Bone scintigraphy of severe hypercalcemia following simvastatin induced rhabdomyolysis

Mirza, Zubair B; Hu, Sophia; Amorosa, Louis F.

doi:10.11138/ccmbm/2016.13.3.257

Cited by 6 publications

(3 citation statements)

References 14 publications

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“…The prevalence of hypercalcaemia in rhabdomyolysis is quoted to be between 9.2 and 34% ( 6 , 7 , 8 ). The variable prevalence is probably related to incomplete identification of these subjects due to the late occurrence of hypercalcaemia (often in the polyuric or recovery phase of AKI) and its mild, often asymptomatic nature.…”

Section: Discussionmentioning

confidence: 99%

Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder

Ravindran

Witczak

Bahl

et al. 2020

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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Summary A 53-year-old man who used growth hormone (GH), anabolic steroids and testosterone (T) for over 20 years presented with severe constipation and hypercalcaemia. He had benign prostatic hyperplasia and renal stones but no significant family history. Investigations showed – (1) corrected calcium (reference range) 3.66 mmol/L (2.2–2.6), phosphate 1.39 mmol/L (0.80–1.50), and PTH 2 pmol/L (1.6–7.2); (2) urea 21.9 mmol/L (2.5–7.8), creatinine 319 mmol/L (58–110), eGFR 18 mL/min (>90), and urine analysis (protein 4+, glucose 4+, red cells 2+); (3) creatine kinase 7952 U/L (40–320), positive anti Jo-1, and Ro-52 antibodies; (4) vitamin D 46 nmol/L (30–50), vitamin D3 29 pmol/L (55–139), vitamin A 4.65 mmol/L (1.10–2.60), and normal protein electrophoresis; (5) normal CT thorax, abdomen and pelvis and MRI of muscles showed ‘inflammation’, myositis and calcification; (6) biopsy of thigh muscles showed active myositis, chronic myopathic changes and mineral deposition and of the kidneys showed positive CD3 and CD45, focal segmental glomerulosclerosis and hypercalcaemic tubular changes; and (7) echocardiography showed left ventricular hypertrophy (likely medications and myositis contributing), aortic stenosis and an ejection fraction of 44%, and MRI confirmed these with possible right coronary artery disease. Hypercalcaemia was possibly multifactorial – (1) calcium release following myositis, rhabdomyolysis and acute kidney injury; (2) possible primary hyperparathyroidism (a low but detectable PTH); and (3) hypervitaminosis A. He was hydrated and given pamidronate, mycophenolate and prednisolone. Following initial biochemical and clinical improvement, he had multiple subsequent admissions for hypercalcaemia and renal deterioration. He continued taking GH and T despite counselling but died suddenly of a myocardial infarction. Learning points: The differential diagnosis of hypercalcaemia is sometimes a challenge. Diagnosis may require multidisciplinary expertise and multiple and invasive investigations. There may be several disparate causes for hypercalcaemia, although one usually predominates. Maintaining ‘body image’ even with the use of harmful drugs may be an overpowering emotion despite counselling about their dangers.

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Section: Discussionmentioning

confidence: 99%

Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder

Ravindran

Witczak

Bahl

et al. 2020

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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“…Disturbance in calcium homeostasis has been observed previously in cases of rhabdomyolysis-induced acute renal failure. 4 Initial hypocalcaemia may be observed predominantly due to sequestration of calcium associated with marked hyperphosphatemia on the destroyed muscle cell. Subsequent hypercalcaemia may be severe, as in this case, as this calcium is released back into the circulation possibly exacerbated by an initial temporary rise in PTH levels responding to the initial hypocalcaemia.…”

Section: Discussionmentioning

confidence: 99%

Rhabdomyolysis and severe biphasic disturbance of calcium homeostasis secondary to COVID-19 infection

Thomas

Gökmen

et al. 2021

BMJ Case Rep

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We report a case of severe hypercalcaemia secondary to rhabdomyolysis in a woman with COVID-19 (SARS CoV-2) infection. The patient presented with myalgia and anuria with an acute kidney injury requiring haemodialysis. Creatine kinase peaked at 760 000 IU/L. A biphasic calcaemic response was observed with initial severe hypocalcaemia followed by severe, symptomatic hypercalcaemia, persistent despite haemodialysis. Control of the calcium levels was achieved by continuous haemofiltration.

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“…Further putative therapeutic effects include decrease of hippocampal amyloid-beta abundance in Alzheimer’s disease [16], anticoagulation [10], inhibition of inflammatory disease, such as asthma [1, 17-19], protection against contrast-induced nephropathy [20], protection of cardiac allografts against ischemia/reperfusion injury [21], as well as counteraction of osteoporosis and support of bone fracture healing [22, 23]. Side effects of simvastatin include rhabdomyolysis [6, 8, 24-29] and thrombocytopenia [30]. …”

Section: Introductionmentioning

confidence: 99%

Simvastatin, a Novel Stimulator of Eryptosis, the Suicidal Erythrocyte Death

Bhuyan

Nüßle

Cao

et al. 2017

Cell Physiol Biochem

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Background/Aims: The 3-hydroxy-3-methyl-glutaryl-Coenzyme A (HMG-CoA) reductase inhibitor simvastatin has been shown to trigger apoptosis of several cell types. The substance has thus been proposed as an additional treatment of malignancy. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal erythrocyte death. Hallmarks of eryptosis include cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the extracellular face of the erythrocyte cell membrane. Signaling contributing to stimulation of eryptosis include increase of cytosolic Ca²⁺ activity ([Ca²⁺]_i), induction of oxidative stress, increase of ceramide abundance, and activation of SB203580-sensitive p38 kinase. The present study explored, whether simvastatin induces eryptosis and aimed to shed light on cellular mechanisms involved. Methods: Flow cytometry was employed to quantify phosphatidylserine exposure at the cell surface from annexin-V-binding, cell volume from forward scatter, [Ca²⁺]_i from Fluo3-fluorescence, reactive oxygen species (ROS) abundance from DCFDA dependent fluorescence, and ceramide abundance utilizing specific antibodies. Hemolysis was estimated from hemoglobin concentration in the supernatant. Results: A 48 h exposure of human erythrocytes to simvastatin (1 µg/ml) significantly decreased the forward scatter, significantly augmented the percentage of annexin-V-binding cells, significantly increased Fluo3-fluorescence, and significantly enhanced DCFDA fluorescence. Simvastatin tended to increase ceramide abundance, an effect, however, escaping statistical significance. The effect of simvastatin on annexin-V-binding was significantly blunted by removal of extracellular Ca²⁺ and by addition of SB203580 (2 µM). Conclusions: Simvastatin stimulates eryptosis, an effect at least in part due to Ca²⁺ entry, oxidative stress, and p38 kinase.

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Bone scintigraphy of severe hypercalcemia following simvastatin induced rhabdomyolysis

Cited by 6 publications

References 14 publications

Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder

Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder

Rhabdomyolysis and severe biphasic disturbance of calcium homeostasis secondary to COVID-19 infection

Simvastatin, a Novel Stimulator of Eryptosis, the Suicidal Erythrocyte Death

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