The association between serum total testosterone and progression of hyperglycemia: a 15-year prospective cohort study.

BACKGROUND: The association between low testosterone concentration and increased risk of hyperglycemia in men has been demonstrated in observational and interventional studies. However, considering a variety of confounding factors, limited population-based studies have so far been conducted. Also, no information is available regarding the effect of testosterone on progressive development of dysglycemia. OBJECTIVE: To examine the effect of total testosterone on development of pre-diabetes/diabetes in normoglycemic middle-aged and older men. MATERIALS AND METHODS: Data were obtained from the Tehran Lipid and Glucose Study, a community-based prospective cohort of an Iranian population. Analyses were conducted on 903 normoglycemic eligible men aged 30-70 years. An illness-death model was applied to estimate the probabilities of three transitional phases of normoglycemia→diabetes, normoglycemia→pre-diabetes, and pre-diabetes→diabetes. RESULTS: Over a median follow-up of 12 years, 0.9% individuals developed diabetes. Per unit increase (ng/mL) in testosterone concentration, the transition rate from normoglycemia to pre-diabetes decreased by 6% [hazard ratios (HRs): 0.94 (95% confidence interval (CI): 0.90, 0.99)]. However, no effect for testosterone on the progression of diabetes from normoglycemia or pre-diabetes was observed [HRs: 0.79 (95% CI: 0.44, 1.41) and 0.98 (95% CI: 0.84, 1.16), respectively]. High body mass index was a strong predictor of hyperglycemia within all transitions. DISCUSSION: Independent of major confounding factors, low testosterone was associated with normoglycemia progression to pre-diabetes, but not with pre-diabetes to diabetes, which might indirectly highlight the stronger impact of other risk factors after occurrence of pre-diabetes. CONCLUSION: Low testosterone concentrations in men are associated with progression from normoglycemia to pre-diabetes, but not from pre-diabetes to diabetes.

Is sudden infant death syndrome associated with Helicobacter pylori infection in children?

Helicobacter pylori infection has recently been implicated in the pathogenesis of sudden infant death syndrome (SIDS). We investigated this association. Twenty-five pairs of gastric and tracheal tissue specimens obtained from autopsies of 25 children with previous diagnoses of SIDS were available for this study. The presence of H. pylori organisms was evaluated by three different methods: histology (hematoxylin-eosin or Giemsa staining), immunohistochemistry, and nested polymerase chain reaction technique. We were unable to confirm the presence of H. pylori organisms by the first two methods. H. pylori DNA was identified by nested polymerase chain reaction in six different tissue specimens (stomach, 4; trachea, 2). In no case was H. pylori DNA detected in both tissues. We concluded that H. pylori infection is most likely not associated with SIDS.