Decreased bone mass has been reported in patients with idiopathic hypercalciuria. Previous studies, using bioassays, have suggested a role of interleukin-1 (IL-1), in the decreased bone mineral density (BMD) of fasting hypercalciuria. The present study was designed to determine which IL-1 fraction (alpha or beta) correlates with bone resorption and whether other known bone resorting cytokines like interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) may play a role in this process. Cytokines production was determined by quantitative and specific analysis, enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase polymerase chain reaction (RT-PCR). Dual-energy X-ray absorptiometry and cytokine production by unstimulated and lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMCs) were determined in a group of 29 patients with recurrent nephrolithiasis (17 hypercalciurics and 12 normocalciurics), and 12 healthy controls. The hypercalciuric subjects showed lower vertebral BMD than the normocalciuric or normal controls. There was no difference in spinal or femoral BMD between absorptive or fasting hypercalciurics. A significant negative correlation existed between urinary calcium excretion and vertebral BMD (r = -0.55, P < 0.01). Basal IL-1 alpha production correlated with vertebral BMD (r = -0.45, P < 0.02). This correlation was not seen with IL-1 beta, IL-6 or TNF-alpha production. LPS-induced IL-6 and TNF-alpha production were enhanced in the hypercalciuric patients, when compared to normocalciurics or controls. Control and normocalciuric subjects showed minimal amounts of IL-1 alpha mRNA. In contrast, hypercalciuric patients showed a significant increase of spontaneous IL-1 alpha mRNA transcription. These results suggest that different cytokines could be involved in the bone resorption process observed in hypercalciuria.

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Symptoms in patients suffering from spontaneous osteonecrosis of the knee (SONK) may be reduced by high tibial osteotomy (HTO). However, the fate of the necrotic lesion is unknown and needs further investigation. We conducted a prospective study to evaluate magnetic resonance imaging (MRI) changes after operative and nonoperative treatment. Ten consecutive patients suffering from SONK of the medial compartment were given two treatment options: either HTO (n = 6) or conservative treatment with partial weight bearing for 3 months (n = 4). We measured the greatest extent of well-defined subchondral low signal intensity abnormality, considered to represent necrosis, and the surrounding area of intermediate signal intensity, considered to represent perifocal bone marrow edema, on T1-weighted coronal MRI images before and after treatment. The MRI follow-up period was 17.5 months (range 12-27) in the HTO group and 14.5 months (range 8-25) in the nonoperative group. At follow-up the MRI evaluation revealed a decrease in the low signal intense areas (necrosis) in five of the six patients in the HTO group. Only one of the four nonoperative patients showed a decrease in the low signal intense area. The intermediate intense areas (edema) decreased in all patients in the HTO group and in three of four in the nonoperative group. The mean decrease in the area of perifocal edema was significantly greater in the HTO group than in the nonoperative group (P = 0.019). No statistically significant difference was found for the area of necrosis between the two groups (P = 0.171). A clinical improvement was observed in all patients of the HTO group but in only two of the four patients of the nonoperative group. We conclude that the decrease in perifocal bone marrow edema seems to be associated with improved patient comfort. The MRI appearance of the necrotic lesion does not alter with either treatment mode.

A retrospective study in a hospital-based sample of Venezuelan patients with rheumatoid arthritis was made to estimate the lag time between onset of symptoms, diagnosis, and initiation of DMARD treatment. Medical records and in-person interview of patients to fill in a questionnaire collecting information on demographics and initiation of symptoms, first consultation with any physician, time of diagnosis, and initiation of first disease-modifying anti-rheumatic drug were reviewed. We performed descriptive statistics and multivariable linear regression analysis. Mean lag time between symptom onset and diagnosis of rheumatoid arthritis was 40.5 months (range 1-424). Mean lag time between onset of symptoms and first consultation with a physician and between first consultation and diagnosis was 16.3 and 23.9 months, respectively. Mean lag time between onset of symptoms and initiation of DMARD treatment was 56.9 months. A definitive diagnosis of rheumatoid arthritis was done by a rheumatologist in 251 patients (92.3%). First consultation with an orthopedist or a primary care physician, first consultation in a public versus a private health center, and diagnosis before 2000 were associated with longer lag time between onset of symptoms and diagnosis. Venezuelan patients with rheumatoid arthritis had a marked delay from disease onset to diagnosis and initiation of first DMARD. First consultation with an orthopedist and consultation in a public versus a private health center were the variables with the strongest effect on lag time to diagnosis and to initiation of first DMARD.