medium-sized blood vessels in the dermis and subcutaneous tissue. Clinically, calciphylaxis causes livedo racemosa, which progresses to retiform purpura and skin necrosis. First-line treatment is with sodium thiosulfate. We present a review of the calcifying disorders of the skin, focusing on their diagnosis and treatment

Calcinosis Cutis and Calciphylaxis.

Calcinosis cutis (CC) is defined as the deposition of calcium salts in the skin. The condition is divided into 5 types: calciphylaxis and dystrophic, metastatic, idiopathic, and iatrogenic CC. Dystrophic CC is the most common form and usually occurs in association with autoimmune diseases. CC can be treated surgically or with the use of drugs such as diltiazem, bisphosphonates, warfarin, ceftriaxone, probenecid, minocycline, or aluminum hydroxide. Calciphylaxis is defined as calcification of the media of small- and medium-sized blood vessels in the dermis and subcutaneous tissue. Clinically, calciphylaxis causes livedo racemosa, which progresses to retiform purpura and skin necrosis. First-line treatment is with sodium thiosulfate. We present a review of the calcifying disorders of the skin, focusing on their diagnosis and treatment.