Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary thymic carcinoma is a rare neoplasm that in contradistinction to thymoma, is not supposed to be associated with a paraneoplastic syndrome. A 73-year-old man, with new onset of disorientation, was found to have an elevated serum calcium level as the cause. Computed tomography demonstrated a mediastinal mass, pericardial invasion, and metastases to the lung. Examination of a biopsy specimen revealed thymic squamous cell carcinoma. Thus, a paraneoplastic syndrome, in this case hypercalcemia, does not exclude primary carcinoma of the thymus.
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PMID:Squamous cell carcinoma of the thymus with paraneoplastic hypercalcemia. 777 75

We recently reported that mice treated with 1,25-dihydroxyvitamin D3 ( 1,25-(OH)2D3) or 19-nor-1,25-(OH)2D2 experienced a severe loss of their thymocytes and decreased proliferation in response to concanavalin A mitogen. The present study investigated the effect of short-term treatment with 1,25-(OH)2D3 on the thymic architecture and thymocyte subsets. Daily treatment with 1,25-dihydroxyvitamin D3 at 20 ng per mouse for 4 days induced significant involution of thymic tissue. The atrophy was predominantly observed in the cortical component. Flow cytometric analysis of thymocyte subsets showed that the CD4 + CD8 + population was the primary target. Since the treated mice experienced profound hypercalcemia, we studied the effect of 1,25-(OH)2D3 on animals fed a vitamin D-deficient, low calcium diet or the same diet containing vitamin D for 25 days prior to treatment. The low calcium fed mice showed severe hypocalcemia and slight thinning of thymic cortex. Treatment with 1,25-(OH)2D3 moderately improved the hypocalcemia but had no further effect on the thymus of these animals. On the other hand, hypercalcemia and thymic atrophy were found in the animals fed the diet containing vitamin D. Overall, the atrophy effect on the thymus caused by 1,25-(OH)2D3 treatment was prevented by eliminating the hypercalcemia observed in + D + Ca treated animals. Thus, thymic atrophy probably resulted from hypercalcemia and not from 1,25-(OH)2D3 itself.
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PMID:Effect of 1,25-dihydroxyvitamin D3 on mouse thymus: role of extracellular calcium. 860 Sep 85

A total of 220 patients have undergone cervical exploration for hyperparathyroidism by the author. A review of 125 cases was published in 1991. An additional 95 patients have been explored in the subsequent four years. Subtotal parathyoidectomy was performed in 39 patients with chronic renal failure. Exploration was successful in over 97% of the 181 patients diagnosed with primary hyperparathyroidism. Single adenomas were found in 146, double adenomas in 11, and multiple gland hyperplasia in 19 patients. Two of the five patients in whom cervical exploration failed were ultimately diagnosed with benign familial hypocalciuric hypercalcemia. Twenty-four adenomas were ectopic. Preoperative thallium-technetium scans and ultrasound correctly localized only 61% of the adenomas. Technetium sestamibi scans were correct in two of four adenomas. Only 47% of ectopic adenomas were correctly localized by isotope scanning and 29% by ultrasound. All four glands should be examined at initial exploration. Because of the occurrence of double adenomas, contralateral exploration is always indicated regardless of whether an enlarged gland and a normal one are found on the first side. All enlarged parathyroids should be removed when dealing with single or multiple adenomas; subtotal parathyroidectomy (3-1/2 glands) should be performed in multiple gland hyperplasia. Frozen section confirmation of excised parathyroid tissue is essential. If exploration is unsuccessful, ectopic locations, such as the retroesophageal areas, thymus, anterior and posterior mediastinum, carotid sheath and thyroid lobe, must be examined carefully. Preoperative localization studies are not as reliable as an experienced parathyroid surgeon.
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PMID:Parathyroid update: a review of 220 cases. 876 6

