Pulmonary hydatid cyst disease mimicking necrotizing pneumonia in a child with leukocytoclastic vasculitis.

The diagnosis and management of pulmonary hydatid cyst disease represents an important clinical problem in countries of the world that are endemic to echinococcal infection. Atypical clinical and radiologic findings including multiple cavitary lesions in the lung and pleural effusion may lead to misdiagnosis or delay in diagnosis in these patients. We report a patient who was followed up in our hospital with rashes and, clinical and radiologic findings of necrotizing pneumonia in whom there was no response to broad spectrum antibiotherapy. Lung computed tomography showed multiple thick-walled cystic lesions and pleural effusion and the diagnosis of pulmonary hydatid cyst disease was confirmed by surgical and serologic examinations. Antibiotic treatment was changed to albendazole 10 mg/kg/day. There was no liver involvement in terms of cyst hydatid disease with ultrasonographic examination. Skin biopsy showed leukocytoclastic vasculitis. Complete clinical and radiologic improvement was achieved in three months and albendazole treatment lasted six months.

Intraperitoneal mesenchymal stem cell administration ameliorates allergic rhinitis in the murine model.

Previous studies showed that bone marrow-derived mesenchymal stem cells (BMSCs) could ameliorate a variety of immune-mediated and inflammatory diseases due to their immunomodulatory and anti-inflammatory effects. In this study, we developed a mouse model of ovalbumin (OVA) induced allergic inflammation in the upper airways and evaluated the effects of the intraperitoneal administration of BMSCs on allergic inflammation. Twenty-five BALB/c mice were divided into five groups; group I (control group), group II (sensitized and challenged with OVA and treated with saline-placebo group), group III (sensitized and challenged with OVA and treated with 1 × 106 BMSCs), group IV (sensitized and challenged with OVA and treated with 2 × 106 BMSCs), and group V (sensitized and challenged with phosphate buffered saline (PBS) and treated with 1 × 106 BMSCs). Histopathological features (number of goblet cells, eosinophils and mast cells, basement membrane, epithelium thickness, and subepithelial smooth muscle thickness) of the upper and lower airways and BMSCs migration to nasal and lung tissue were evaluated using light and confocal microscopes. Levels of cytokines in the nasal lavage fluid and lung tissue supernatants were measured using enzyme-linked immunosorbent assay (ELISA). Confocal microscopic analysis showed that there was no significant amount of BMSCs in the nasal and lung tissues of group V. However, significant amount of BMSCs were observed in group III and IV. In OVA-induced AR groups (group II, III, and IV), histopathological findings of chronic asthma, such as elevated subepithelial smooth muscle thickness, epithelium thickness, and number of goblet and mast cells, were determined. Furthermore, the number of nasal goblet and eosinophil cells, histopathological findings of chronic asthma, and IL-4, IL-5, IL-13, and NO levels was significantly lower in both BMSCs-treated groups compared to the placebo group. Our findings indicated that histopathological findings of chronic asthma were also observed in mice upon AR induction. BMSCs migrated to the nasal and lung tissues following intraperitoneal delivery and ameliorated to the airway remodeling and airway inflammation both in the upper and lower airways via the inhibition of T helper (Th) 2 immune response in the murine model of AR.

Idiopathic cold urticaria and anaphylaxis.

Cold urticaria (CU) is a subtype of physical urticaria characterized by the development of urticaria and angioedema after cold exposure. Symptoms typically occur minutes after skin exposure to cold air, liquids, and objects. Most common method to confirm the diagnosis of CU is through ice cube challenge test, but 20% of patients with CU have negative ice cube challenge test results. The greatest risk with this kind of urticaria is the development of systemic reaction resulting in a hemodynamic collapse during generalized cold exposure. We report a case of a patient who developed CU and anaphylaxis during swimming and diving in the sea.

Neuroprotective effects of recombinant human erythropoietin in the developing brain of rat after lithium-pilocarpine induced status epilepticus.

Status epilepticus triggers a mixture of apoptotic and necrotic cell death within the hippocampus. This neuronal loss may result in the development of epilepsy and cognitive deficits. Erythropoietin mediates a number of biological actions within the central nervous system and has been shown to be neuroprotective. In the present study, we investigated the effects of recombinant human erythropoietin on hippocampus of rat after lithium-pilocarpine induced status epilepticus. Twenty-one dam reared Wistar male rats, 21-day-old were divided into three groups: control group, lithium-pilocarpine induced status epilepticus and lithium-pilocarpine induced status epilepticus and erythropoietin treated group. Erythropoietin treated group received recombinant human erythropoietin 10 U/g intraperitoneally 40 min after pilocarpine injection for 5 days. Rats were sacrificed and brain tissues were collected at 5th day of experiment. Neuronal cell death and apoptosis were evaluated. Histopathological examination showed that erythropoietin significantly decreased neuronal cell death in CA1, CA2, CA3 and dentate gyrus regions of hippocampus. It also diminished apoptosis in the CA1 and dentate gyrus regions of hippocampus. In conclusion, erythropoietin may preserve the number of neurons and decrease apoptosis in model of status epilepticus induced by lithium-pilocarpine. This experimental study suggests that erythropoietin administration may be neuroprotective in status epilepticus.