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Insulin resistance before and after parathyroidectomy in patients with primary hyperparathyroidism--a pilot study. 2010
Rudman A1, Pearson ER, Smith D, Srivastava R, Murphy MJ, Leese GP.
Primary hyperparathyroidism (PHPT) is associated with insulin resistance and an increased cardiovascular mortality. We aimed to see if parathyroidectomy improved insulin resistance.
Twelve PHPT patients undergoing parathyroidectomy and ten control patients undergoing non-neck surgery were recruited to the study. Fasting venous blood samples were collected immediately pre-operatively and again at five to six weeks post-operatively. Samples were assayed for plasma glucose, serum insulin, total cholesterol, triglycerides, calcium, alkaline phosphatase, magnesium, parathyroid hormone (PTH), and haemoglobin A1c (HbA1c). Insulin resistance was calculated from fasting insulin and glucose values using Homeostasis Model Assessment (HOMA).
Parathyroidectomy decreased serum calcium (mean pre-op = 2.85 mmol/L, post-op 2.28 mmol/L, P < 0.001) and PTH concentrations (mean pre-op = 23.33 pmol/L, post-op = 10.23 pmol/L, P < 0.001) and increased phosphate concentration. However, there was no improvement in insulin resistance in the PHPT group at between 5 and 6 weeks post-operatively (geometric mean; pre-op = 0.88 (95% CI 0.59 - 1.33) vs. post-op = 0.88 (0.66 - 1.17) P = 0.95). In the control group, an increase in serum calcium was observed post-operatively (mean pre-op = 2.29 mmol/L, post-op = 2.35 mmol/L, P = 0.03). No change in insulin resistance was observed (geometric mean; pre-op = 1.37 (95% CI 0.89 - 2.11) vs. post-op = 1.38 (0.72 - 2.67) P = 0.96).
In summary, no significant change in insulin resistance post-parathyroidectomy in patients with PHPT was observed. This indicates that surgical treatment of PHPT does not improve insulin resistance for patients currently selected for parathyroidectomy.
Excess parathyroid hormone adversely affects lipid metabolism in chronic renal failure. 1990
Hyperlipidemia is common in chronic renal failure (CRF), but the underlying mechanisms are not clearly defined. Certain data points toward a potential role for the state of secondary hyperparathyroidism of CRF in its pathogenesis. We examined the effects of parathyroid hormone (PTH) on lipid metabolism utilizing intravenous fat tolerance test (IVFTT) and post-heparin lipolytic activity in five normal dogs, in six animals with CRF and secondary hyperparathyroidism (NPX) and in six normocalcemic-thyroparathyroidectomized dogs (NPX-PTX) with comparable degree and duration of CRF. NPX dogs had fasting hypertriglyceridemia (82 + 6.0 mg/dl vs. 49 +/- 2.7 mg/dl in normal dogs, P less than 0.01), abnormal IVFTT, and reduced post-heparin plasma LPL activity (151 +/- 10 vs. 275 +/- 15 mumol fatty acids/ml/min in normal dogs, P less than 0.01). The NPX-PTX dogs had normal fasting levels of serum triglycerides (42 +/- 0.6 mg/dl), normal IVFTT, and normal post-heparin plasma LPL (317 +/- 19 mumol fatty acids/ml/min) despite CRF. Post-heparin HL activity in plasma was not different between NPX and NPX-TPX dogs. The results show that excess blood levels of PTH and not other consequences of CRF are mainly responsible for the abnormalities in lipid metabolism. The data are consistent with the notion that excess PTH reduces post-heparin LPL activity in plasma, which in turn results in impaired lipid removal from the circulation and consequently hyperlipidemia.