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BACKGROUND/AIMS: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study histopathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflammation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). METHODS: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. RESULTS: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS-induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). CONCLUSIONS: The present study demonstrated that significant and serious histopathological changes directly associated with colitis occur in the lungs in IBD.

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Hyperthyroidism is a pathologic condition in which the body is exposed to excessive amounts of circulating thyroid hormones. Skeletal muscle is one of the major target organs of thyroid hormones. We evaluated hand grip strength and function in patients with overt hyperthyroidism. Fifty-one patients newly diagnosed with hyperthyroidism and 44 healthy controls participated in this study. Age, height, weight, and dominant hand of all participants were recorded. The diagnosis of hyperthyroidism was confirmed by clinical examination and laboratory tests. Hand grip strength was tested at the dominant hand with a Jamar hand dynamometer. The grooved pegboard test (PGT) was used to evaluate hand dexterity. The Duruöz Hand Index (DHI) was used to assess hand function. No significant differences were found in terms of clinical and demographic findings between the patients with hyperthyroidism and healthy controls (p > 0.05). Significant differences were found between the patients with hyperthyroidism and healthy controls regarding PGT and DHI scores (p < 0.05). Hyperthyroidism seemed to affect hand dexterity and function more than hand grip strength and seemed to be associated with reduced physical function more than muscle strength. This may also indicate that patients with hyperthyroidism should be evaluated by multidisplinary modalities.

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BACKGROUND: The aim of this study was to evaluate the serum lipoxin A4 (LXA4) and neutrophil/lymphocyte (Ne/Ly) ratio in individuals with achieved systemic risk factors for periodontitis. MATERIAL AND METHODS: One hundred and eighty volunteers (69 male, 111 female) who were categorized as systemically healthy control, diabetes, hyperlipidemia, obese and menopause were recruited for this cross-sectional study. Sociodemographic characteristics and oral health behaviors were recorded via questionnaire. Clinical periodontal parameters, including plaque index (PI), gingival index (GI), probing pocket depth (PD), clinical attachment level (CAL), sulcus bleeding index (SBI) and decayed, missing, and filled teeth index (DMFT), were assessed. Systemic parameters and LXA4 levels were evaluated in serum samples. RESULTS: Clinical periodontal parameters and DMFT were higher in subjects with achieved systemic risk factors than in healthy subjects. The systemically healthy with periodontitis group had higher serum LXA4 levels than the systemically healthy with non-periodontitis group (P<0.05). The Ne/Ly ratio was higher in the hyperlipidemic group with periodontitis than in the hyperlipidemic group with non-periodontitis (P<0.05). In the control group, serum LXA4 levels were positively correlated with the PD, CAL and SBI. CONCLUSIONS: In the presence of periodontitis, an increase in LXA4 levels and the Ne/Ly ratio in hyperlipidemic patients could contribute to the hypothesis that these parameters could be an indicator in periodontitis and its systemic risk factors.

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Thionamide induced vasculitis is a multisystem disease. The patients may present with different clinical signs and findings due to organ involvement. These patients are almost always perinuclear antineutrophil cytoplasmic antibody (pANCA) or antimyeloperoxidase (MPO) positive. Clinical findings are not seen in all of the patients who are ANCA positive while using thionamide. Although symptoms usually resolve with drug discontinuation, some patients, however, require high-dose steroids, immunosuppressants, or plasmapheresis. We present here a case of alveolar hemorrhage induced by propilthiouracil (PTU) during treatment with PTU for Graves' disease; patients completely recovered with corticosteroid, cyclophosphamide, and plasmapheresis.

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The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on amphotericin B induced nephrotoxicity in rat models. Male Wistar-Albino rats were randomly divided into four groups: (I) control group (n = 10), (II) CAPE group (n = 9) which received 10 µmol/kg CAPE intraperitoneally (i.p.), (III) amphotericin B group (n = 7) which received one dose of 50 mg/kg amphotericin B, and (IV) amphotericin B plus CAPE group (n = 7) which received 10 µmol/kg CAPE i.p. and one dose of 50 mg/kg amphotericin B. The left kidney was evaluated histopathologically for nephrotoxicity. Levels of malondialdehyde (MDA), nitric oxide (NO), enzyme activities including catalase (CAT), and superoxide dismutase (SOD) were measured in the right kidney. Histopathological damage was prominent in the amphotericin B group compared to controls, and the severity of damage was lowered by CAPE administration. The activity of SOD, MDA, and NO levels increased and catalase activity decreased in the amphotericin B group compared to the control group (P = 0.0001, P = 0.003, P = 0.0001, and P = 0.0001, resp.). Amphotericin B plus CAPE treatment caused a significant decrease in MDA, NO levels, and SOD activity (P = 0.04, P = 0.02, and P = 0.0001, resp.) and caused an increase in CAT activity compared with amphotericin B treatment alone (P = 0.005). CAPE treatment seems to be an effective adjuvant agent for the prevention of amphotericin B nephrotoxicity in rat models.

