Cardiac structure and functions in patients with asymptomatic primary hyperparathyroidism.

BACKGROUND: The data about cardiovascular (CV) changes in patients with asymptomatic primary hyperparathyroidism (PHPT) are scarce. AIM: The aim of this study is to compare cardiac structure and functions in patients with asymptomatic PHPT and controls by using tissue Doppler echocardiography. SUBJECTS AND METHODS: Thirty-eight patients with asymptomatic PHPT and 31 sex- and age-matched controls with similar cardiac risk factors were evaluated. RESULTS: There was no significant difference in ejection fraction (EF) between the patients and the controls [64±5.95 vs 62±3.25% (p=0.094)]. Left ventricular mass index (LVMI) was significantly higher in patients than controls [105.96 (66.45-167.24) vs 93.79 (64.25- 139.25) g/m2, p=0.014]. There was a significant correlation between LVMI and serum calcium (Ca) (r=0.240, p<0.005). Myocardial performance index (MPI) was significantly higher in patients than controls [0.49 (0.35-0.60) vs 0.39 (0.33-0.62), p<0.001]. There was positive correlation between theMPI and serumCa levels (r=0.505, p<0.001), parathyroid hormone (PTH) levels (r=0.464, p<0.001) and LVMI (r=0.270, p<0.005). When the normotensive patients and controls were evaluated, the difference between the groups remained statistically significant considering LVMI and MPI [109 (66.45-167.24) g/m2 vs 94.17 (64.25-75.10) g/m2, p=0.03; and 0.49 (0.35-0.60) vs 0.39 (0.33-0.62), p<0.01, respectively]. There were significant correlations between MPI and Ca (r=0.566, p<0.001), and PTH (r=0.472, p<0.001). CONCLUSIONS: Our study results showed that cardiacmorphology and diastolic functions are altered in the patients with asymptomatic PHPT. High serum PTH and Ca levels may have an impact on these CV changes. Whether these subtle CV changes would affect cardiac systolic functions and mortality in patients with asymptomatic PHPT should be investigated in further prospective studies.

Acute and chronic effects of different concentrations of free fatty acids on the insulin secreting function of islets.

INTRODUCTION: Lipotoxic effects of free fatty acids (FFAs) on insulin secreting function of islet beta-cells have been demonstrated in recent studies. This toxic effect is especially prominent on postprandial hypertriglyceridemic period. Hypertriglyceridemia and high FFAs levels are the most common metabolic disturbances seen in diabetes mellitus (DM), in particular in uncontrolled cases. AIM OF STUDY: To investigate acute and chronic effects of different concentrations of FFAs on insulin secreting function of pancreas islet beta-cells. MATERIAL AND METHOD: We determined the acute and chronic effects of FFAs on insulin secretion dynamics of isolated rat islets. The insulinotropic effects of four D-glucose concentrations (Nil, 5.6, 8.3 and 27.7 mM) were studied in freshly isolated and perifused islets in the presence of two different concentrations (250 micromol/l and 1,250 micromol/l) of three FFAs (palmitate, stearate and oleate) to determine the acute effects. Chronic effects were investigated similarly on islet cells incubated for 72 hours in the presence of nil, 250 micromol/l and 1,250 micromol/l concentrations of FFAs. RESULTS: There was only a slight increase in insulin secretion at both concentrations of FFAs in freshly isolated islets, and the recovery was complete with a slight decrease in pathologic FFA channel. However, after 72 hour incubation at physiological or higher concentrations of FFAs, insulin secretion was significantly lower, even in the presence of high levels of D-glucose when compared to either nil channel results, or results of the fresh samples. Insulin levels of recovery phase were slightly but significantly lower in physiological and pathologically high FFA conditions when compared to nil condition. In addition, first phase insulin release response was lost in these islets. CONCLUSION: FFAs slightly increased the insulin output of normal fresh pancreas beta-cells. However, chronic exposure to FFAs resulted in loss of first phase insulin release and blunted insulin secretion response to various levels of D-glucose stimulation.