Diagnosis and Treatment > Medication
Search for other papers by Ravikumar Ravindran in
Google Scholar
PubMed
Search for other papers by Justyna Witczak in
Google Scholar
PubMed
Search for other papers by Suhani Bahl in
Google Scholar
PubMed
Centre for Endocrine and Diabetes Sciences, University Hospital of Wales, Cardiff, UK
Search for other papers by Lakdasa D K E Premawardhana in
Google Scholar
PubMed
Search for other papers by Mohamed Adlan in
Google Scholar
PubMed
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.
Msc Metabolic Bone Diseases, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece
Search for other papers by Nikolaos Asonitis in
Google Scholar
PubMed
Msc Metabolic Bone Diseases, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece
Search for other papers by Eva Kassi in
Google Scholar
PubMed
Search for other papers by Michalis Kokkinos in
Google Scholar
PubMed
Search for other papers by Ilias Giovanopoulos in
Google Scholar
PubMed
Search for other papers by Foteini Petychaki in
Google Scholar
PubMed
Search for other papers by Helen Gogas in
Google Scholar
PubMed
Summary
Hypercalcemia of malignancy is the most common cause of hypercalcemia in hospitalized patients. It is associated with a poor prognosis, since it reflects an advanced cancer stage. Among all cancer in females, breast cancer is the most common malignancy, and it has the highest prevalence of hypercalcemia. Approximately 70% of patients with breast cancer have bone metastases and 10% of them will have hypercalcemia as a complication at some point in the disease. Herein, we report a 69-year-old female patient with metastatic breast cancer, who developed severe hypercalcemia in the course of her disease and was diagnosed with humoral hypercalcemia of malignancy (HHM). Intense hydration along with corticoisteroids and antiresorptive medication (calcitonin, bisphosphonates and denosumab) were administered to the patient. Despite the above treatment, serum calcium levels remain elevated and calcimimetic cinacalcet was added. Upon discontinuation of cinacalcet, calcium levels were raised and returned back to the normal levels following re-initiation of the calcimimetic. Her calcium level restored to normal, and she was discharged with the following medical treatment: denosumab monthly, and cinacalcet at a titrated dose of 90 mg per day. The patient is followed as an outpatient and 11 months later, her calcium level remained within the normal range.
Learning points:
-
Hypercalcemia of malignancy is the most common cause of hypercalcemia in hospitalized patients.
-
Breast cancer has the highest prevalence of hypercalcemia.
-
The cornerstone of therapy remains the intense hydration and intravenous bisphosphonates (preferably zoledronic acid).
-
In case of persistent hypercalcemia of malignancy, the administration of calcimimetic cinacalcet could be an additional effective therapeutic option.
