The benefit of adjuvant use of corticosteroids in patients with septic shock remains controversial. In this international, multicenter, double-blind, placebo-controlled trial, adjunctive therapy with hydrocortisone in nearly 500 patients with septic shock was not found to be clinically helpful. This lack of benefit was also found in a subgroup of patients who did not have a response to a corticotropin test.

Optimal glucose control and fluid resuscitation in patients with septic shock remain a challenge. In this study involving more than 500 patients, the potential benefit of maintaining euglycemia through intensive insulin therapy and optimal fluid resuscitation with either pentastarch or Ringer's lactate was assessed. There was no benefit in the intensive-therapy group with respect to either 28-day survival or organ function; there was more severe hypoglycemia in the intensive-therapy group and more acute renal failure in the pentastarch group.

In this open-label trial, patients with tuberous sclerosis or lymphangioleiomyomatosis — conditions with constitutive activation of signaling by the mammalian target of rapamycin (mTOR) — received rapamycin (now called sirolimus) for 1 year and were observed for an additional year. Angiomyolipomas regressed with sirolimus therapy but generally increased after therapy was stopped. Pulmonary function improved after treatment in some patients. Suppression of mTOR signaling may hold therapeutic promise in these conditions.

From a database of 12,550 trained athletes, 81 were identified who had markedly abnormal electrocardiograms (ECGs) in the absence of apparent structural heart disease. During 9 years of follow-up, cardiomyopathies developed in five of these athletes, including one who died suddenly and one who had cardiac arrest. No cardiomyopathies developed in 229 matched control subjects with normal ECGs.

Hypoxia-inducible factor (HIF) α is a transcription factor that modulates erythropoiesis, angiogenesis, and cellular metabolism. This study of a family with isolated erythrocytosis revealed a mutation in the gene for the HIF-2α isoform, HIF2A, that prevents the hydroxylation of the protein by prolyl hydroxylase–domain protein 2 under normoxic conditions and hence blocks the normal step of degradation by the von Hippel–Lindau protein.