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Asymptomatic primary hyperparathyroidism
Author(s) -
Mitlak Bruce H.,
Daly Margaret,
Potts John T.,
Schoenfeld David,
Neer Robert M.
Publication year - 1991
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650061422
Subject(s) - osteopenia , medicine , asymptomatic , creatinine , urology , hyperparathyroidism , azotemia , primary hyperparathyroidism , renal function , parathyroid hormone , endocrinology , osteoporosis , bone mineral , calcium
Of 118 consecutive white patients referred for asymptomatic primary hyperparathyroidism, the diagnosis was clinically confirmed in 100, of whom 85 adults had a serum calcium less than 3.0 mM (12 mg/dl) and no skeletal, rheumatic, or significant neuropsychiatric symptoms, azotemia, or other significant illnesses. Among these 85, 68 had both asymptomatic and medically uncomplicated hyperparathyroidism, whereas 17 had historical, radiographic, or ultrasonic evidence of renal stone disease. The 20% with past or present renal calculi concentrated their urine significantly better than the 68 others ( p = 0.05), but these two groups were otherwise not distinguished by the tests we performed, so all 85 patients were analyzed together. Systolic and diastolic blood pressures were normal, but premature osteopenia and/or impaired renal function were present in 29–36% of the patients. Micrometer measurements of metacarpal radiographs and 125 I photon absorptiometry at the shaft of the radius revealed cortical osteopenia. Osteopenia was equally significant in the distal radius (cortical plus trabecular bone). These quantitative measurements were superior to routine bone radiography, and ROC analysis showed that 125 I absorptiometry at either site was superior ( p < 0.01) to metacarpal cortex measurements for detecting premature osteopenia, which was present in more than a third of these patients. Creatinine clearances (24 h) and maximum urine concentrating capacity (overnight dehydration plus the synthetic vasopressin analog DDAVP) were each significantly reduced, despite all patients' normal BUN and serum creatinine levels. Sequential performance of a 24 h creatinine clearance and a urine concentration test revealed abnormalities in the renal function of 27 of 74 patients (36%), with a specificity of 95% and a higher sensitivity than either test alone (27–29%). Testing the kidneys' ability to acidify the urine to pH 5.3 or less identified only 1 additional abnormal patient. Silent complications of primary hyperparathyroidism are thus common in “asymptomatic” patients with mild hypercalcemia. Their presence was only weakly correlated with urinary calcium excretion (measured on a low‐calcium diet) and serum alkaline phosphatase. From these data, it is not possible to predict whether these complications progress in the absence of treatment or diminish with successful treatment of the primary hyperparathyroidism.

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