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Severe hypophosphatemia and decreased parathyroid hormone: case report A 76-year-old woman developed severe hypophosphatemia during treatment with alendronic-acid and decreased parathyroid hormone level during treatment with calcium-carbonate and colecalciferol for postmenopausal osteoporosis [not all routes and outcomes stated]. The woman presented with a CT scan demonstrating a non-traumatic vertebral compression fracture. Previously, she had been diagnosed with anaemia due to iron deficiency. For which she had received ferrous sulfate. She also had a history of hypertension, hypercholesterolemia, type 2 diabetes and ischaemic heart disease and her medications included amlodipine, enalapril, atorvastatin, metformin, vildagliptin and aspirin [acetylsalicylic acid]. Following investigation, she was diagnosed with postmenopausal osteoporosis without clinical symptoms on May 2018. On blood tests, normal phosphate and p-parathyroid hormone level were observed at that time. Subsequently, she started receiving oral alendronic-acid [Alendronate] 70mg once weekly, and calcium carbonate 800mg and colecalciferol 20µg daily along with magnesium hydroxide. Thereafter, she was found with good compliance with medications at a follow-up after 4 months. However, the blood test performed on September 2018 demonstrated severe hypophosphatemia, suppressed p-parathyroid hormone levels, and the pre-existing hypomagnesaemia. Therefore, she was hospitalised. At that time, her only problem was the pain in both feet. She did not have a prior history of diarrhoea, alcohol misuse or nutritional issues. Her vital parameters were normal, and an ECG and telemetry did not show any signs of arrhythmias. Severe hypophosphatemia was reconfirmed by a blood test. The decrease in p-parathyroid hormone levels was attributed to calcium carbonate and colecalciferol. Consequently, the woman’s alendronic-acid, calcium-carbonate and colecalciferol were discontinued. She was treated with phosphate replacement therapy, and phosphate levels and p-parathyroid hormone levels were restored within 3 days of hospitalisation. After that, she was discharged, and a slightly elevated phosphate level was noted on a short follow-up after discharge which normalised spontaneously. At a follow-up on January 2019, after 4 months of the episode of severe hypophosphatemia, the woman’s plasma phosphate levels and p-parathyroid hormone levels were normal. Hence, alendronic-acid, calcium-carbonate and colecalciferol were restarted. One month after, again she presented with unaffected severe hypophosphatemia and decreased parathyroid hormone and was hospitalised. At that time, she had pain and muscular weakness of left hip and leg as well as difficulty walking. Thereafter, her alendronic-acid, calcium-carbonate and colecalciferol were discontinued, and hypophosphatemia was managed with phosphate on the first day and followed by phosphate replacement therapy. As a result, her p-Phosphate was normalised within 2 days and was discharged after 10 days. Thereafter, her osteoporos