Exercise-associated hyponatremia, renal function, and nonsteroidal antiinflammatory drug use in an ultraendurance mountain run.

OBJECTIVE: To study biochemical parameters and renal function in runners completing a 60 km mountain run and to investigate the incidence of exercise-associated hyponatremia (EAH). To assess the effects of nonselective nonsteroidal antiinflammatory medication (NSAIDs) and cyclooxygenase-2 (COX-2) selective nonsteroidal antiinflammatory medication (COXIBs) on these parameters. DESIGN: Observational cohort study. SETTING: Kepler Challenge 60 km mountain run, Te Anau, New Zealand, December 2003. PARTICIPANTS: One hundred thirty-one of the 360 runners entered in the race were prospectively enrolled as volunteers on the day before the race. MAIN OUTCOME MEASURES: Subjects were weighed at race registration the day before the race and at the finish line. Blood was taken within 5 minutes of finishing and was analyzed for serum sodium, creatinine, urea, and potassium concentrations, and hematocrit. Participants were questioned about medication use in the 24 hours before and during the race (NSAIDs, COXIBs, other medications). RESULTS: Complete data sets were obtained on 123 runners. Five athletes were biochemically hyponatremic [(Na) 130-134 mM] and four were hypernatremic [(Na) 146-148 mM]. Hyponatremia was associated with a mean weight gain of 1.32 kg (range, -1.5 to 1.6 kg). Serum [Na] varied inversely with weight change. Estimated creatinine clearance did not vary with percent weight loss. Estimated creatinine clearance declined with increasing runner age. Sixty-five percent of runners did not use any medication, whereas 20% had used NSAIDs and 15% had taken COXIBs. There were no statistically significant differences between NSAID and COXIB users in any measured parameters or between all NSAID and COXIB users when compared with nonusers. CONCLUSIONS: Mild asymptomatic EAH was found to occur in 4% of the volunteer ultraendurance mountain runner study group and was associated with a mean weight gain of 1.32 kg (range, -1.5 to 1.6 kg) during the race. Seven percent gained weight but remained normonatremic, suggesting other compensatory mechanisms. Hypernatremia was found in 3% and was associated with a mean weight loss. Postrace serum sodium concentration varied inversely with percent weight change. Runners using any NSAID were more likely to become hyponatremic. Estimated creatinine clearance increased with increasing age. Elevated serum creatinine concentration at the end of the race returned to normal when remeasured the week after the race. Thirty-five percent of runners were found to use NSAIDs or COXIBs. The measures of weight change and of serum sodium, potassium, urea, and creatine concentration did not differ between NSAID and COXIB users or between all nonsteroidal antiinflammatory users and nonusers.

Subepithelial corneal deposits in IgG lambda myeloma.

A 46-year-old female presented with disseminated IgG lambda myeloma and unusual, translucent, subepithelial deposits in the periphery of both corneas. Electrophoretic studies showed that the deposits consisted of an IgG lambda paraprotein identical to that found in the serum. Minute amounts of the papaprotein were also present in the tears.

Euthyroid hyperthyroxinaemia due to endogenous antibodies to thyroxine and tri-iodothyronine. A case report.

A case of euthyroid hyperthyroxinaemia caused by auto-antibodies to thyroxine and tri-iodothyronine is presented. Gel filtration chromatography of the patient's serum showed increased binding of radio-labelled thyroxine analogue to a macromolecular component, which migrated in the gammaglobulin region on electrophoresis. Precipitation by protein A confirmed that this was an immunoglobulin. The importance of recognising this condition so that inappropriate therapy can be avoided is stressed.

Dual pathways of calcium entry in spike and plateau phases of luteinizing hormone release from chicken pituitary cells: sequential activation of receptor-operated and voltage-sensitive calcium channels by gonadotropin-releasing hormone.

It has previously been shown that, in pituitary gonadotrope cells, the initial rise in cytosolic Ca2+ induced by GnRH is due to a Ca2+ mobilization from intracellular stores. This raises the possibility that the initial transient spike phase of LH release might be fully or partially independent of extracellular Ca2+. We have therefore characterized the extracellular Ca2+ requirements, and the sensitivity to Ca2+ channel blockers, of the spike and plateau phases of secretion separately. In the absence of extracellular Ca2+ the spike and plateau phases were inhibited by 65 +/- 4% and 106 +/- 3%, respectively. Both phases exhibited a similar dependence on concentration of extracellular Ca2+. However, voltage-sensitive Ca2+ channel blockers D600 and nifedipine had a negligible effect on the spike phase, while inhibiting the plateau phase by approximately 50%. In contrast, ruthenium red, Gd3+ ions, and Co2+ ions inhibited both spike and plateau phases to a similar extent as removal of extracellular Ca2+. A fraction (35 +/- 4%) of spike phase release was resistant to removal of extracellular Ca2+. This fraction was abolished after calcium depletion of the cells by preincubation with EGTA in the presence of calcium ionophore A23187, indicating that it depends on intracellular Ca2+ stores. Neither absence of extracellular Ca2+, nor the presence of ruthenium red or Gd3+ prevented mobilization of 45Ca2+ from intracellular stores by GnRH. We conclude that mobilization of intracellular stored Ca2+ is insufficient by itself to account for full spike phase LH release.(ABSTRACT TRUNCATED AT 250 WORDS)