Methamphetamine-Induced Hypoglycemia: A Case Report and Literature Review.

We present a rare case of a 34-year-old male patient with a history of schizophrenia who was found to be persistently hypoglycemic after a positive toxicology screen for methamphetamine. The patient has had multiple admissions to the hospital for persistent hypoglycemia and was then transferred to our in-patient behavioral health unit (BHU). At this time, his toxicology screen was negative for methamphetamines. During his stay in the BHU, he was compliant with his psychiatric medications and was euglycemic despite having a poor appetite until he was discharged home. This patient was shortly readmitted to the hospital and found to be severely hypoglycemic and methamphetamine positive. Here, we present this rare case of methamphetamine-induced hypoglycemia. We emphasize our work-up, treatment, and our suggested theory of why methamphetamines are the likely cause of hypoglycemia.

Association of plasma folate, plasma total homocysteine, but not methylenetetrahydrofolate reductase C667T polymorphism, with bone mineral density in postmenopausal Iranian women: a cross-sectional study.

Polymorphisms of methylenetetrahydrofolate reductase (MTHFR) have been well documented to cause hyperhomocysteinemia, and recent studies suggest an association of C677T mutation of methylenetetrahydrofolate reductase with low bone mineral density (BMD). In this study, the association of plasma total homocysteine (Hcy), plasma folate, and vitamin B12 as well as methylenetetrahydrofolate reductase C667T polymorphism with bone mineral density at neck of femur and lumbar spine in 271 postmenopausal Iranian women was investigated. Bone mineral density was measured by dual-energy X-ray absorptiometry. Restriction fragment length polymorphism was used for genotyping the methylenetetrahydrofolate reductase polymorphism. Plasma total homocysteine, plasma folate, and vitamin B12 were also determined. The bone mineral densities at the neck of femur and lumbar spine together with other clinical characteristics among methylenetetrahydrofolate reductase genotypes (CC, CT, and TT) were examined. Bone mineral densities at both neck of femur (r = -0.18, P = 0.003) and lumbar spine (r = -0.16, P = 0.01) were significantly and negatively correlated with the logarithm of plasma total homocysteine. Bone mineral density at the lumbar spine was also significantly and positively associated with plasma folate (r = 0.14, P = 0.02). However, no correlation between methylenetetrahydrofolate reductase polymorphism with bone mineral density at neck of femur (r = -0.01, P = 0.81) and lumbar spine (r = -0.04, P = 0.51) was observed. The negative association of plasma total homocysteine with bone mineral density was no longer significant when adjusted for folate and vitamin B12. Plasma folate and age were the main predictors of plasma total homocysteine explaining 15.3% and 5.2% of the variance of plasma total homocysteine, respectively. Methylenetetrahydrofolate reductase polymorphism, however, was not associated with plasma folate (r = 0.086, P = 0.17) or vitamin B12 (r = 0.05, P = 0.4). Plasma folate was one of the main predictors explaining 3.0% and 1.7% of variance of the bone mineral density at femoral neck and lumbar spine, respectively. Results from this study suggest hyperhomocysteinemia as a result of folate deficiency, but not methylenetetrahydrofolate reductase polymorphism, is independently associated with low bone mineral density and may contribute to the pathogenicity of osteoporosis in postmenopausal Iranian women.