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BACKGROUND/AIMS: Previous studies have shown that the prevalence of abnormal acid reflux in fibrotic lung disease patients is high, and in particular, patients with secondary pulmonary fibrosis show higher esophageal acid exposure than normal controls. There are also some findings that, in patients with pathological reflux, pulmonary fibrosis may develop. The aim of this study is to investigate if pulmonary fibrosis is involved in the pathogenesis of chronic cough due to Gastroesophageal Reflux. MATERIALS AND METHODS: A prospective study was performed in twenty-one patients with chronic cough due to gastroesophageal reflux who was diagnosed as reflux esophagitis by upper gastrointestinal endoscopy, histology, and in ten healthy controls without GER or any lung disease. All participitants underwent laryngoscopic examination and gastroesophageal scintigraphy with late lung imaging. Bronchoalveolar lavage fluid total and differential cell counts, T and B cell subsets, and the concentrations of IL- 1ß and TNF-α were measured. RESULTS: Reflux extending into the proximal esophagus was noted in 52.5%, and posterior laryngitis was present in 90.5% of the patients. No evidence of pulmonary aspiration was noted in the patients with reflux on scintigraphic examination. No significant difference was found between the GER and control groups in terms of cellular content, IL-1ß and TNF-α levels or mean T cell subsets and B cell counts in bronchoalveolar lavage fluid. Forced expiratory volume in one second, forced vital capacity FEV1/FVC, total lung capacity, and carbon monoxide diffusion capacity values were within normal limits in the gastroesophageal reflux group. CONCLUSION: Our findings do not support the hypothesis that gastroesophageal reflux leads to chronic cough by triggering alveolar epithelial injury and subsequent pulmonary fibrosis.

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BACKGROUND: Our aim is to identify the relation of leptin, adiponectin and insulin resistance to bone mineral density (BMD) in type 2 diabetic postmenopausal women and compare it with that experienced by nondiabetics. MATERIAL AND METHODS: Seventy six postmenopausal female patients were included in the study. Postmenopausal type 2 diabetic (n = 19) and nondiabetic patients (n = 19) with spine and/or hip BMD T score lower than -2 were included in the study, and postmenopausal type 2 diabetic (n = 20) and nondiabetic women (n = 18) with normal BMD (T score > -1) were selected as control groups. Those receiving therapy for osteoporosis, over the age of 65, those who had a disease and were taking a medication that could affect bone metabolism were excluded. Biochemical tests, as well as leptin, adiponectin and insulin levels, were measured and insulin resistance was calculated using the HOMA test. RESULTS: There was no correlation between low BMD and leptin, adiponectin and insulin resistance. There was only a negative correlation between leptin and femur Ward's triangle BMD. CONCLUSION: Further large-scale studies must to be performed in order to analyse the effects of leptin, adiponectin and insulin resistance on bone metabolism in type 2 diabetic patients.

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The association of polymyalgic symptoms and lymphoma is a rare event whose pathogenesis remains to be clarified. Here, we describe a case of a 75-year old man with Hodgkin's lymphoma, who had presented with polymyalgic symptoms suggesting polymyalgia rheumatica. An intensive investigation with respect to malignancy was initially negative. Corticosteroid treatment was administered first and a dramatic clinical improvement was achieved. Four months later, when the corticosteroid treatment was tapered off, the initial manifestations reappeared. After the development of lymph node enlargement, the patient was diagnosed by lymph node biopsy as having Hodgkin's lymphoma. The lymphadenopathy and musculoskeletal manifestations all responded well to chemotherapy. Hodgkin's lymphoma should be considered in the differential diagnosis of PMR. These musculoskeletal syndromes should alert the physician to possible paraneoplastic manifestations of an evolving neoplasm.

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