Background The aim of this study was to investigate the familiality and clustering of type 2 diabetes (T2DM) and metabolic syndrome (MES) predominantly in families with young-onset diabetes from the Hong Kong Family Diabetes Study.

SummaryWe report a patient with a biochemically and radiologically confirmed parathyroid adenoma, which underwent spontaneous resolution by necrosis. The patient was followed-up over the subsequent two years during which time the tumour and hypercalcaemia recurred. Sequential radiological and biochemical changes at the time of diagnosis, spontaneous necrosis and recurrence are documented fully. Keywords: hyperparathyroidism; hypocalcaemia; apoplexy Primary hyperparathyroidism is one of the commonest endocrine disorders. However, spontaneous resolution by necrosis of a parathyroid adenoma is rare. Although there have been approximately 10 reported cases since the condition was first described in 1946, 1 in most cases the infarcted gland was removed soon after diagnosis. Therefore, the natural history, biochemical and hormonal changes following spontaneous infarction are not well known. We report a patient who had spontaneous infarction of her parathyroid adenoma, while awaiting surgery, with detailed documentation of the above-mentioned features. Case reportA 78-year-old woman was referred to our clinic for further management of Type 2 diabetes. She gave a history of renal stone, with right nephrectomy, 8 years before. She was put on oral hypoglycaemic therapy. She was found incidentally to have hypercalcaemia with a calcium concentration of 3.43 mmol/l (normal range 2.20-2.62 mmol/l) together with a reduced phosphate concentration of 0.55 mmol/l (0.82-1.40 mmol/l). Alkaline phosphatase was normal at 85 IU/l (45-145 IU/l). There was renal impairment with a plasma creatinine concentration of 160 µmol/l (44-107 µmol/l), but she had stable glycaemic control as indicated by a HbA 1c concentration of 7.4%. Physical examination revealed mild peripheral neuropathy and the nephrectomy scar, but no obvious neck mass. Further investigations confirmed primary hyperparathyroidism. Her parathyroid hormone (PTH) was 44 pmol/l (1.16-5.67 pmol/l, intact PTH assay; coefficient of variation 7%) with concomitant plasma calcium of 3.40 mmol/l and ionized calcium of 1.61 mmol/l (1.13-1.32 mmol/l).Ultrasound of the abdomen confirmed the previous right nephrectomy but showed no other abnormality. Her hypercalcaemia improved to approximately 2.8 mmol/l with adequate hydration, a low calcium diet and oral phosphate solution. She was referred for parathyroidectomy and was on the waiting list for surgery. During subsequent follow-up, her alkaline phosphatase gradually increased to 1465 IU/l, indicating development of parathyroid bone disease. Her glycaemic control was stable on oral hypoglycaemic therapy and there was no further deterioration of diabetic complications.She was put on the waiting list for surgery, which was very long in our hospital. Two years later, she underwent pre-operative imaging to localise the parathyroid adenoma. Computed tomography (CT) showed a 2.5 × 1.5 cm welldefined parathyroid adenoma posterior to the upper pole of the left lobe of the thyroid. The adenoma was of homogenous soft tissue attenuation and revea...

neck ultrasound showed a large parathyroid tumour beside the right lower lobe of the thyroid measuring 2·3 ern in diameter. Bone mineral density (BMD) was measured using a Hologic QDR 2000 Dual Energy X-ray Densitometer (Hologic, Waltham, MA, USA). Bone mineral density (BMD) of the whole body, lumbar spine and hip was 0-492, 0·562 and 0·108 g/cm 2 , respectively. Total T-score of the hip was -7,42. Bone biopsy of the posterior superior iliac crest showed mixed hyperparathyroidism and osteomalacia. There was evidence of active bone resorption with trabeculae showing a focal irregular scalloped appearance, abutted by osteoclasts and vascular fibroblastic tissue. There was prominent paratrabecular fibroblastic proliferation in the marrow with many dilated vessels. In other areas, the osteoid was thickened and the mineralization front could not be seen Additional key phrases: hypercalcaemia; 25-hydroxyvitamin D; alkaline phosphatase ultrasound-guided ethanol injection; remineralization CASE HISTORYA 66-year-old Chinese man was referred for investigation of weakness. He complained of weakness and wasting of the thighs for 4 years and low back pain for 2 years. He was homebound for 2 years and had very little exposure to sunlight. Home helpers brought him three meals a day. He also complained of polydipsia, polyuria and constipation at times. In the past, he had been an intravenous drug addict but had discontinued the habit 2 years earlier. He also smoked and suffered from chronic obstructive airways disease.The patient weighed 31·8 kg and he was 144 ern tall. He had a kyphoscoliosis and pseudoclubbing of the fingers. The gluteal and quadriceps muscles were weak and wasted. Reflexes and sensation were normal. He had poor chest expansion. The peak expiratory flow rate was 140 L/min. His blood pressure was 150/ 90 mmHg.Investigations indicated evidence of severe hyperparathyroidism and increased bone turnover as shown in Table 1. Serum total 25 hydroxyvitamin D (250HD) was within the reference range. There was no aminoaciduria or glycosuria. The patient's urea was 12·6 mmol/L on admission and became normalized (8 mmol/L) upon rehydration.His skull X-ray (Fig. la) showed a pepper-pot appearance and the hand X-rays revealed distal resorption of terminal phalanges consistent with hyperparathyroidism. A looser's zone was identified over the left ulnar bone. There was generalized osteopenia and bone softening of the pelvis. Both femurs were fractured and the inferior pubic rami were widened. The chest Xray showed fracture of the right clavicle in addition to multiple bullae in the upper zones. A