Hyperthyroid hearts are shown to display a phenotype of cardioprotection against ischemic stress, but the underlying signaling mechanisms remain largely unknown. The present study investigated the possible relation of HSP70 to the thyroid hormone induced cardioprotection. HSP70 is a redox-regulated molecular chaperone, and enhances cell survival under stress. Thyroxin (25 microg/100 g body weight) was administered to Wistar male rats for four days (THYR-4d) and two weeks (THYR-14d), respectively, while untreated animals served as controls (CON-4d, CON-14d). Isolated hearts from control and thyroxin treated rats were subjected to 20 min zero-flow ischemia followed by 45 min of reperfusion (I/R). The amount of HSP70 in the myocardium for THYR-14d was 1.85 times the levels of CON-14d (p < 0.05). The levels of HSP70 expression were no different between THYR-4d and CON-4d, p > 0.05. This was only accompanied by an increase in MDA levels (used as an index of oxidative stress) in THYR-14d compared to untreated hearts. These changes corresponded to a differential response of the heart to I/R; post-ischemic recovery of function was significantly increased in THYR-14d compared to CON-14d, and was no different between the THYR-4d and CON-4d hearts. In conclusion, long-term thyroxin administration results in increased tolerance of the myocardium to I/R and enhances the expression of HSP70 which may, at least in part, account for this response.

OBJECTIVE To study the urological manifestations of familial multiple endocrine neoplasia type 1 (MEN‐1). PATIENTS AND METHODS The study included 26 adults (median age 38.5 years, range 18–80) from two unrelated MEN‐1 pedigrees. In 15 of the patients the diagnosis was confirmed by genetic analysis, while in the rest the diagnosis was based on clinical criteria combined with genealogy data. RESULTS Urolithiasis associated with primary hyperparathyroidism was present in 65% of MEN‐1 patients and in 77% of those who were symptomatic. In 68% of patients complications of urolithiasis (renal/ureteric colic, urinary tract infection) were the presenting clinical manifestations of MEN‐1, whereas in 50% they constituted the only clinical manifestation of the syndrome. The mean time from the onset of symptoms of urolithiasis to the diagnosis of the polyendocrinopathy was 17.2 years. Initial failure to recognize the presence of MEN‐1 in patients with primary hyperparathyroidism led to conservative parathyroid surgery, with subsequent relapse of the hyperparathyroidism, requiring re‐operation. Serious renal morbidity included one case of pyonephrosis necessitating nephrectomy. While urolithiasis was a cardinal clinical manifestation of MEN‐1, there was otherwise considerable phenotypic polymorphism, even among patients bearing the same MEN1 gene mutation. CONCLUSION In patients with familial MEN‐1 the complications of urolithiasis are the commonest presenting clinical manifestations and the cause of significant morbidity. In the presence of a family history of renal stones, appropriate investigations may lead to the timely diagnosis of this important, albeit rare, disorder.

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