In this study, the clinical and laboratory features of children with lymphadenopathy were evaluated. Over a 3-year period, 126 patients were referred to the clinic for lymphadenopathy. Twenty-eight of cases have diseases mimicking lymphadenopathy; 98 (mean age: 86+/-55 months) have lymphadenopathy. Localized, limited, and generalized involvement was found in 52%, 30%, and 18% of patients. The most common localization was the head and neck region. The causes of lymphadenopathy were benign diseases in 75 patients. Sixty percent were reactive lymphadenopathy, 39% were lymphadenitis. Lymphadenitis was more frequently localized and bigger than 3 cm compared with reactive adenopathy (p=.02, p=.004). Twenty-three patients have malignant diseases whose mean age was higher than others (p=.002). The enlargement of supraclavicular nodes was more likely due to malignant disease (p=.001). The risk of malignant disease was higher in patients who had generalized lymphadenopathy, lymph nodes bigger than 3 cm, hepatosplenomegaly, and high lactate dehydrogenase levels. In conclusion, this study pointed out the important clues for the differential diagnosis, which were present in the history, physical, and laboratory findings.

Leptin has important effects on bone metabolism. Possible relationships between leptin and bone mineral density were evaluated in the survivors of the childhood leukemia and lymphoma. Twenty patients were included the study. Anthropometric parameters, growth hormone response to provocative test, serum calcium, phosphorus, alkaline phosphates, osteocalcin, leptin levels, urinary calcium and deoxyypyridinoline levels, and bone mineral density were obtained. Anthropometric parameters of patients were not significantly different from those of a control group. Growth hormone provocative test was abnormal in 3 patients who received cranial radiotherapy. The osteocalcin levels and bone mineral density of patients were significantly lower than in the control group (p=.001, p=.02). Nine patients were in the osteopenic and 7 were in the osteoporotic range. The leptin levels of patients were significantly lower (p=.01) than in the control group. Bone mineral density (BMD) was significantly correlated with leptin level, age, body mass index, and Tanner stage in simple correlation analysis. However, in multivariate analysis only age was significant (p<.000, r: .752). Markers of bone metabolism, BMD, and leptin levels were not related with the growth hormone status of patients and did not present a correlation with the cumulative doses of drugs. There are a few studies evaluating the relationship between BMD and leptin levels in childhood cancer. Although this study did not find any correlation between the leptin level and BMD, detailed studies of larger numbers of patients are necessary to evaluate causes of decreased leptin level and the possible role of leptin on osteopenia observed in survivors of childhood cancer.