Hyperparathyroidism parathyroidectomy

Parathyroid hormone (PTH) produces CNS effects in normal subjects and neuropsychiatric symptoms are frequently encountered in patients with primary hyperparathyroidism, where EEG changes resemble those described in acute renal failure. Circulating PTH is not removed by hemodialysis. In uremic patients both EEG changes and neuropsychiatric symptoms are improved by either parathyroidectomy or medical suppression of PTH. The mechanism whereby PTH causes disturbances of CNS function is not well understood, but it has been suggested that increased PTH might facilitate the entry of Ca2+ into the cell resulting in cell death. 

In contrast to the hypocalcemia that is more often associated with chronic kidney disease, some patients may become hypercalcemic from two other possible causes (in addition to overzealous treatment with calcium). The most common cause of hypercalcemia is the development of severe secondary (sometimes referred to as tertiary) hyperparathyroidism. In such cases, the PTH level in blood is very high. Serum alkaline phosphatase levels also tend to be high. Treatment often requires parathyroidectomy. 

Hyperparathyroidism and aluminium hydroxide lead to aluminium-related bone disease however, total parathyroidectomy does not lead to failure of aluminium mobilization after renal transplantation. This man had satisfactory graft function, and the aluminium excretion that was achieved by deferoxamine suggests that the renal transplant was not the limiting factor for the mobihzation of aluminium. The most likely explanation was that he developed adynamic bone through a combination of vitamin D deficiency, hypoparathyroidism, and aluminium deposition. Vitamin D supplementation failed to prevent the osteodystrophy on its own. When aluminium chelation therapy was used, bone healing occurred and his symptoms improved. 

Hyperparathyroidism— primary Parathyroidectomy 60 11 Pratley et al. (P36) See also Table 8. 

Spiegel, A. M., Marx, S. ]., Brennan, M. F., Brown, E. M., Koehler, J. O., and Aur-bach, G. D., Urinary cAMP excretion during surgery An index of successful parathyroidectomy in patients with primary hyperparathyroidism. J. Clin. Endocrinol. 47, 537-542 (1978). 

It is g erally assumed that it is the concentration of ionic calcium in the extracellular fluid which the parathyroid glands control by this action on the skeleton and that the variations in total plasma calcium are strictly proportional. However, Freeman and Breen (Fll) have shown that parathyroidectomy is followed by a rise in the proportion of protein-boimd calcium and that this can be reduced by injection of the hormone. This accords with the observations of Lloyd and Rose in hyperparathyroidism (L6 see Section 4.2) and with the clinical observation that hypo-parathyroid patients may develop tetany at surprisingly high levels of total plasma calcium. The effects of Ae hormone on add-base balance may be concerned in this phenomenon since acidemia reduces the proportion of protein-bound calcium. 

Experiments with everted sacs of rat intestine have shown a fall in the transport of calcium-45 across the intestinal wall after thyroparathyroid-ectomy (D9) and after parathyroidectomy (R2), and it has been suggested that the hormone may promote calcium absorption. It is said that calcium is particularly well absorbed in hyperparathyroidism, but this may be a nonspecific response of the absorptive mechanism to hyper-calcuria (Jl). 

Polyuria is a recognized clinical feature of primary hyperparathyroidism (CIO). It has been shown to be associated with a reduction in maximum tubular water reabsorptive capacity which cannot be explained by general impairment of renal function and which has been found to improve after parathyroidectomy, as shown in Table 6 (R8). Hellstrom (H4) has found that it is unusual for a case of primary hyperparathyroid-... 

Potassium depletion has been reported in hyperparathyroidism (B9). This would be expected if there was impaired hydrogen ion secretion into the renal tubule such impairment may be associated with a compensatory increase in potassium secretion in exchange for sodium. Magnesium depletion has also been described, and parathyroidectomy is followed by magnesium retention (Bl). It is thought that these effects may be the result of the action of the hormone on bone (F6). 

There is a high incidence of peptic ulceration in primary hyperparathyroidism (H5, SI), but the cause of this is not established. Parathyroidectomy did not change gastric secretion in 4 out of 5 patients (D8), but did do so in one who had a duodenal ulcer. Four cases of hyperparathyroidism were identified in a series of 300 consecutive cases of peptic ulcer who were screened for this purpose (F7). 

Once the hypercalcemic crisis has resolved, or in patients with milder calcium elevations, longterm therapy can be initiated. Parathyroidectomy remains the definitive therapy for primary hyperparathyroidism. As described below, a Ca mimetic that stimulates the CaSR is a promising therapy for hyperparathyroidism. If the hypercalcemia results from malignancy, therapy ideally is directed at the underlying cancer. When this is not possible, intermittent dosing of parenteral bisphosphonates has been used to keep serum Ca within an acceptable range. 

The ultimate therapeutic goal of managing hyperparathyroid hypercalcemia is returning blood PTH, calcium and phosphate levels to their normal range. In IPTH, when active bone, renal or 61 symptoms are present, surgery is the most effective treatment modality when the offending parathyroid adenoma can be identified. In MENl or hyperplasia, controversy exists as to whether total parathyroidectomy... 

In chronic renal failure treated by renal transplantation, hyperparathyroidism may persist, as discussed above. In most cases, the parathyroid glands involute to normal within 3 years (11,59,M,, 66). However, since severe or prolonged hypercalcemia impairs renal function and may cause permanent renal graft injury, subtotal parathyroidectomy must be considered for patients with persistent hypercalcemia or acute hypercalcemic crisis. 

---