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PubMed1976

Surgical management of parathyroid disease.

One hundred fifty patients who had operation for hyperparathyroidism at the National Institutes of Health are reviewed. The series is composed of several groups of patients, including 18 with normocalcemic hyperparathyroidism, 13 with hyperparathyroidism associated with MEA II, and 24 patients with a history of previous parathyroid operation. Selective venous catherization and radioimmunoassay of parathormone was carried out in 81 patients and was interpreted as being localizing in 65 cases. Following operation, six patients remained hypercalcemic. There were nine instances of permanent hypocalcemia and four cases in which permanent recurrent nerve injuries were experienced. The operative management of these patients is outlined in detail, stressing an approach which includes the surgeon, the internist and the pathologist. Based upon pathological evidence, the importance of identifying by frozen section four glands is emphasized.

Adenoma↗
PubMedDate not supplied

The molecular biology of parathyroid disease.

Advances in molecular genetics have shed important new light on the understanding of the basis for human tumors. The application of these methods has allowed for characterization of endocrine neoplasms at a level of resolution that was not previously possible. A variety of molecular techniques have been applied to the study of parathyroid tumors at the DNA level. Studies of the clonal derivation of adenomas and hyperplasia suggest that these entities arise through fundamentally different mechanisms. The gene for parathyroid hormone (PTH) has been cloned and mapped within the human genome. In a small subset of parathyroid tumors, a rearrangement of the PTH gene has been described which may have contributed to their pathogenesis. A separate gene has been identified which appears to be responsible for the humoral hypercalcemia of malignancy. Chromosomal deletions which appear to be involved in the pathogenesis of multiple endocrine neoplasia type 1 have also been found in sporadic parathyroid adenomas. Characterization of tumors at the DNA level may make it possible to correlate specific genetic abnormalities with the biologic behavior of different parathyroid neoplasms and may be useful in distinguishing between adenoma, hyperplasia, and carcinoma.

Chromosome Deletion↗
PubMed1986

[Diagnostic tests in parathyroid diseases].

The diagnosis of primary hyperparathyroidism (PHP) depends increasingly on laboratory tests, since the majority of patients are elderly people without typical symptoms. A mean plasma calcium level close to the upper normal limit serves to diagnose hypercalcemia. To rule out malignant disease, the most common cause of hypercalcemia, measurement of plasma PTH is the most appropriate test. Determination of blood phosphorus, chloride, and alkaline phosphatase, and of urinary calcium and phosphorus, contribute to the investigation of the metabolic effects of the given disease but are not very useful for causal diagnosis. Urinary and nephrogenous cyclic AMP reflect PTH secretion but can be elevated in paraneoplastic hypercalcemia. Diagnosis of subtle forms of PHP by dynamic tests is largely of scientific interest, since they do not necessarily need treatment. The diagnosis of hypoparathyroidism is primarily clinical. PTH measurements rarely distinguish normal from low values. In severe hypocalcemia of non-parathyroid origin, plasma PTH is elevated (except in hypomagnesemia). In borderline cases, measurement of urinary cyclic AMP or of plasma PTH after attempted stimulation by EDTA infusion is helpful, especially in distinguishing between subtle hypoparathyroidism and tetany induced by hyperventilation.

Adenoma↗
PubMed1992

[Acid-base disturbance in adrenal and parathyroid diseases].

Aldosterone stimulates sodium absorption in the collecting tubule, which makes the potential more lumen-negative, and secondarily stimulates proton and potassium secretion. Potassium depletion stimulates ammonia synthesis, which increases distal buffer delivery, increases luminal pH in the collecting tubule, and secondarily stimulates proton secretion. This stimulation of the distal nephron acidification by aldosterone can result in metabolic alkalosis. Inversely, aldosterone deficiency can produce characteristic metabolic acidosis with hyperkalemia (type IV renal tubular acidosis). Acute administration of parathyroidhormone (PTH) decreases renal bicarbonate reabsorption in the proximal tubule. Since the effect of PTH is overridden by other factors, such as PTH-induced base release from bone, hyperparathyroidism does not uniformly cause metabolic acidosis.

Acidosis↗
PubMedDate not supplied

Clinicopathological peculiarities in parathyroid disease with hypercalcaemic crisis.