These results in difficult patients with previously missed parathyroid adenomas demonstrate that a prospective strategy to treat these patients surgically can be used with a high degree of success. This strategy required collaboration among endocrinologists, radiologists, and surgeons. Prospectively, only patients with symptomatic persistent or recurrent primary hyperparathyroidism were included. Operative reports and pathology results from the initial operation and all previous operations were reviewed in detail. Patients with FHH or hypercalcemia from other causes were excluded. State-of-the-art radiologic localization procedures were used to localize the abnormal parathyroid gland. Most patients had only noninvasive procedures, such as the sestamibi scan, but some whose results were equivocal underwent invasive localization, including selective angiography and venous sampling. All patients underwent surgery even if the localization procedures were negative. The operative approach and strategy were dependent on the previous operative result and results of the imaging studies. Operative techniques like IOUS and urinary cAMP determination helped facilitate a more rapid successful outcome. However, in some patients, operative success was only achieved by complete dissection and removal of all tissue that might harbor the adenoma such as a lobe of the thyroid or the thymus. Abnormal parathyroid tissue was cryopreserved for possible subsequent autotransplantation in the event of hypoparathyroidism. The reoperative success rate for missed adenoma was 97%, the highest ever reported with a very acceptable complication rate and no deaths. Postoperative hypoparathyroidism, which was really a complication of the initial previous operations during which normal parathyroid tissue was removed, was treated by autotransplantation of cryopreserved tissue in 12 patients, and 8 functioned perfectly. With attention to details and possible pitfalls, reoperations for missed parathyroid adenomas can be performed safely and effectively.
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PMID:Reoperation for missed parathyroid adenoma. 940 98

We report two women presenting with parathyroid cysts. A 20 years old woman presented with goiter and a cystic lesion in the left thyroid lobe was identified on ultrasound examination and CAT scan. The patient had hypercalcemia and elevated PTH levels. The content of the cyst, obtained by needle aspiration, had an extremely high PTH concentration. The patient was operated, removing the cyst and a remaining thymus. Pathological study confirmed the diagnosis of a parathyroid cyst. An 11 years old girl presented with a mass in the left thyroid lobe. An ultrasound examination disclosed the presence of a cystic nodule. The patient was otherwise asymptomatic and laboratory work up was normal. The patient was operated and pathological examination of the surgical piece revealed a parathyroid cyst.
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PMID:[Functioning and non-functioning parathyroid cysts: entities with different origin and clinical characteristics in 2 cases]. 959 97

We report a case of a 35-year-old male, with a history of diarrhea, renal lithiasis with frequent expulsions of calculus and hypercalcemia during the last 2 years. The patient was studied and diagnosed with a multiple endocrine neoplasia type I (MEN I), familiar (mother with MEN I). A scintigraphic study with 99mTc-MIBI was performed in order to localize hyperfunctioning parathyroid glands because of biochemical diagnosis of primary hyperparathyroidism. Double phase 99mTc-MIBI scan detected one hyperfunctioning parathyroid gland and a large anterior mediastinal mass. Subsequent, plain radiograph and CT of the chest showed a soft-tissue mass in that localization. Punch biopsy of the lesion guided by CT revealed malignant cells of neuroendocrine tumor. The tumor was removed and histologically confirmed as a carcinoid within a thymus in a MEN type I syndrome. MEN I patients can benefit from the examination with this agent which can potentially localize not only parathyroid endocrine pathology but also unknown associated tumors.
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PMID:Thymic carcinoid and parathyroid hyperplasia detection with 99mTc-MIBI men type 1. 1061 32

Familial hyperparathyroidism (HPT) is a hereditary disease in which HPT is transmitted in an autosomal dominant fashion. It includes a variety of diseases: multiple endocrine neoplasia (MEN) type 1 and type 2, and familial isolated hyperparathyroidism (FIHPT). We screened for MEN 1 mutations by direct nucleotide sequencing of all protein-coding regions and identified the germline mutations of the MEN 1 gene in two families with familial HPT. Patients with FIHPT have multiple abnormal parathyroid glands and are prone to both recurrent and persistent HPT. They frequently present with profound hypercalcemia, in contrast to patients with MEN-associated HPT or sporadic HPT. We recommend subtotal or total parathyroidectomy plus autotransplantation in patients with MEN-associated HPT and patients with FIHPT. Because parathyroid remains or supernumerary glands are often present in the thymus or perithymic tissue, we advocate routine bilateral dissection of the central zone with bilateral cervical thymectomy.
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PMID:Familial hyperparathyroidism. 1091 86

