Metabolie Complications of Primary Hyperparathyroidism

Gerhard Prager, MD ■ Claudette Abela, MD ■ Bruno Niederle, MD

In 1925, the Viennese surgeon Felix Mandl removed for the first time a parathyroid tumor in a patient with symptomatic primary hyperparathyroidism (PHPT).1 The patient was confined to bed and suffered from classic renal and osseous symptoms: recurrent renal calculi, osteitis cystica fibrosa, disabling bone pain, and fatigue. Postoperatively, the patient improved dramatically but unfortunately died 10 years later from the consequences of progressive renal disease.1,2 Since then there has been a dramatic improvement in the outcome of patients with PHPT after parathyroidectomy.3 Careful analysis of patients with PHPT reveals that postoperative metabolic complications occur in patients with a long history of PHPT.3,4 For example, the death rate related directly or indirectly to PHPT ranges from 1% to 12%. Death in patients with PHPT is mainly caused by cardiovascular disease (<68%5) and acute or chronic renal failure (<8%3).

Over the last 50 years, the clinical picture of PHPT has changed from a "rare" illness characterized by bone disease and renal calculi to a "common" disease characterized by more subtle or no clinical manifestations.6 Articles from Scandinavia and North America7,8 have documented an increasing number of patients with PHPT who are diagnosed because hypercalcemia is detected on undirected routine serum calcium determinations and the diagnosis confirmed by parathyroid immunoassays.4,9"11 PHPT is a relatively common, worldwide disorder with a reported incidence ranging from 0.1% in Central Europe,10 Australia,12 and South Africa13 to as high as 0.52% in Sweden.4,7,9 Heath14 in England reported that among his patients with PHPT, fewer than 10% have renal calculi and fewer than 10% have bone disease, whereas more than 80% have either vague ill health or are asymptomatic.

PHPT patients may be classified as symptomatic, minimally symptomatic, or asymptomatic. Symptomatic patients have renal, skeletal, or gastrointestinal disease or a combination. Osseous disease is defined as osteitis fibrosa, subperiosteal resorption, pathologic bone fractures, and acro-osteolysis. Minimally symptomatic patients have bone pain, diffuse osteopenia, or hypertension and the so-called hypercalcemia syndrome, which includes depression, lethargy, apathy, weakness, loss of memory, confusion, insomnia, headaches, and myopathy with muscular weakness as well as other general manifestations like polyuria and polydypsia, weight loss, vomiting, nausea, or epigastric discomfort without any apparent organic origin.3 Asymptomatic patients have neither symptoms nor signs attributable to PHPT (Table 42-1).

In this chapter, we describe metabolic manifestations and complications other than the typical well-known, classic manifestations in both treated and untreated patients with PHPT that are described elsewhere in this textbook.

Several metabolic complications are not usually attributed to PHPT. Patients with PHPT, for example, may have impaired glucose tolerance and diabetes mellitus.15,16 Both hyperuricemia5,17 and hyperlipidemia18 may be increased in patients with PHPT. These conditions may have an adverse effect on hypertension and concomitant cardiovascular disease, and these conditions may contribute to the increased morbidity and mortality in patients with PHPT, even after successful parathyroidectomy.11,19,20

The severity of the metabolic manifestations that occur in patients with PHPT cannot be predicted by the presence or absence of symptoms. Age, serum calcium level, and renal function are similar in patients with or without symptoms,21"23 although asymptomatic patients appear to have slightly lower serum calcium levels (Table 42-2). Some symptoms and metabolic changes improve, at least in part, after parathyroidectomy.24,25 On the other hand, about one quarter of asymptomatic patients develop symptoms of PHPT within 1 decade.26

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