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Barry M Wall - One of the best experts on this subject based on the ideXlab platform.
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reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism
The American Journal of the Medical Sciences, 2007Co-Authors: Asif S Kazmi, Barry M WallAbstract:A 71-year-old man presented with acute pulmonary edema related to new onset of severe left ventricular dysfunction (ejection fraction, 30%). His symptoms did not improve with emergency therapy with diuretics and dobutamine. He was noted to be severely hypocalcemic (5.5 mg/dL) and subsequently showed dramatic improvement in symptoms and ejection fraction (58%) with correction of hypocalcemia with intravenous calcium and calcitriol replacement. Hypocalcemia was related to surgically induced hypoparathyroidism. The patient had been instructed to decrease calcium supplements and to discontinue calcitriol 3 months previously due to hypercalcemia. Additional factors that may have contributed to hypocalcemia included vitamin D deficiency, alendronate therapy for osteoporosis, and chronic kidney disease. We concluded that the patient's congestive heart failure was precipitated by severe hypocalcemia and resolved with correction of hypocalcemia. Hypocalcemia is a rare cause of reversible congestive heart failure that should be in the differential diagnosis in any patient presenting with heart failure and not responding to traditional therapy.
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reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism
The American Journal of the Medical Sciences, 2007Co-Authors: Asif S Kazmi, Barry M WallAbstract:A 71-year-old man presented with acute pulmonary edema related to new onset of severe left ventricular dysfunction (ejection fraction, 30%). His symp- toms did not improve with emergency therapy with diuret- ics and dobutamine. He was noted to be severely hypocal- cemic (5.5 mg/dL) and subsequently showed dramatic improvement in symptoms and ejection fraction (58%) with correction of hypocalcemia with intravenous calcium and calcitriol replacement. Hypocalcemia was related to surgically induced hypoparathyroidism. The patient had been instructed to decrease calcium supplements and to discontinue calcitriol 3 months previously due to hyper- calcemia. Additional factors that may have contributed to hypocalcemia included vitamin D deficiency, alendronate therapy for osteoporosis, and chronic kidney disease. We concluded that the patient's congestive heart failure was precipitated by severe hypocalcemia and resolved with correction of hypocalcemia. Hypocalcemia is a rare cause of reversible congestive heart failure that should be in the differential diagnosis in any patient presenting with heart failure and not responding to traditional therapy. KEY IN- DEXING TERMS: Congestive heart failure; Hypocalcemia; Hypoparathyroidism. (Am J Med Sci 2007;333(4):226- 229.)
Xi Liuderyke - One of the best experts on this subject based on the ideXlab platform.
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hypocalcemia in trauma patients receiving massive transfusion
Journal of Surgical Research, 2016Co-Authors: Amanda Giancarelli, Kara L Birrer, Rodrigo F Alban, Brandon Hobbs, Xi LiuderykeAbstract:Abstract Background Massive transfusion protocol (MTP) is increasingly used in civilian trauma resuscitation. Calcium is vital for coagulation, but hypocalcemia commonly occurs during massive transfusion due to citrate and serum calcium chelation. This study was conducted to determine the incidence of hypocalcemia and severe hypocalcemia in trauma patients who receive massive transfusion and to compare characteristics of patients with severe versus nonsevere hypocalcemia. Materials and methods This was a retrospective study of trauma patients who received massive transfusion between January 2009 and November 2013. The primary outcome was the incidence of hypocalcemia (ionized calcium [iCa] Results There were 156 patients included; 152 (97%) experienced hypocalcemia, and 111 (71%) had severe hypocalcemia. Patients were stratified into iCa ≥ 0.90 (n = 45) and iCa 1.12. Conclusions Hypocalcemia is common during MTP, and vigilant monitoring is warranted. Research is needed to effectively manage hypocalcemia during massive transfusion.
G. Tsvetov - One of the best experts on this subject based on the ideXlab platform.
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denosumab induced hypocalcemia in patients with osteoporosis can you know who will get low
Osteoporosis International, 2020Co-Authors: G. Tsvetov, O. Amitai, T. Shochat, I. Shimon, A. Akirov, Talia DikercohenAbstract:Hypocalcemia was reported at low rates (0.05–1.7%) in denosumab-treated postmenopausal women with osteoporosis. This real-life study shows a 7.4% rate of denosumab-induced hypocalcemia in community-dwelling osteoporotic men and women. Pretreatment serum calcium and creatinine levels are major predictors for this complication. Serum-calcium monitoring may help to identify and prevent severe hypocalcemia. RCTs have reported a 0.05–1.7% rate of hypocalcemia in denosumab-treated postmenopausal women with osteoporosis, but long-term real-life data are lacking. We assessed the rate of hypocalcemia in osteoporotic community-dwelling patients treated with denosumab. A retrospective analysis was conducted based on medical records (2010–2018) from a large HMO. An albumin-adjusted serum calcium concentration lower than 8.5 mg/dL was defined as hypocalcemia. We included 2005 patients (93% women, mean age 76 ± 9 years). Hypocalcemia developed during treatment in 149 patients (7.4%; 1% less than 8 mg/dL): in 66 after 0.5–1 years; 48 after 1–2 years; 35 after > 2 years. On comparison of the hypocalcemic and normocalcemic patients, the strongest predictors of hypocalcemia were pretreatment levels of albumin-adjusted serum calcium (9.1 ± 0.4 vs. 9.4 ± 0.5 mg/dL, respectively; p < 0.05) and creatinine (0.9 ± 0.5 vs. 0.8 ± 0.3 mg/dL, respectively; p < 0.05). The hypocalcemia rate increased in parallel to a decrease in eGFR (p = 0.032 for the difference between eGFR ranges). Baseline calcium level ≤ 9.31 mg/dL predicted hypocalcemia with a sensitivity of 77% and specificity of 56%. A model of (− 2)*calcium + creatinine predicted hypocalcemia (3.7% when lower and 17.1% when higher than − 17.4). Gender, age, 25-hydroxyvitamin-D, parathyroid hormone, alkaline phosphatase, and whether denosumab was given as first or advanced line of osteoporotic therapy had no predictive value. Real-life rates of denosumab-induced hypocalcemia are higher than previously reported. Hypocalcemia might develop after each dose of denosumab in ongoing treatment. Adequate calcium and vitamin D supplementation are needed. Serum calcium monitoring is advised in high-risk patients for early detection of severe hypocalcemia.
