Calcium gluconate

Abstract

Myocardial and skeletal muscle calcification: case report A 24-year-old man developed myocardial and skeletal muscle calcification during treatment with calcium gluconate for hypocalcaemia. The man presented with severe epigastric pain and fever for two weeks. On admission, CT scan showed cervical, supraclavicular, axillary, paraaortic and inguinal lymphadenopathies, bilateral pleural effusion, ascites and hepatosplenomegaly. Soon after admission, he was started on haemodialysis and mechanical ventilation for anuria and dyspnoea. Additionally, he was started on methylprednisolone pulse therapy after excluding bacterial infections, followed by IV methylprednisolone as maintenance therapy. In spite of haemodialysis and ventilatory support, his vital signs not stable. Also, his plasma calcium level decreased, suggesting hypocalcaemia, on day 17 of admission. As the hypocalcemia was refractory to therapy, he was initiated on IV calcium gluconate [calcium gluconate hydrate; dosage not stated] for a total of 8 days. Afterwards, laboratory test showed low vitamin D and high intact parathyroid hormone levels, as seen in patients with chronic kidney disease. Finally, his plasma calcium levels were maintained within the normal range. A bone marrow biopsy demonstrated hypercellular marrow with an elevated number of megakaryocytes. Based on the results, he was diagnosed with TAFRO syndrome. He was started on biologic tocilizumab 8 mg/kg weekly treatment, along with tapering glucocorticoids on day 32. However, on day 76, he presented with syncope secondary to sick sinus syndrome. Myocardial and skeletal muscle calcification were noted on CT scans, on day 47 of admission. In the first few months, subsequent CT scans revealed progressive worsening of the degree of calcification. The calcification was attributed to calcium gluconate therapy. At this time, temporary pacing was not possible due to the risk of haemorrhage after persistently low platelet levels and coagulopathy. He repeatedly suffered from various infections including catheter related blood stream infection, pyothorax, intraabdominal abscess and infectious endocarditis. He also developed cardiac arrest. However, he was continued on tocilizumab, except when the infection was very severe. On day 173, he was started on romiplostim as his platelet count remained persistently low. The treatment soon resulted in recovery of platelet count to baseline. His urine volume also gradually began to increase, five months after the onset of anuria. Thereafter, calcification of the rectus abdominis muscle also gradually diminished, as observed by CT scans. But no remarkable changes were noted in that of the myocardium. Despite some life-threatening events during his prolonged admission, he was finally discharged from the hospital in an ambulatory condition, with residual calcific lesions on day 410 of admission. Sick sinus syndrome also resolved along with improvement in his general condition. Thus, permanent pacemaker implantation was not unnecessary. At the time of this report, he was receiving regular haemodialysis and tocilizumab therapy without evidence of recurrence for one year following discharge.