A complementary DNA (cDNA) encoding the rat homologue of receptor activator of NF-kappaB ligand/osteoprotegerin ligand/osteoclast differentiation factor/tumor necrosis factor (TNF)-related activation-induced cytokine (RANKL/OPGL/ODF/TRANCE) was cloned and sequenced from tibias of ovariectomized (OVX) rats. The predicted amino acid sequence of rat RANKL (rRANKL) has 84% and 96% identity to that of human and mouse RANKL, respectively, and 35% and 37% similarity to that of human and mouse TNF-related apoptosis-inducing ligand (TRAIL), respectively. RANKL transcripts were expressed abundantly in the thymus and bone tissues of OVX rats. rRANKL has a single hydrophobic region between residues 53 and 69, which is most likely to serve as a transmembrane domain. The long C-terminal region containing beta-sheet-forming sequences of the TNF-like core is considered the extracellular region. Three truncated domains within the TNF-like core region were expressed as glutathione S-transferase (GST) fusion proteins and investigated for their ability to induce osteoclastogenesis. The results showed that GST-rRANKL (aa160-318) containing the full TNF-like core region had the highest capability to induce the formation of osteoclast-like cells from RAW264.7 cells. GST-rRANKL (aa239-318 and aa160-268) had lesser degrees of osteoclast inductivity. Furthermore, the GST-rRANKL (aa160-318) is capable of (1) inducing osteoclast formation from rat spleen cells in the presence of macrophage colony-stimulating factor (M-CSF), (2) stimulating mature rat osteoclast polarization and bone resorption ex vivo, and (3) inducing systemic hypercalcemia in vivo; thus the full TNF-like core region of rRANKL is an important regulator of calcium homeostasis and osteoclastic function.
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PMID:Cloning, sequencing, and functional characterization of the rat homologue of receptor activator of NF-kappaB ligand. 1109 98

The majority of patients with adult T-cell leukemia/lymphoma (ATL) resulting from human T-cell lymphotropic virus type-1 (HTLV-1) infection develop humoral hypercalcemia of malignancy (HHM). We used an animal model using severe combined immunodeficient (SCID)/beige mice to study the pathogenesis of HHM. SCID/beige mice were inoculated intraperitoneally with a human ATL line (RV-ATL) and were euthanized 20 to 32 days after inoculation. SCID/beige mice with engrafted RV-ATL cells developed lymphoma in the mesentery, liver, thymus, lungs, and spleen. The lymphomas stained positively for human CD45RO surface receptor and normal mouse lymphocytes stained negatively confirming the human origin of the tumors. The ATL cells were immunohistochemically positive for parathyroid hormone-related protein (PTHrP). In addition, PTHrP mRNA was highly expressed in lymphomas when compared to MT-2 cells (HTLV-1-positive cell line). Mice with lymphoma developed severe hypercalcemia. Plasma PTHrP concentrations were markedly increased in mice with hypercalcemia, and correlated with the increase in plasma calcium concentrations. Bone densitometry and histomorphometry in lymphoma-bearing mice revealed significant bone loss because of a marked increase in osteoclastic bone resorption. RV-ATL cells contained 1.5 HTLV-1 proviral copies of the tax gene as determined by quantitative real-time polymerase chain reaction (PCR). However, tax expression was not detected by Western blot or reverse transcriptase (RT)-PCR in RV-ATL cells, which suggests that factors other than Tax are modulators of PTHrP gene expression. The SCID/beige mouse model mimics HHM as it occurs in ATL patients, and will be useful to investigate the regulation of PTHrP expression by ATL cells in vivo.
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PMID:Humoral hypercalcemia of malignancy: severe combined immunodeficient/beige mouse model of adult T-cell lymphoma independent of human T-cell lymphotropic virus type-1 tax expression. 1139

The diagnosis of primary hyperparathyroidism in children is often delayed and is usually based on symptoms of hypercalcemia rather than abnormal laboratory values alone. We report the case of an 8-year-old boy with hypercalcemia, hypophosphatemia and mildly, but inadequately elevated intact parathyroid hormone (iPTH) who presented without any symptoms of hyperparathyroidism. Although imaging studies were misleading and four normal parathyroid glands were found intraoperatively, exploration of the thymus revealed an ectopic parathyroid adenoma. After removal of the ectopic gland, a rapid iPTH immunoassay proved immediate normalization of iPTH. This is the first report of sporadic isolated primary hyperparathyroidism diagnosed in an asymptomatic child on the basis of hypercalcemia and hypophosphatemia.
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PMID:Asymptomatic hypercalcemia due to an ectopic parathyroid adenoma in an 8-year-old boy. 1140 3


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