Talia Dikercohen - One of the best experts on this subject based on the ideXlab platform.
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denosumab induced hypocalcemia in patients with osteoporosis can you know who will get low
Osteoporosis International, 2020Co-Authors: G. Tsvetov, O. Amitai, T. Shochat, I. Shimon, A. Akirov, Talia DikercohenAbstract:Hypocalcemia was reported at low rates (0.05–1.7%) in denosumab-treated postmenopausal women with osteoporosis. This real-life study shows a 7.4% rate of denosumab-induced hypocalcemia in community-dwelling osteoporotic men and women. Pretreatment serum calcium and creatinine levels are major predictors for this complication. Serum-calcium monitoring may help to identify and prevent severe hypocalcemia. RCTs have reported a 0.05–1.7% rate of hypocalcemia in denosumab-treated postmenopausal women with osteoporosis, but long-term real-life data are lacking. We assessed the rate of hypocalcemia in osteoporotic community-dwelling patients treated with denosumab. A retrospective analysis was conducted based on medical records (2010–2018) from a large HMO. An albumin-adjusted serum calcium concentration lower than 8.5 mg/dL was defined as hypocalcemia. We included 2005 patients (93% women, mean age 76 ± 9 years). Hypocalcemia developed during treatment in 149 patients (7.4%; 1% less than 8 mg/dL): in 66 after 0.5–1 years; 48 after 1–2 years; 35 after > 2 years. On comparison of the hypocalcemic and normocalcemic patients, the strongest predictors of hypocalcemia were pretreatment levels of albumin-adjusted serum calcium (9.1 ± 0.4 vs. 9.4 ± 0.5 mg/dL, respectively; p < 0.05) and creatinine (0.9 ± 0.5 vs. 0.8 ± 0.3 mg/dL, respectively; p < 0.05). The hypocalcemia rate increased in parallel to a decrease in eGFR (p = 0.032 for the difference between eGFR ranges). Baseline calcium level ≤ 9.31 mg/dL predicted hypocalcemia with a sensitivity of 77% and specificity of 56%. A model of (− 2)*calcium + creatinine predicted hypocalcemia (3.7% when lower and 17.1% when higher than − 17.4). Gender, age, 25-hydroxyvitamin-D, parathyroid hormone, alkaline phosphatase, and whether denosumab was given as first or advanced line of osteoporotic therapy had no predictive value. Real-life rates of denosumab-induced hypocalcemia are higher than previously reported. Hypocalcemia might develop after each dose of denosumab in ongoing treatment. Adequate calcium and vitamin D supplementation are needed. Serum calcium monitoring is advised in high-risk patients for early detection of severe hypocalcemia.
Rajesh V Thakker - One of the best experts on this subject based on the ideXlab platform.
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diseases associated with the extracellular calcium sensing receptor
Cell Calcium, 2004Co-Authors: Rajesh V ThakkerAbstract:The human calcium-sensing receptor (CaSR) is a 1078 amino acid cell surface protein, which is predominantly expressed in the parathyroids and kidney, and is a member of the family of G protein-coupled receptors. The CaSR allows regulation of parathyroid hormone (PTH) secretion and renal tubular calcium reabsorption in response to alterations in extracellular calcium concentrations. The human CaSR gene is located on chromosome 3q21.1 and loss-of-function CaSR mutations have been reported in the hypercalcaemic disorders of familial benign (hypocalciuric) hypercalcaemia (FHH, FBH or FBHH) and neonatal severe primary hyperparathyroidism (NSHPT). However, some individuals with loss-of-function CaSR mutations remain normocalcaemic. In addition, there is genetic heterogeneity amongst the forms of FHH. Thus, the majority of FHH patients have loss-of-function CaSR mutations, and this is referred to as FHH type 1. However, in one family, the causative gene for FHH is located on 19p13, referred to as FHH type 2, and in another family it is located on 19q13, referred to as FHH type 3. Gain-of-function CaSR mutations have been shown to result in autosomal dominant Hypocalcaemia with hypercalciuria (ADHH) and Bartter's syndrome type V. CaSR auto-antibodies have been found in FHH patients who did not have loss-of-function CaSR mutations, and in patients with an acquired form (i.e. autoimmune) of hypoparathyroidism. Thus, abnormalities of the CaSR are associated with three hypercalcaemic and three hypocalcaemic disorders.