Hypercalcemia in sarcoidosis all are true except?
Parathormone level is increased
PTHrP level is increased
Calcitriol level is increased
Oral steroids are useful
Ans. is 'a' i.e., Parathormone level is increased Calcium metabolism in sarcoidosis* Extrarenal synthesis ofcalcitriol is central to the pathogenesis of abnormal calcium metabolism in sarcoidosis.* Sarcoidosis causes an increase in 1, 25-dihydroxy vitamin D, the active metabolite of vitamin D, which is usually hydroxylated within the kidney, but in sarcoidosis patients hydroxylation of vitamin D can occur outside the kidneys, mainly inside the immune cells found in the granulomas and produces 1 alpha, 25(OH)2D3, which is the main cause for hypercalcemia in sarcoidosis.* Gamma-interferon produced by activated lymphocytes and macrophages, also plays a major role in the synthesis of 1 alpha, 25(OH)2D3.* Above 1-ahydroxylation is controlled by PTH and calcitriol. PTH is stimulated by circulating vitamin D metabolites and low levels of ionized calcium to form a bioregulatory loop 8c PTH release is inhibited by hypercalcaemia and high levels ofcalcitriol, which explains why the PTH level is suppressed in sarcoidosis.* PTHrP has similar properties to PTH, stimulating 1 -a hydroxylation of 25(OH)2D3 and affecting bone turnover but unlike PTH, PTHrP gene expression is not regulated by calcium and vitamin D metabolites, but rather by TNFa and IL-6, two cytokines that are up-regulated in sarcoidosis. They are produced by macrophages and have autocrine actions, up-regulating PTHrP expression and therefore increasing calcitriol synthesis* To date corticosteroids have been the first-line therapy in hypercalcaemic sarcoidosis because of their effectiveness in rapidly restoring normocalcaemia and the lack of a recognized alternative therapy.* It is generally accepted that a corrected serum calcium concentration of >3.0 mmol/1 or evidence of renal complications in the presence of a lesser degree of hypercalcaemia is an indication for therapy.
Endocrine