leptin and Hyperparathyroidism--Secondary

Leptin has been implicated in bone metabolism, but the association with parathyroid gland function has not been fully clarified. This review aimed to summarize evidence of the association between leptin and hyperparathyroidism, both primary and secondary, elucidating the potential pathophysiologic and therapeutic consequences between leptin and parathyroid hormone, hopefully prompting the design of new studies.. Experimental studies indicate a positive loop between leptin and parathyroid hormone in primary hyperparathyroidism. Dissimilar, parathyroid hormone seems to inhibit leptin expression in severe secondary hyperparathyroidism. Data from clinical studies indicate higher leptin levels in patients with primary hyperparathyroidism than controls, but no association between parathyroid hormone and leptin levels, as well as a minimal or neutral effect of parathyroidectomy on leptin levels in patients with primary hyperparathyroidism. Clinical data on secondary hyperparathyroidism, mainly derived from patients with chronic kidney disease, indicate a potential inverse association between leptin and parathyroid hormone in some, but not all studies. This relationship may be affected by the diversity of morbidity among these patients.. Data from experimental studies suggest a different association between leptin and parathyroid hormone in primary and secondary hyperparathyroidism. Data from clinical studies are conflicting and potentially affected by confounders. More focused, well-designed studies are warranted to elucidate a potential association between leptin and parathyroid hormone, which may have specific clinical implications, i.e., targeting obesity and hyperleptinemia in patients with hyperparathyroidism.

Topics: Adipose Tissue, White; Animals; Anti-Obesity Agents; Chief Cells, Gastric; Hormone Replacement Therapy; Humans; Hyperparathyroidism, Primary; Hyperparathyroidism, Secondary; Insulin Resistance; Leptin; Models, Biological; Obesity; Parathyroid Glands; Parathyroid Hormone; Recombinant Proteins; Reproducibility of Results; Severity of Illness Index

Risks of chronic metabolic acidosis in patients with chronic kidney disease. Metabolic acidosis is associated with chronic renal failure (CRF). Often, maintenance dialysis therapies are not able to reverse this condition. The major systemic consequences of chronic metabolic acidosis are increased protein catabolism, decreased protein synthesis, and a negative protein balance that improves after bicarbonate supplementation. Metabolic acidosis also induces insulin resistance and a decrease in the elevated serum leptin levels associated with CRF. These three factors may promote protein catabolism in maintenance dialysis patients. Available data suggest that metabolic acidosis is both catabolic and anti-anabolic. Several clinical studies have shown that correction of metabolic acidosis in maintenance dialysis patients is associated with modest improvements in nutritional status. Preliminary evidence indicates that metabolic acidosis may play a role in beta2-microglobulin accumulation, as well as the hypertriglyceridemia seen in renal failure. Interventional studies for metabolic acidosis have yielded inconsistent results in CRF and maintenance hemodialysis patients. In chronic peritoneal dialysis patients, the mitigation of acidemia appears more consistently to improve nutritional status and reduce hospitalizations. Large-scale, prospective, randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in maintenance hemodialysis patients. To avoid adverse events, an aggressive management approach is necessary to correct metabolic acidosis. Clinicians should attempt to adhere to the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines for maintenance dialysis patients. The guidelines recommend maintenance of serum bicarbonate levels at 22 mEq/L or greater.

Topics: Acidosis; Amino Acids, Branched-Chain; Animals; Firefly Luciferin; Humans; Hydrocortisone; Hyperparathyroidism, Secondary; Insulin Resistance; Kidney Failure, Chronic; Leptin; Luciferases; Nutritional Status; Rats

 Disturbances in endothelial function, adipokines, and mineral metabolism due to secondary hyperparathyroidism (SHPT) shorten the lifespan in hemodialysis (HD) patients..  The aim of the study was to evaluate the effect of SHPT treatment with cinacalcet on selected adipokines and markers of endothelial injury in HD patients..  Soluble thrombomodulin (sTM), E-selectin, leptin, and adiponectin levels were measured in patients with SHPT at baseline and at 6 months of cinacalcet treatment..  A total of 18 patients completed the study. SHPT treatment with cinacalcet decreased calcium, phosphate, and intact parathormone (iPTH) levels; however, no significant changes in sTM, E-selectin, leptin, or adiponectin were observed. iPTH levels after treatment correlated with age (r = -0.51, P = 0.031), mean cinacalcet dose (r = 0.65, P = 0.004), as well as baseline calcium (r = 0.65 P = 0.003), iPTH (r = 0.59, P = 0.01), E-selectin (r = 0.56, P = 0.016), and leptin (r = -0.49, P = 0.039)..  Cinacalcet treatment does not affect the markers of endothelial function and selected adipokines. Effectiveness of treatment may be modulated by E-selectin and leptin.

Topics: Adipokines; Aged; Biomarkers; Calcimimetic Agents; Cinacalcet; E-Selectin; Endothelium, Vascular; Female; Humans; Hyperparathyroidism, Secondary; Leptin; Male; Middle Aged; Naphthalenes; Renal Dialysis; Treatment Outcome