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Q1 What is the differential diagnosis based on the history and the MRI giant cell tumour, brown tumour, chondrosarcoma, secondaries in the bone
The differential diagnosis is giant cell tumour and brown tumour. A lytic lesion in a young woman with an associated pathological fracture and soft tissue mass raises several possibilitiesfor example, giant cell tumour, eosinophilic granuloma, brown tumour, or a primary bone tumour. Brown tumours are focal bone lesions caused by an increased osteoclastic activity and fibroblastic proliferation within primary hyperparathyroidism PHP or more rarely secondary hyperparathyroidism. They are named after their typical brown haemorrhagic stroma with, also typical, giant cell formations. A brown tumour should always be ruled out in such a clinical situation by serum calcium concentration and parathyroid hormone assay. A preoperative biopsy is mandatory for the other lesions. A finding of giant cells on histopathology does not exclude a brown tumour. A giant cell tumour is characterised by the presence of multinucleated giant cells. Although the tumour is regarded as benign and has an indolent course, up to 50 of cases may recur locally. Typical giant cell tumours are radiologically easily distinguished from other bone tumours. Giant cell tumours are lytic, subarticular, eccentric, and often lack a sclerotic rim.
Q2 What other relevant blood investigations should be ordered in such patients calcium, parathyroid hormone, alkaline phosphatase, acid phosphatase
Other relevant blood investigations are calcium and parathyroid hormone. The final histopathology report raised the suspicion of hyperparathyroidism. On testing the patients blood, the corrected calcium concentration was 32.5 mmoll, with an increased concentration of parathyroid hormone of 314 mgml. Ultrasonography of the neck revealed a parathyroid adenoma in the vicinity of the inferior pole of the right thyroid. The adenoma was successfully excised. In any such lytic lesion of the bone, the possibility of brown tumour should always be kept and blood calciumparathyroid hormone assay should be mandatory to prevent surgical misadventure.
In women of childbearing age the estimated incidence of PHP is eight per 100000 population per year.1 Usually, pregnant women with PHP are asymptomatic or have minor complaints such as early fatigability, constipation, thirst, or depression.2 These are common complaints that are usually attributed to pregnancy by patients. It is mandatory to correct PHP before childbirth to prevent postpartum hypercalcaemic crisis in the mother and hypocalcaemic crisis in the fetus. The hypercalcaemia can manifest itself in symptoms such as hyperemesis, pathological fractures, renal stones, pancreatitis, abortion, or fetal death.3 A hypercalcaemic crisis in the immediate postpartum period may be dangerous as the maternal efflux of calcium to the fetus is suddenly stopped. A neonate born to such a mother is at risk of tetany and convulsions within 514days of the birth because of transient hypocalcaemia. Though PTH and calcitonin do not cross the placental barrier,3 calcium is actively transported across the placenta with the help of fetal 1,25dihydroxycholecalciferol.3 Maternal PHP results in high concentrations of serum calcium that acts to suppress the fetuss PTH concentration. If this is not corrected beforehand, at birth the neonate is suddenly deprived of calcium and this is compounded by an inability to mobilise calcium from bone because of the high concentrations of calcitonin. This will result in acute neonatal hypocalcaemia causing tetany and convulsions by 2weeks of age but can be delayed if the infant is breast fed.4 All neonates with tetany or seizures in first few weeks of life should have their mothers serum calcium concentrations checked to exclude PHP.5 Oral or parenteral calcium and magnesium are usually required for a short period only and it resolves within three to five months.