Progression of atypical femur stress fracture after discontinuation of bisphosphonate therapy.

Atypical femur fracture (AFF) is an uncommon complication of long-term bisphosphonate use, but the risk declines substantially after treatment cessation. We report a case of a 70-year-old woman with osteopenia treated with alendronate for 9 years who presented with right mid-thigh pain and radiographic findings of focal lateral cortical thickening in the right mid-femur and lateral cortex irregularity in the proximal-mid left femur. Alendronate was discontinued, but she remained on estrogen for menopausal symptoms. Four years later, a horizontal linear translucent defect was seen in the right mid-femur area of cortical hypertrophy, consistent with an incomplete AFF. The patient underwent prophylactic intramedullary rodding of the right femur and estrogen was discontinued. Three years later (7 years after initial presentation), the cortical irregularities in the left femur were more prominent and three small horizontal linear translucent defects were now evident, consistent with early incomplete atypical fracture development. The patient also suffered a wrist fracture. She was treated with teriparatide for 1.5 years with resolution of the translucent defects in the left but not the right femur, although abnormal thickening of the lateral cortex persisted in both femurs. Our case demonstrates incomplete atypical femur fracture progression in a patient with long-term bisphosphonate exposure, even after treatment cessation. These findings highlight the importance of follow-up for patients who develop diaphyseal femur stress fractures and the potential for early healing with anabolic therapy. This case also demonstrates the challenge in managing older patients with incomplete AFF at risk for progression to complete AFF and osteoporotic fracture.

Adverse health effects of lead exposure on children and exploration to internal lead indicator.

Our research on adverse effects of lead exposures on physical and neurobehavioral health of children aged 6-12years in 4 villages, labeled as K, M, L, and X, in rural China, was reported in this article. Lead in blood (PbB), urine (PbU), hairs (PbH), and nails (PbN) were measured by graphite furnace atomic absorption spectrometry. Abbreviated Symptom Questionnaire of Conner's instruments and Revised Raven's Standard Progressive Matrices were applied to evaluate childhood attention deficit/hyperactivity disorders (ADHD) and intelligences. Geometric means (SD) of PbB, PbU, PbH and PbN concentrations were 71.2 microg/L (1.56), 11.7 microg/g (1.75), 12.5 microg/g (2.82), and 25.3 microg/g (2.79), respectively. 54 (17.0%) children had PbB levels of > or =100 microg/L. Boys, 6-10 years old, and living in village K were 2.11, 2.48, and 9.16 times, respectively, more likely to be poisoned by lead than girls, aged 11-12 years, and residing in X. 18 (5.7%) and 37 (11.7%) subjects had ADHD and mental retardations, respectively. Inverse relationships between intelligences and natural log transformed PbU and PbH levels were observed with respective odds ratios (95%CI) of 1.79 (1.00-3.22) and 1.46 (1.06-2.03) or 1.28 (1.04-1.58) and 1.73 (1.18-2.52) by binary or ordinal logistic regression modeling. ADHD prevalence was different by gender and age of subjects. PbU, PbH, and PbN related to PbB positively with respective correlation coefficients of 0.530, 0.477, and 0.181. Receiver operating characteristic (ROC) curves of the three measurements revealed areas under curves (AUCs) being 0.829, 0.758, and 0.687, respectively. In conclusion, children had moderate levels of lead exposures in this rural area. Intelligence declines were associated with internal lead levels among children. ROC analysis suggests PbU an internal lead indicator close to PbB.

Study on the cytotoxicity of microcystin-LR on cultured cells.

The toxicity of purified blue-green algal toxin, microcystin-LR, on permanent cell lines KB, NIH/3T3, H-4-II-E, HeLa, Vero, Hep G2, Caco-2 and HL-60 was studied. Assessment of cell viability using colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays indicated that purified microcystin-LR induced toxic effect on KB and H-4-II-E cell lines after 96 h incubation at toxin concentrations greater than 18.75 microg/ml. KB cell line was selected for further study when reproducibility, consistency and sensitivity were considered. Significant amounts of lactate dehydrogenase (LDH) were released from KB cells when incubation durations were 72 and 96 h with toxin concentrations of 18.75 microg/ml and higher. Although previous studies suggested that microcystin-LR had no cytotoxic effect on permanent cell lines, LDH release assay performed on KB cells indicated that exposure to microcystin-LR could result in damage to the cell membrane.