Cases reported "Hyperparathyroidism"

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1/19. Course and outcome of pregnancy in a patient with mild, asymptomatic, primary hyperparathyroidism diagnosed before conception.

    Primary hyperparathyroidism (PHP) during pregnancy is well known to confer an increased risk of complications to both the mother and the fetus. However, the risks and optimal management of patients with mild, asymptomatic disease during pregnancy are much less clear. We observed a patient with mild, asymptomatic PHP who was diagnosed before conception through pregnancy. The patient remained asymptomatic through the first 22 weeks of pregnancy, and her calcium levels remained under 11 mg/dL. This occurred despite a dramatic elevation in the level of 1,25-dihydroxyvitamin D and marked hypercalciuria. Parathyroid surgery was performed at 22 weeks of gestation and a parathyroid adenoma was removed. Postoperatively, the patient's calcium level normalized and the rest of the pregnancy was uncomplicated. The patient delivered a healthy baby at 40 weeks of gestation. The neonatal course was unremarkable. We conclude that mild, asymptomatic PHP during early pregnancy is compatible with normal fetal development and an uncomplicated pregnancy and that the serum calcium level in such patients can remain stable with medical management alone, despite the marked changes in maternal calcium metabolism that characterize normal pregnancy.
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2/19. Primary neonatal hyperparathyroidism. Report of a case and review of the literature.

    The seventh case in the world literature of primary hyperparathyroidism in a neonate is reported. This is the fifth case in which an autopsy was performed. The clinical and anatomic findings in all seven cases are reviewed and compared. Neonates with primary hyperparathyroidism show diffuse hyperplasia of the parathyroid glands. The bones show disturbed osteogenesis, bone resorption, and widespread fibrosis of the marrow cavities. Bony cysts are not appreciated. Pathologic fractures are common. Marked hypercalciuria or hyperphosphaturia is usually not observed, perhaps because the immature renal tubules fail to respond to the influence of excess parathormone. Aminoaciduria and anemia are commonly observed. The prognosis is grave, and the etiology of this syndrome remains unexplained.
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3/19. Familial hypercalcemia and hypercalciuria: no mutations in the Ca2 -sensing receptor gene.

    A 6-year-old boy presented with persistent hypercalcemia, hypercalciuria and nephrocalcinosis from early infancy. His 40-year-old father also had hypercalcemia and hypercalciuria. In both individuals serum values of intact parathyroid hormone (PTH) were repeatedly normal. Although these findings suggest a functional abnormality of the calcium-sensing receptor (CaR), no mutations in coding regions of the CaR gene could be demonstrated.
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4/19. Inactivating mutations of calcium-sensing receptor results in parathyroid lipohyperplasia.

    Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant disease characterized by mild hypercalcemia, an inappropriately high parathyroid hormone level, and absence of hypercalciuria. Heterozygous inactivating mutations of calcium-sensing receptor (CaSR) are found in about two thirds of patients with FHH. Histologic examination of parathyroid glands in FHH is reported to show normal histology or chief cell hyperplasia. Thus, histologic features of the parathyroid glands in FHH vary, and there is no clear histologic criterion that indicates FHH. The authors have encountered three hypercalcemic patients with characteristic histologic features of enlarged parathyroid glands. Clusters of parenchymal cells were mixed with fat cells, and the area of fat cells was 33% to 49% of the total area. These features are similar to those described as parathyroid lipohyperplasia. Postoperative evaluation showed that fractional excretion of calcium was low in these patients. Direct sequencing of the polymerase chain reaction product showed that the first patient was heterozygous for an already reported inactivating mutation of CaSR (P55L). The second patient was also heterozygous for a novel inactivating mutation (R220W). The third was homozygous for an inactivating mutation (Q27R). These results indicate that histologic features of parathyroid lipohyperplasia suggest the presence of inactivating mutations of CaSR.
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5/19. Coexistence of a parathyroid adenoma and parathyroid cyst causing primary hyperparathyroidism.

