Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder

Autor: Lakdasa Premawardhana, Mohamed Adlan, Suhani Bahl, Ravikumar Ravindran, Justyna Witczak
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Male
Hypercalcaemia
Ejection fraction
Ventricular hypertrophy
Focal segmental glomerulosclerosis
Endocrinology
Diabetes and Metabolism

Echocardiogram
Pamidronate
White
lcsh:Diseases of the endocrine glands. Clinical endocrinology
Gastroenterology
Ultrasound scan
Rhabdomyolysis
chemistry.chemical_compound
0302 clinical medicine
Furosemide
Testosterone
CD-45
FT4
Estimated glomerular filtration rate
Vitamin D
Myositis
Bisoprolol
Urea and electrolytes
biology
TSH
Calcimimetics
Acute kidney injury
Bisphosphonates
Hypervitaminosis
GH
Proteinuria
Nephrology
July
030220 oncology & carcinogenesis
Creatinine
Phosphate (serum)
Steroids
Cinacalcet
Renal biopsy
Calcium (serum)
PTH
MRI
Muscle biopsy
Adult
medicine.medical_specialty
Kidney stones
Prednisolone
Thyroxine (T4)
Histopathology
030209 endocrinology & metabolism
03 medical and health sciences
Internal medicine
Fluid repletion
Glomerulosclerosis
Internal Medicine
medicine
Vitamin A
Mycophenolate
Hypervitaminosis A
Creatine kinase
Bone
Glucocorticoids
Enlarged prostate
Aortic stenosis
lcsh:RC648-665
business.industry
Albumin
CD-3
Hyperparathyroidism (primary)
Tamulosin
medicine.disease
Unique/Unexpected Symptoms or Presentations of a Disease
United Kingdom
Oedema
Myocardial infarction
chemistry
25-hydroxyvitamin-D3
biology.protein
Lansoprazole
business
Constipation
Calcification
Zdroj: Endocrinology, Diabetes & Metabolism Case Reports
Endocrinology, Diabetes & Metabolism Case Reports, Vol 1, Iss 1, Pp 1-5 (2020)
ISSN: 2052-0573
Popis: 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.
Databáze: OpenAIRE