Lofgren's syndrome: an acute variant of sarcoidosis diagnosed by mediastinoscopy

Lofgren's syndrome is an acute clinical form of sarcoidosis that is first described by Sven Lofgren as bilateral hilar lymphadenopathy together with Erythema Nodosum [EN] and accompanying arthritis/arthralgia. This syndrome has some differences in terms of treatment, prognosis and recurrence compared to sarcoidosis. In this report, we describe a 70 years old lady who admitted with multiple erythematous lesions and arthralgia of both lower extremities and she was diagnosed as Lofgren's syndrome via mediastinoscopy

Carotid body tumors and adrenal pheocchromocytomas in siblings of a turkish family

This is a report of 2 hypertensive siblings with a history of carotid body tumors and subsequent benign adrenal pheochromocytomas [pheos] in a family where the mother had died of possible adrenal carcinoma. The first case was a 35-year-old woman with paroxysmal hypertensive attacks and a right adrenal mass. She had earlier undergone surgery to remove bilateral carotid body tumors. Investigation revealed excessive excretion of catecholamines and their metabolites in the urine. Abdominal MRI and 131I-MIBG scintigraphy revealed a right adrenal tumor. Right adrenalectomy was performed. The second case, the 45-year-old brother of the first case, was found to have a left adrenal mass on abdominal MRI. Catecholamines and their metabolites in the urine were found to be increased. He had also had surgery to remove bilateral carotid body tumors of the neck. Left adrenalectomy was performed. Both siblings showed no evidence of other familial syndromes, such as multiple neoplasia type 2, von Hippel-Lindau disease or neurofibromatosis type 1. Although the combination of familial carotid body tumors and pheo is rare, a patient who remains hypertensive after removal of a carotid body tumor deserves a careful evaluation to exclude pheo. Such tumors may be extra-adrenal or multifocal

Coagulation and fibrinolysis parameters in type 2 diabetic patients with and without diabetic vascular complications

To investigate the markers of endogenous coagulation/fibrinolysis and vascular endothelial cell function, and to assess the relationships between hemostatic parameters and diabetic vascular complications in type 2 diabetic patients. Materials and Coagulation and fibrinolysis parameters were measured in 92 type 2 diabetic patients [43 male, 49 female, mean age 50.1 ' 13.4 years] with [n = 44] and without [n = 48] vascular diabetic complications, and in 40 nondiabetic healthy subjects [20 male, 20 female, mean age 49.8 ' 15.1 years]. Common lipid parameters were also measured. The plasma levels of fibrinogen, antithrombin III [AT III], plasminogen activator inhibitor-1 [PAI-1], von Willebrand factor [vWF] activity and prothrombin time were found to be significantly increased in the type 2 diabetic patients compared with the healthy subjects. Glycosylated hemoglobin lc was inversely correlated with plasma protein S and activated prothrombin time. Protein C and S activities were positively correlated with plasma vWF activity, and were negatively correlated with plasma t-PA levels. vWF activity was negatively correlated with plasma t-PA levels. AT III levels were positively correlated with plasma total cholesterol levels, plasma low density lipoprotein cholesterol levels, plasma triglycerides and D-dimer levels. Plasma PAI-1 levels and factor V activity in diabetic patients with microvascular complications were significantly higher than those of the diabetic patients without microvascular complications. The plasma PAI-1 and platelet count were increased in patients with diabetic retinopathy compared with the diabetic patients without retinopathy. Plasma PAI-1 levels and factor VII activity were significantly higher in the diabetic patients with nephropathy than in diabetic patients without nephropathy. Plasma concentrations of fibrinogen and PAI-1 were significantly higher in the diabetic patients with neuropathy than the diabetic patients without neuropathy. The data demonstrated that patients with type 2 diabetes mellitus had a hypercoagulable state and hypofibrinolysis, thereby indicating that activation of coagulation with a reduced fibrinolytic activity may contribute to the increased risk of vascular disease in type 2 diabetic patients