    The association of a functional parathyroid cyst with a parathyroid adenoma is an uncommon finding. In this report we describe the clinical history of a 60-yr-old man, presenting with the following findings: hypercalcemia (18.9 mg/dl), elevated serum parathormone levels (1320 pg/dl), hypercalciuria (228 mg/dl), and hyperphosphaturia (155 mg/dl). neck ultrasound, magnetic resonance imaging (MRI) and 99Tc Sestamibi scintigraphy led to the identification of a left parathyroid adenoma, located at the lower pole of the left thyroid gland lobe, associated with a parathyroid cyst, located at the upper extremity of the same thyroid lobe. parathyroidectomy was performed and the histological examination confirmed the diagnosis of a parathyroid adenoma with aspects of cystic degeneration and an upper parathyroid cyst. Analysis of the crystal clear intracystic fluid showed elevated parathyroid hormone (PTH) levels (137.000 pg/ml). The patient is normocalcemic at 2 yr after surgery without signs of recurrent parathyroid enlargements. Aetiology, diagnosis and management of parathyroid cyst will be discussed.
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6/19. multiple myeloma presenting with recurrent hypercalcemia in a patient with a history of primary hyperparathyroidism: report of case and review of literature.

    OBJECTIVE: To report a case of primary hyperparathyroidism (PHPT) that presented with recurrent hypercalcemia due to multiple myeloma after successful parathyroidectomy. methods: The initial manifestations, investigations, and postoperative follow-up of a case of hypercalcemia due to PHPT are described. The studies performed for evaluation for recurrent hypercalcemia and the subsequent diagnosis of multiple myeloma are discussed. The association between these disorders and reports of similar cases in the literature are reviewed. RESULTS: A 72-year-old woman was referred for incidentally discovered hypercalcemia. She had no history of kidney stones or fractures. Further investigations revealed a high parathyroid hormone (PTH) level, hypercalciuria, and low bone mass, particularly at the cortical sites. parathyroidectomy was performed, and a right inferior parathyroid adenoma was removed. Postoperatively, both the calcium and PTH levels normalized. She presented 9 months later with a 3-week history of pain in her left hip, polyuria, nausea, and vomiting. The patient had severe hypercalcemia and a suppressed PTH level. Further investigations revealed multiple bony lytic lesions, abnormalities on serum protein electrophoresis, and features consistent with multiple myeloma on a bone marrow biopsy specimen. CONCLUSION: hypercalcemia can occur in patients with PHPT and multiple myeloma; however, the occurrence of both disorders in the same patient is rare. review of the literature revealed only a few cases similar to ours. Evidence in the literature suggests that monoclonal gammopathies occur more often in patients with PHPT than in the general population; therefore, screening for monoclonal gammopathy may be warranted in patients with PHPT.
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7/19. Primary hyperparathyroidism in infants. Diagnostic and therapeutic difficulties.

    On the basis of 3 infants with primary congenital hyperparathyroidism we discuss problems in the early diagnosis and interpretation of the results of laboratory findings. The lack of increased renal echogenicity and hypercalciuria, which is regularly present in idiopathic hypercalcaemia is emphasized. In contrast to secondary hyperparathyroidism caused by prolonged hypocalcaemia, e.g. in patients treated by longterm haemodialysis, the aetiology of primary hyperparathyroidism (pHPT) remained unclear although molecular genetic studies suggest that the development of parathyroid adenoma may be due to gene mutation in a cell. Congenital pHPT is a particularly rare condition usually due to diffuse hyperplasia of all parathyroid glands. Its inheritance is known to be autosomal. Three infants with congenital primary hyperparathyroidism were treated at the child health Centre in the years 1987-1988.
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8/19. Self-limited neonatal familial hyperparathyroidism associated with hypercalciuria and renal tubular acidosis in three siblings.

    Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin d and calcitonin seemed to be intact. hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.
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9/19. 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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10/19. 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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