Short-course treatment in neurobrucellosis: A study in Iran

Neurobrucellosis is a rare neurological complication of brucellosis. This report describes 19 patients of neurobrucellosis and they accounted for 8% of all cases of brucellosis admitted to Shiraz University Hospitals over a period of eight years. Headache, fever, fatigue, drowsiness and neck stiffness were the common clinical features. Cerebrospinal fluid (CSF) showed pleocytosis in 100%, elevated protein levels in 89% and low glucose level in 47% of the patients. All the patients improved with specific antibiotic treatment. Of the 19 patients, 10 (52.5%) patients received treatment for 8 to 28 weeks. Duration of antibiotic treatment was: 8-14 weeks in 8 (42%) patients; 24-28 weeks in 2 (10.5%) patients; 6 months in 7 (37%) patients; 12 months in 1 (5.3%) patient; and 18 months in 1 (5.3%) patient. Clinicians in endemic areas should consider the likelihood of neurobrucellosis in patients with unexplained neurological and psychiatric symptoms

RAGE is a Potential Cause of Onset and Progression of Nonalcoholic Fatty Liver Disease

Objective. Fatty liver is a rising global health concern, significantly increasing the burden of health care cost. Nonalcoholic fatty liver disease (NAFLD) has a correlation with metabolic syndrome and its complications. Method. We reviewed the literature regarding the mechanisms of developing NAFLD through AGE-RAGE signaling. Results. NAFLD, metabolic syndrome, and production of advanced glycation end-products (AGEs) share many common risk factors and appear to be connected. AGE induces production of the receptor for AGE (RAGE). AGE-RAGE interaction contributes to fat accumulation in the liver leading to inflammation, fibrosis, insulin resistance, and other complications of the fatty liver disease. The immune system, especially macrophages, has an important defense mechanism against RAGE pathway activities. Conclusion. Soluble form of RAGE (sRAGE) has the capability to reduce inflammation by blocking the interaction of AGE with RAGE. However, sRAGE has some limitations, and the best method of usage is probably autotransplantation of transfected stem cells or monocytes, as a precursor of macrophages and Kupffer cells, with a virus that carries sRAGE to alleviate the harmful effects of AGE-RAGE signaling in the settings of fatty liver disease

Adiponectin as a Protective Factor Against the Progression Toward Type 2 Diabetes Mellitus in Postmenopausal Women.

Serum adiponectin levels have been suggested to be predictors of type 2 diabetes mellitus in diverse populations. However, the relationship between circulating adiponectin levels and the risk of development of type 2 diabetes in postmenopausal women has not been investigated.A total of 382 healthy postmenopausal women who participated in a prospective cohort study were followed for 5.8 years. Type 2 diabetes mellitus was defined according to the criteria set out by the American Diabetes Association. Adiponectin, osteoprotegerin (OPG), and high-sensitivity C-reactive protein (hs-CRP) levels were measured using ELISA.Of 195 women who did not have diabetes at baseline and who were reexamined in the second phase of the study for diabetic status, 35 subjects (17.9%) developed type 2 diabetes mellitus during the 5.8 years follow-up period. The women with type 2 diabetes had lower adiponectin levels than the healthy postmenopausal women. Multiple regression analysis showed that, after adjustments were made for age, cardiovascular risk factors, OPG, and hs-CRP levels, higher baseline adiponectin levels were associated with a lower relative risk (RR) of having type 2 (RR = 0.07, confidence interval [CI]: 0.01-0.66, P = 0.021).Higher baseline adiponectin levels functioned as a predictor of a lower risk of developing type 2 diabetes mellitus among postmenopausal women during a 5.8 years follow-up study. Therefore, it is suggested that elevated adiponectin levels may offer protection against the development of type 2 diabetes mellitus after the menopause

Evaluation of adipokines, adiponectin, visfatin, and omentin, in uncomplicated type I diabetes patients before and after treatment of diabetic ketoacidosis

Background: Diabetic ketoacidosis (DKA) is potentially a lethal complication of uncontrolled, especially type 1, diabetes. Understanding the mechanisms underlying adipokine involvement in the regulation of glucose metabolism is important to prevent complications of hyperglycemia. The role of novel adipokines during DKA in human remains unclear. Method: The method is to determine the changes in the circulating levels of adiponectin, visfatin, and omentin after treating DKA in the patients referred to Shohadaye Khalij-e-Fars hospital at the Bushehr University of Medical Sciences. Measuring adipokines (adiponectin, visfatin, and omentin) in 31 patients with DKA who are admitted in Shohadaye Khalij-e-Fars hospital at the Bushehr University of Medical Sciences. Adipokines are measured at the time of admission and after recovery from DKA, using ELISA method. Results: After recovery from DKA, omentin-1 serum concentration decreased significantly (from 183 to 165), but adiponectin and visfatin did not change significantly. Conclusion: Omentin-1 may play a significant role in insulin resistance during the DKA and could be potentially recommended as a marker of recovery in DKA

Oncogenic osteomalacia secondary to glomus tumor

Oncogenic osteomalacia secondary to glomus tumor is extremely rare. Localization of causative tumors is critical as surgical resection can lead to a complete biochemical and clinical cure. We present a case of oncogenic osteomalacia treated with resection of glomus tumor. A 39-year-old woman with a history of chronic sinusitis presented with chronic body ache and muscle weakness. Biochemical evaluation revealed elevated alkaline phosphatase hypophosphatemia, increased urinary phosphate excretion, low calcitriol, and FGF23 was unsuppressed suggestive of oncogenic osteomalacia. Diagnostic studies showed increase uptake in multiple bones. Localization with MRI of paranasal sinuses revealed a sinonasal mass with concurrent uptake in the same area on the octreotide scan. Surgical resection of the sinonasal mass was consistent with the glomus tumor. The patient improved both clinically and biochemically postoperatively. Along with the case of oncogenic osteomalacia secondary to a glomus tumor, we have also discussed in detail the recent development in the diagnosis and management of oncogenic osteomalacia. Learning points: •• Tumor-induced osteomalacia is a rare cause of osteomalacia caused by the secretion of FGF23 from mesenchymal tumors. •• Mesenchymal tumors causing TIO are often difficult to localize and treat. •• Resection of the tumor can result in complete resolution of biochemical and clinical manifestations in a very short span of time. •• Glomus tumor can lead to tumor induced osteomalacia and should be surgically treated