Cases reported "Hyperparathyroidism"

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21/39. Primary hyperparathyroidism exacerbated by pregnancy.

    Primary hyperparathyroidism may remain subclinical as long as there is adequate calcium in the diet. If the demand for calcium increases, as in pregnancy, the symptoms become evident. Any giant cell growths should alert the oral surgeon to the possibility of hyperparathyroidism. Untreated, hyperparathyroidism ultimately leads to fractures, irreversible kidney damage, and death by renal failure. tetany must be guarded against after parathyroid surgery. Finally, the brown tumors of hyperparathyroidism need not be removed surgically since bone will regenerate if the disease is correctly treated by removal of the parathyroid adenoma.
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22/39. hypercalcemia in squamous cell carcinoma of the renal pelvis? Parathyroid or paraendocrine in origin.

    hypercalcemia associated with metastatic cancer may be due to osteolytic invasion or paraendocrine effects of the neoplasm. A patient with refractory hypercalcemia of long duration underwent cervical parathyroid exploration; three glands were found, but hypercalcemia persisted. After localization studies, a fourth gland was uncovered from the mediastinum. hypercalcemia persisted, and at operation for kidney stones, squamous cell carcinoma of the renal pelvis was discovered, which progressed to cause the patient's death in hypercalcemia.
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23/39. A case with persistent nephrogenic diabetes insipidus following parathyroidectomy for hyperparathyroidism.

    A 25-year-old woman with persistent nephrogenic diabetes insipidus (NDI) following parathyroidectomy for primary hyperparathyroidism is described. NDI is a well recognized complication of primary hyperparathyroidism, generally imputed to hypercalcemia, and promptly reversible after correcting it. In our case, the impaired concentrating ability of the renal tubule was irreversible after the removal of the parathyroid adenoma and the correction of the hypercalcemia, presumptively due to the morphological irreversible changes in the kidney. In addition, hypercalciuria persisted and was the cause of a compensatory hyperparathyroidism. Treatment with thiazide diuretic was effective to decrease relative hypercalciuria, thus reversing the compensatory hyperparathyroidism.
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24/39. medullary sponge kidney and hyperparathyroidism.

    medullary sponge kidney (MSK), parathyroid adenoma, renal cell carcinoma, and renal-leak hypercalciuria coincided in 1 female patient. Renal-leak hypercalciuria was not corrected by removal of a parathyroid adenoma. Since the patient had renal tubular acidosis (RTA), alkali treatment was conducted and resulted in the correction of hypercalciuria. Renal cell carcinoma eventually developed and MSK was confirmed histologically. This case suggests that MSK and primary hyperparathyroidism occurred independently.
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25/39. The hypercalcemia of malignancy.

    The hypercalcemia of malignancy is mediated by complex and heterogeneous mechanisms. Once thought of as a simple paraneoplastic syndrome mediated by the effects of tumor production of PTH, it is now clear that multiple mechanisms are involved and that these mechanisms involve abnormalities in calcium transport in bone, kidney, and gut. calcium homeostasis in normal individuals is complex and tightly regulated. Although much has been learned over the last 20 years about the effects of individual hormones on target organs, much remains to be understood about how these hormonal systems interact to control extracellular fluid calcium. Future studies on disturbances in calcium homeostasis, such as that occurring in association with malignant disease, should do much to clarify how these complex hormonal mechanisms function in the normal individual.
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26/39. Ectopic prolactinoma in a patient with hyperparathyroidism and abnormal sellar radiography.

    In a patient with hyperparathyroidism and chronic renal failure due to polycystic kidney disease, a finding of destroyed sellar and parasellar structures and hyperprolactinemia suggested the diagnosis of invasive pituitary prolactinoma. At surgery no tumor was found, and pathological examination of the sphenoid bone revealed a parathyroid bone lesion (brown tumor) as well as ectopic prolactinoma in the clivus. This patient demonstrates that a tumor may develop in ectopic pituitary tissue. The combination of radiographically abnormal sellar structures with pituitary hormone hypersecretion should not be regarded as absolute proof of a pituitary adenoma.
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27/39. Hypercalcaemia due to hyperparathyroidism in a patient with chronic renal failure and renal carcinoma.

