Henoch-Schönlein purpura (HSP) is the most common form of childhood vasculitis. Various viral and bacterial infections, drugs, vaccines, food allergy and even insect bites have been considered as triggering factors in pathogenesis of HSP. Epstein-Barr virus (EBV) infection, which is associated with HSP, have been rarely reported. Herein we present HSP patient possibly caused by EBV infection. A 8-year old boy was admitted to our department with fever, rashes on legs and arms and intermittent mild abdominal pain. Multiple purpuric rashes were on his extremities, abdomen and buttock. Laboratory investigations revealed that monospot test was positive, EBV serology tests; Anti-EA-D Ig G: 3+, Anti-VCA gp125 Ig G: 3+, Anti-VCA p19 Ig M: 2+, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig G: negative. The patient was interpreted as the primary active acute EBV infection. A skin biopsy showed leucocytoclastic vasculitis. The other viral and bacterial investigations were negative. The patient was diagnosed as HSP vasculitis according to EULAR criteria and treated with intravenous hydration and ibuprofen. He was discharged after 15 days with normal laboratory findings and physical examination. We think that EBV infection may be stimulant factor for autoimmune reactions and may cause HSP vasculitis. Hence, it may be useful to investigate the EBV infection in etiology of HSP cases.

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The aim of this experimental study was to investigate effects of prostaglandin E1 and E2 analogues on mucosal structure and bacterial translocation during small bowel obstruction. The study was carried out on 40 Wistar rats equally divided into four groups; group 1 = control, group 2 = intestinal obstruction by ligation of distal ileum, and groups 3 and 4 = obstruction and administration of PGE2 and PGE1, respectively. Intestinal bacterial content and translocation to mesenteric lymph nodes and to the blood were determined by microbiological analysis. Mucosal structural changes were assessed by histopathological examination and expressed as a structural damage score and as the thickness of the mucosal layer. Bacterial overgrowth was determined in all obstruction groups. Mucosal thickness was 39.7 microm in group 1 and 26.8 microm in group 2 (p <.001). The thickness was significantly preserved by administration of PGE1 and PGE2 (p <.001). Mean structural damage score was 0.4 in group 1 and 6.7 in group 2 (p <.001). The damage scores were significantly lower in groups treated with PGE1 and PGE2 than obstruction alone group (p <.001). Better scores were obtained in rats treated with PGE1 than rats treated with PGE2 (p =.0026). Translocation to the lymph nodes did not occur in group 1, but was 70% in group 2 (p =.0015); significantly lower rates of translocation to lymph nodes were observed in rats treated with PGE1 (p =.035), but not with PGE2. We conclude that mucosal structure is partly maintained by administration of PGE1 and PGE2 during intestinal obstruction; PGE1 is more effective than PGE2 for ameliorating mucosal injury. PGE1 prevents bacterial translocation by preserving structural integrity of the mucosa. PGE2 partially prevents mucosal damage but not bacterial translocation.

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The association of lupus erythematosus (LE) and erythema multiforme (EM) in the presence of anti-nuclear antibodies (ANA), Sjogren syndrome antigen B (autoantigen La) (anti-SS-B/La) and rheumatoid factor (RF) positivity has been described as a new syndrome by Rowell et al. in 1962. In 2012, Torchia et al. suggested novel diagnostic criteria for Rowell syndrome (RS). However, a number of cases, which lack the full diagnostic criteria, have been reported as RS in the literature. The EM-like lesions seen in these cases have been proposed as a subtype of subacute cutaneous LE. This article presents the case of a 34-year-old female patient with histopathologically diagnosed discoid LE, EM-like lesions, and speckled-pattern ANA positivity. Localizations of malar rash, discoid rash and EM-like lesions were not typical in the patient, and there was no triggering factor. Due to the lack of fully novel diagnostic criteria for RS, we conclude that our case is an instance of SLE exacerbated with EM-like lesions. (Turkderm 2015; 49: 85-8)