OBJECTIVE: To draw attention to some hitherto unnoticed clinicopathological aspects of primary hyperparathyroidism in patients who develop hypercalcaemic crisis. DESIGN: Retrospective review of records and histopathological archive material. SETTING: University hospital. SUBJECTS: 54 patients treated for primary hyperparathyroidism with hypercalcaemic crisis between 1961 and 1988. MAIN OUTCOME MEASURES: Correlation of age, serum calcium concentration, histopathological appearance and size of tumours associated with hypercalcaemic crisis. RESULTS: 11/54 (20%) of the patients with hypercalcaemic crisis were younger than 40 years of age. Among 460 patients treated at the same hospital for primary hyperparathyroidism without hypercalcaemic crisis, 23 (5%) belonged to the same age category (p less than 0.001). There was no difference between the two groups of patients regarding histopathological characteristics, with the exception of mitotic activity which was remarkably high in some benign lesions causing hypercalcaemic crisis. The correlation between tumour size and degree of hypercalcaemia was poor, and one-third of the adenomas did not exceed 2 cm in diameter. CONCLUSIONS: Young age is a risk factor regarding the development of hypercalcaemic crisis in primary hyperparathyroidism; the proportions of the pathological entities causing hypercalcaemic crisis do not differ markedly from other cases of primary hyperparathyroidism; the correlation between adenoma size and degree of hypercalcaemia is poor; oxyphil adenomas are as likely to be associated with hypercalcaemic crisis as other types of parathyroid adenoma; and some benign parathyroid lesions associated with hypercalcaemic crisis (hyperplastic glands as well as adenomas) show high mitotic activity.

Adenoma↗
PubMed1982

[Plasma vitamin D metabolites in parathyroid diseases (author's transl)].

The basal values of plasma vitamin D metabolites were evaluated in patients with primary hyperparathyroidism (1 degree HPT, n = 31), hypoparathyroidism (HP, n = 7), pseudohypoparathyroidism (PHP, n = 4) and normal controls (n = 21). Plasma 25-hydroxyvitamin D (25-OH-D) in 1 degree HPT (9.0 +/0 7.3 ng/ml, mean SD) was significantly lower than that of normal controls (17.9 +/- 5.5ng/ml)(p less than 0.001), and in particular 1 degree HPT classified as the skeletal type showed extremely low value (4.7 +/- 4.6 ng/ml). Plasma 1, 25-dihydroxyvitamin D [1, 25-(OH)2D] was significantly higher in 1 degree HPT (69.1 +/- 31.4pg/ml)(p less than 0.001) and significantly lower in Hp (15.2 +/- 11.0 pg/ml) (p less than 0.001) compared to normal controls (37.2 +/- 13.8pg/ml), although there was no significant difference in PHP (22.3 +/- 17.5 pg/ml). Plasma 24, 25-dihydroxyvitamin D [24,, 25-(OH)2D] in 1 degree HPT (1.06 +/- 0.55 ng/ml) was significantly lower than that of normal controls (1.73 +/- 0.62 ng/ml) (p less than 0.05), and particularly 1 degree HPT classified as the skeletal type showed a marked low value (0.85 +/- 0.27 ng/ml), whereas no significant differences were seen in HP (1.84 +/- 0.46 ng/ml) or PHP (1.34 +/- 0.22 ng/ml). There were slight but significant correlations between either plasma 25-OH-D and 1, 25-(OH)2D (r = -0.350, p less than 0.05), or plasma 25-OH-D and 24, 25-(OH)2D (r = 0.356, p less than 0.05), or plasma 1, 25-(OH)2D and 24, 25-(OH)2D (r = -0.444, p less than 0.01) in all subjects. In addition, relationships between plasma vitamin D metabolites and other indicators of parathyroid function in all subjects were analyzed. There were positive correlations between plasma 1, 25-(OH)2D and serum Ca (r = -0.621, p less than 0.001) or urinary cAMP (r = -0.671, p less than 0.001) or nephrogenous cAMP (r = -0.689, p less than 0.001), while negative correlations were seen between plasma 1, 25-(OH)2D and serum P (r = -0.680, p less than 0.001) or %TRP (r = -0.663, p less than 0.001). On the other hand, there were negative correlations between plasma 24, 25-(OH)2D and serum Ca (r = -0.457, p less than 0.01) or urinary cAMP (r = -0.562, p less than 0.005) or nephrogenous cAMp (r = -0.561, p less than 0.005), and a positive correlation was seen between plasma 24, 25-(OH)2D and %TRP (r = 0.519, p less than 0.005). After parathyroidectomy, a distinct depression of plasma 1, 25-(OH)2D and reciprocal elevation of plasma 24, 25-(OH)2D were observed in 1 degree HPT. Furthermore, there was a clear elevation of plasma 24, 25-(OH)2D as well as plasma 1, 25-(OH)2D after treatment with maintenance doses of 1 alpha-OH-D3 or 1 alpha, 25-(OH)2D3 in HP and PHP. It is concluded that plasma vitamin D metabolites are very useful as the indicators of parathyroid function.

25-Hydroxyvitamin D 2↗