    A 65-year-old woman with a history of a left heminephrectomy for renal carcinoma developed hypercalcaemia 11 years after the operation. The same kidney was found to contain a recurrent renal carcinoma. After the radical nephrectomy of the left kidney, hypercalcaemia remitted but reappeared 11 months later. The right kidney was small but functioned at a level of creatinine clearance of 10--15 ml/min. Metastatic work-up was negative, and secondary causes of hypercalcaemia were excluded. A neck exploration revealed a parathyroid adenoma. With parathyroid resection the serum calcium declined to normal, and the risk of hypercalcaemic nephropathy in the remaining kidney was precluded.
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28/39. Total parathyroidectomy and autotransplantation for tertiary hyperparathyroidism in children with chronic renal failure.

    An association between chronic renal failure and skeletal deformities in the adolescent patient was first documented by Lucas in 1883. Since then it has been established that the kidneys play a major role in the regulation of calcium, phosphate, and parathyroid hormone, and that chronic renal failure is characterized by profound alterations in the normal metabolic homeostasis of the human body. With the hyperphosphatemia of uremia, compensatory hyperparathyroidism is also a well known complication. Due to these factors, loss of normal renal function ultimately leads to derangement in mineral and bone metabolism resulting in severe skeletal deformities. Reports in the English literature suggest that the changes of renal osteodystrophy are much more pronounced in the pediatric patient, as compared to those in the adult. In the last two decades, renal transplantation has come to be recognized as a satisfactory modality for controlling renal failure and its complications. This procedure is often not available as an option, however, in small patients, especially those under three years of age. The pediatric nephrologist is often forced to manage these patients for long periods with conservative therapy, in an attempt to control the ravages of renal osteodystrophy. The problem becomes unmanageable when the compensatory hyperparathyroidism proceeds to autonomy. When this occurs, despite maintenance of normal serum calcium levels, the renal osteodystrophy progresses rapidly, producing pain, deformities and growth retardation. At this point, the condition is often refractory to medical management and resection of parathyroid tissue remains the only satisfactory modality for control.(ABSTRACT TRUNCATED AT 250 WORDS)
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29/39. Reversible hypocalciuric hypercalcemia associated with hypothyroidism.

    hypothyroidism is known to affect calcium homeostasis by decreasing bone turnover and serum calcium level, and by increasing parathyroid hormone and 1,25-dihydroxyvitamin D concentrations. A 52-year-old hypothyroid woman is described who had hypercalcemia associated with elevated parathyroid hormone and 1,25-dihydroxyvitamin D levels, but decreased 24-hour urinary calcium excretion and ratio of calcium to creatinine clearance. These parameters normalized following thyroid hormone replacement therapy. hypercalcemia appeared to result from a combination of reduced renal calcium excretion and a change in the "set point" for calcium feedback inhibition of the parathyroid glands. These data suggest that thyroid hormone has a direct effect on the parathyroid glands, regulating parathyroid hormone secretion, and on the kidney's ability to excrete calcium. It is recommended that parathyroid hormone, 1,25-dihydroxyvitamin D, and urinary calcium excretion values be interpreted in light of thyroid hormone status.
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30/39. hyperparathyroidism in patients with X-linked dominant hypophosphatemic rickets--application of the calcium infusion test as an indicator for parathyroidectomy.

    Two children with X-linked dominant hypophosphatemic rickets treated with vitamin-D metabolites and phosphate supplementation, for prolonged periods, developed hyperparathyroidism with nephrocalcinosis. calcium infusion tests were performed in both. In one patient, the initial test was done two weeks after all treatment was stopped. Only moderate decrease in the degree of the phosphaturia was recorded. However, a repeat test, performed after all medications were withheld for another four weeks, showed normal anti-phosphaturic response, and she continued to be treated conservatively. In the other patient, the test was done five weeks after withholding treatment. Failure to suppress the phosphaturia provided strong support for the diagnosis of tertiary hyperparathyroidism. He underwent total parathyroidectomy and the parathyroid histology confirmed the diagnosis. In both, control of parathyroid activity stopped the deterioration in kidney function and improved the response of the basic disorder to treatment. It is concluded that in patients with X-linked dominant hypophosphatemic rickets, the calcium infusion test is useful for the differentiation between secondary-reversible and tertiary-irreversible hyperparathyroidism. To avoid continued stimulation of the parathyroid glands by phosphate administration, we recommend that such calcium infusion test be performed and interpreted after at least six weeks have elapsed without phosphate or vitamin-D administration.
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