Vitamin D status in primary hyperparathyroidism in India

Clinical Endocrinology - Tập 43 Số 3 - Trang 351-358 - 1995
C V Harinarayan1,2, Neerja Gupta1, N Kochupillai1
1Department of Endocrinology and Metabolism, All India Institute of Medical Sciences (AIIMS), New Delhi 110 029, India
2Department of Endocrinology and Metabolism, Sri Venkateswara Institute of Medical Sciences, Tirupati-517 507, Andhra Pradesh, India

Tóm tắt

SummaryOBJECTIVES Primary hyperparathyroidism is a syndrome with variable clinical expression, presenting as asymptomatic hypercalcaemia in Western countries and with predominant bone disease in developing countries. Vitamin D deficiency has been implicated as the cause of bone disease. There is a paucity of information on the vitamin D (25‐OHD3) status of patients with primary hyperparathyroidism presenting with bone disease. The present study aims to evaluate the vitamin D status in patients with primary hyperparathyroidism and to correlate it with the bone disease.DESIGN Twenty consecutive patients with primary hyperparathyroidism admitted to the endocrinology and metabolism wards of the All India Institute of Medical Sciences were analysed to assess their clinical, radiological and biochemical features, as well as parathyroid hormone (mid‐molecular, PTH‐MM) and 25‐OHD3 levels.MEASUREMENTS PTH‐MM levels and 25‐OHD3 levels were measured using RIA kits.RESULTS Bone disease (osteitis fibrosa cystica) was the mode of presentation in 90%. Radiologically, sub‐periosteal resorption was present in 90% of the total group of patients, brown tumours in 60%, and pathological fractures in 40%. Renal stones and/or nephrocalcinosis was present in 50% of patients. Mean serum calcium, phosphate and alkaline phosphatase concentrations (mean of 3 days values) were 2.72 ± 0.24 mmol/l; 1.01 ± 0.28 mmol/l and 425 ± 249 IU/l respectively. The 24‐hour (mean of 3 days values) urine calcium and phosphate excretions were 8.0 ± 4.2 mmol and 19.0 ± 13mmol. Only 50% of the patients had hypercalcaemia (> 2.7 mmol/l). However, 90% of the whole group of patients had hypercalciurla. The mean serum creatinine concentration of patients with hypercalcaemia was 108 ± 38 μmol/l and of those with normocalcaemia 89 ± 33 pmol/l. The mean serum PTH‐MM was 438 ± 350 pmol/l (the detection limit for the kit was 34 pmol/l). Ultrasound examination detected adenomas in 72% of the cases and computerized tomography of the neck localized adenomas in 71 % of the cases. The median weight of the adenoma was 4.6 g (range 0.125–25 g). Two patients had coexistent hyperplasia of the other parathyroid glands and two had recurrent adenomas. 25‐OHD3 levels were assessed in all 20 patients under fasting conditions. The mean value of 25‐OHD3 observed (8.4 ± 51 μg/l) was comparable to the mean value measured in 14 healthy age and sex matched controls (83 ± 25 μg/l).CONCLUSION Patients with primary hyperparathyroidism in India presented with bone and renal diseases; half were normocalcaemic. All the patients had hypercalcuria despite the bone disease. The PTH‐MM levels were increased and 25‐OHD3 levels were low. The predominant bone disease is probably due to prolonged primary hyperparathyroidism coexisting with low calcium intake and/or 25‐OHD3 deficiency. The mean weight of the adenoma was higher than that reported for patients in the Western literature.

Từ khóa


Tài liệu tham khảo

Ahuja M.M.S., 1974, The Proceedings of the Fifth Asian and Oceania Congress of Endocrinology, 201

10.1001/jama.1934.02750160010003

Albright F., 1948, The Parathyroid Glands and Metabolic Bone Disease

Bilezikian J.P., 1991, Characterisation and evaluation of asumptomatic primary hyperparathyroidism, Journal of Bone and Mineral Research, 6

10.1016/S0140-6736(61)90632-8

10.7326/0003-4819-73-2-253

Friedman P.A., 1993, Vitamin D3 accelerates PTH‐dependent calcium transport in distal convuluted tubule cells, American Journal of Physiology, 265, F‐300

Girad R.M., 1982, Primary hyperparathyroidism in children, Canadian Journal of surgery, 25, 11

Gomori G., 1975, Calcium, Phosphorus and Phosphatases: Practical Clinical Biochemistry, 431

10.1001/jama.206.12.2729

Gupta M.M., 1990, Primary hyperparathyroidism, Journal of the Association of Physicians of India, 38, 154

10.1016/S0889-8529(18)30357-8

Heath H., 1991, Clinical spectrum of primary hyperparathyroidism: evolution with change in medical practice and technology, Journal of Bone and Mineral Research, 6

10.1056/NEJM198001243020402

Hellstrom J., 1992, Primary hyperparathyroidism and structural findings in 131 cases, Acta Chirurgica Scandinavica, 294, 1

Hodkins A., 1963, Biochemical aspects of primary hyperparathyroidism: An analysis of 50 cases, Clinical Science, 251, 231

10.1056/NEJM198510313131805

Kapur M.M., 1985, Clinical and biochemical features of primary hyperparathyroidism, Indian Journal of Medical Research, 81, 607

10.1001/archinte.141.13.1761

10.1210/jcem-26-3-309

Lumb G.A., 1974, Parathyroid function in human vitamin D deficiency and in primary hyperparathyroidism, Journal of the American Medical Association, 56, 833, 10.1016/0002-9343(74)90812-2

10.1007/978-1-4613-2970-1

10.1136/pgmj.35.404.330

10.1016/S0140-6736(80)91783-3

10.1016/S0140-6736(60)90836-9

Norris E.H., 1947, The parathyroid adenoma ‐ a study of 322 cases, Surgical Gynaecology and Obstetrics, 84, 1

10.1016/S0022-3468(86)80505-X

Rasbach A.D., 1984, Solitary parathyroid microadenomas, Surgery, 96, 1092

Silverberg S.J., 1989, Skeletal disease in primary hyperparathyroidism, Journal of Bone and Mineral Research, 4, 282, 10.1002/jbmr.5650040302

10.1016/0002-9343(90)90346-F

Shrikande S.S., 1980, Parathyroid tumours: a study of 10 cases, Indian Journal of Cancer, 17, 164

10.1111/j.1440-1673.1973.tb01435.x

10.1097/00000658-197801000-00012

10.1016/0002-9343(69)90222-8

Wilkinson R.H., 1975, Calcium, Phosphorus and Phosphatases: Practical Clinical Biochemistry, 431