Evaluation and Management of Primary Hyperparathyroidism—Author’s Response1

We have reported that, in our practice, most patients with asymptomatic primary hyperparathyroidism who do not meet NIH Consensus Conference guidelines for surgery are followed with no specific intervention (1, 2). In the preceding letter, Dr. S.J. Rosenbloom disagrees with this approach, proposing instead that all patients with primary hyperparathyroidism undergo parathyroidectomy. Surgical cure, he argues, should be undertaken to protect affected patients from the increased cardiovascular morbidity and mortality associated with hypercalcemia. Dr. Rosenbloom raises an important issue in the clinical characterization of primary hyperparathyroidism. Calcium clearly plays a critical role in vascular and cardiac function (3). In addition, parathyroid hormone itself has important inotropic and chronotropic effects on cardiac tissue (4). However, while we agree that primary hyperparathyroidism has the potential to involve the cardiovascular system, there have been no systematic investigations of this possibility in patients with the mild disease we are seeing today. The studies cited by Dr. Rosenbloom describe patients with more severe or certainly more symptomatic primary hyperparathyroidism than we find in our population. The patients of Palmer et al. (5) presented with primary hyperparathyroidism from 1956 to 1979, many before the advent of the serum autoanalyzer, which allowed the diagnosis of asymptomatic disease. Although mortality increased in their population, it was unrelated to the preoperative levels of serum calcium. The cohort of Niederle et al. (6) was completely different from the patients we see in the United States today. Preoperatively, 85% of their patients (181/212) had symptoms of classical primary hyperparathyroidism, including nephrolithiasis, osteitis fibrosa cystica, and impaired renal function, while 11% were classified as having minimal symptoms. Only 4% of their patients were asymptomatic, as opposed to 80% of our cohort. The patients of Stefenelli et al. (7), who had an increased incidence of valvular and myocardial calcifications, had significantly higher serum calcium levels than we see (12 mg/dL vs. 10.7 mg/dL). Furthermore, parathyroid hormone levels were 10 times normal, alkaline phosphatase was twice normal, and 40% of patients had renal calcifications.