scholarly journals Successfully Treating Hypercalcemia Secondary to Subcutaneous Fat Necrosis With Pamidronate: A Case Series

2021 ◽  
Vol 10 (1) ◽  
pp. 6-9
Author(s):  
Ryan J. Dyess ◽  
Prasanthi Pasala Gandham ◽  
Bradly J. Thrasher
Author(s):  
Alexander D Chesover ◽  
Jennifer Harrington ◽  
Farid H Mahmud

Abstract Background Subcutaneous fat necrosis (SCFN) can be complicated by severe hypercalcemia, which is frequently asymptomatic. Nephrocalcinosis is associated with hypercalcemia and, in other clinical settings, has been linked to furosemide and glucocorticoid use. First-line bisphosphonate therapy treating hypercalcemia in neonatal SCFN is not well described. Objectives To describe the biochemical changes and risk of nephrocalcinosis in infants with hypercalcemia, secondary to neonatal SCFN, treated with initial pamidronate. Methods A retrospective chart review of five infants treated with initial pamidronate and without furosemide or glucocorticoids. Data were collected on the following: timing of presentation, therapeutic response, and presence of nephrocalcinosis. Results Hypercalcemia resolved after 2.8±1.7 days; this is compared to 7.6±2.8 days from previously reported cases utilising alternative therapies (P=0.012). There were no episodes of rebound hypercalcemia or hypocalcemia. Nephrocalcinosis was present in four of five cases. When including published cases, age at diagnosis was associated with presenting serum calcium (P=0.003) and nephrocalcinosis was associated with higher serum calcium (P=0.014) and time from SCFN to hypercalcemia diagnosis (P=0.002). Conclusions This retrospective case series demonstrates that first-line pamidronate treatment was effective and safe in the resolution of hypercalcemia. Nephrocalcinosis was observed, despite the avoidance of furosemide and glucocorticoid therapy, and associated with greater disease severity and duration of hypercalcemia.


1982 ◽  
Vol 48 (03) ◽  
pp. 245-246 ◽  
Author(s):  
V Hofmann ◽  
P G Frick

SummaryA female patient is described who developed skin and subcutaneous fat necrosis on two occasions after intake of acenocoumarol.Several months later identical skin changes occurred during an episode of cholestasis associated with a prolongation of the prothrombin time to an extent comparable with therapeutic anticoagulation; intake of oral anticoagulants could be excluded.This association gives new insights in the pathogenetic mechanisms responsible for the so-called coumarin necrosis and indicates that it may be not due to drug toxicity or allergy.


2007 ◽  
Vol 24 (1) ◽  
pp. 93-93 ◽  
Author(s):  
LARISSA L. ZAULYANOV ◽  
SHARON E. JACOB ◽  
GEORGE W. ELGART ◽  
LAWRENCE SCHACHNER

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