The aim of this study was to examine the prevalence of hyperuricemia and its associated factors in an urban area of Izmir, located in western Turkey. Our study group was selected by computerized sampling from the participants of a larger population-based study searching for the prevalence of rheumatoid arthritis in Balcova and Narlidere districts of Izmir. A total of 132 subjects (69 women and 63 men) were included in this study. Serum uric acid, glucose, creatinine and lipid levels were studied. Body composition along with body fat percentage was determined anthropometrically. A total of 16 subjects had hyperuricemia (4 women and 12 men). The overall prevalence of hyperuricemia was 12.1% and the mean uric acid level was 4.9 +/- 1.3 mg/dl. Males had significantly higher uric acid levels than females (P < 0.05; 5.5 +/- 1.3 vs. 4.3 +/- 1.1 mg/dl, respectively). The prevalence of hypertension, diabetes, obesity and metabolic syndrome was 24.4, 5.3, 28 and 26.5%, respectively. There was no gouty subject. Sum of skinfold thickness (SFT) measurements and creatinine levels were the independent predictors of hyperuricemia (beta = 0.45, 0.47, respectively). Uric acid measurement is important not only for inflammatory rheumatic disorders but also for predicting metabolic syndrome and related coronary artery disease. There is sex difference in uric acid levels in favor of women most probably explained by gonadal hormones. Hyperuricemia is significantly predicted by anthropometric measure of SFT which is a simple clinical screening method along with creatinine levels.

The pSS prevalence rates found in the Turkish population in this study were lower than the estimated prevalence rate in a general population.

we showed that sRANKL levels were higher and correlated with bone turnover markers. It may be related to osteoporosis in SSc. The OPG level was unaltered in SSc patients. Higher TRAIL levels associated with skin thickness may indicate vascular dysfunction or injury. Higher DKK-1 and sclerostin levels may be related to a reactive increase in cells and be prominently linked to fibrosis in SSc.

This is the first report of the development of PI-IBS after T. britovi. Consequently, IBS can be considered as a secondary syndrome induced by trichinellosis.

Abstract. Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism and an uncommon form of hypokalemic periodic paralysis. Its differentiation of more common forms of periodic paralysis is important because aggressive treatment can place the patient at risk for rebound hyperkalemia. Treatment of the underlying thyroid dysfunction cures the muscle symptoms. Here we describe a 37-year-old Turkish male with THPP whose paralysis attack recurred soon after administration of radioactive iodine. THYROTOXIC hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism in the Western population. It occurs primarily in males of Asian descent, including patients of Japanese, Chinese, Vietnamese, Korean, Filipino, American Indian, and Hispanic ancestry [1][2][3][4][5][6][7][8][9][10]. Although the association of thyrotoxicosis and periodic paralysis has been wellknown since 1931 [11] it is not reported from Turkey in English literature, most probably because of unfamiliarity with the disorder. We herein report a 37-year-old Turkish male patient with THPP who also experienced a paralysis attack ten days after the administration of radioiodine despite the treatment with propranolol. Case reportA 37-year-old Turkish male patient presented with the complaint of approximately ten episodes of muscle weakness for 2 years. These attacks occurred in all but one episode at night, following exertion or consumption of large carbohydrate meals. He was usually awakened from sleep in the early hours with difficulty of ambulation due to muscle weakness of extremities mainly in his legs. There were no prodromal symptom and no seasonal variation of the attacks. The duration of paralysis attacks ranged from four to 24 hours. He didn't seek medical attention for the paralysis attacks and they all resolved spontaneously. There was no family history of neuromuscular and endocrine abnormality.He was diagnosed as having hyperthyroidism based on the clinical symptoms of occasional palpitation and nervousness and the suppressed thyroid stimulating hormone (TSH) of 0.01 mU/mL (normal, 0.35-4.5 mU/ mL) five months ago. Then he was put on carbimazole therapy (20 mg daily). After the cessation of therapy by his own decision approximately one month ago, he experienced another attack. He denied any weight loss, heat intolerance, or diarrhea. The physical examination including muscle strength and tendon reflexes was unremarkable.His free thyroxine (FT 4 ) level was 5.26 ng/dL (normal, 0.8-1.9 ng/dL) and TSH level was <0.002 mU/mL (normal, 0.4-5.0 mU/mL). The TSH-receptor-stimulating antibody level was 135 U/L (normal, 0-9 U/L). Thyroid scan revealed diffuse uptake in a normal sized gland with a 24-hour radioactive iodine uptake of 52.1%. These findings were found to be most con-