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)

We used the mouse nephrin promoter to express a constitutively active Galphaq [Galphaq(Q>L)] transgene in mice. As previously reported, the transgene was expressed in kidney, pancreas, and brain, and the kidney phenotype was characterized by albuminuria and reduced nephron mass. Additional studies revealed a second phenotype characterized by polyuria and polydipsia. The polyuric phenotype was not caused by abnormal glucose metabolism or hypercalcemia but was accompanied by reduced urinary concentrating ability. Additional studies found that 1) water restriction was associated with an appropriate increase in serum vasopressin levels in transgenic (TG) mice; 2) the urinary concentrating defect was not corrected by administration of desamino-d-arginine vasopressin (DDAVP); and 3) papillary length was similar in TG and non-TG mice. To examine the renal response to DDAVP at the molecular level, we monitored aquaporin 2 (AQP2) and vasopressin V2 receptor (V2R) mRNA levels in mouse kidney. Consistent with the known effects of vasopressin, administration of DDAVP caused a decrease in V2R mRNA levels and an increase in AQP2 mRNA levels in both TG and non-TG animals, suggesting an appropriate renal response to DDAVP in the TG mice. To determine whether the urine concentrating abnormality was the result of primary polydipsia, water intake by TG mice was restricted to the amount ingested by non-TG animals. After 5 days, urinary concentrating ability was similar in TG mice and non-TG littermate controls. These data are consistent with the notion that expression of the Galphaq(Q>L) transgene in the brain induced primary polydipsia in the TG mice.
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PMID:Galphaq-dependent signaling cascades stimulate water-seeking behavior. 1660 48

Nephrogenic diabetes insipidus (NDI) is defined as the inability of the kidney to concentrate urine owing to the insensitivity of the distal nephron to the antidiuretic hormone, arginine vasopressin. NDI can be either a congenital or an acquired disorder. Acquired NDI most commonly is secondary to drugs such as lithium or metabolic disturbances, such as hypokalemia and hypercalcemia. Disturbance of the aquaporin-2 shuttle is the underlying molecular basis of acquired NDI. NDI is diagnosed with the help of a water-deprivation test. Patients with the disorder will have a urinary osmolality of less than 300 mosm/kg H2O despite water deprivation. On administration of aqueous vasopressin, patients with NDI will show little or no increase in urine osmolality. Therapy consists of identifying and correcting the underlying disorder, or withdrawing the offending drug. Other treatment options that may be beneficial include diuretics, nonsteroidal anti-inflammatory drugs, decreased dietary solute intake, and desmopressin (DDAVP).
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PMID:Acquired nephrogenic diabetes insipidus. 1671 97

Nephrogenic diabetes insipidus which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired nephrogenic diabetes insipidus. About 90 percent of patients with congenital nephrogenic diabetes insipidus are males with X-linked recessive nephrogenic diabetes insipidus who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In about 10 percent of the families studied, congenital nephrogenic diabetes insipidus has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (AQP2), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and Cystinosis. Identification of the molecular defect underlying congenital nephrogenic diabetes insipidus is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.
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PMID:[Nephrogenic diabetes insipidus]. 1708 61

Small cell carcinoma (SCC) of the female genital tract is rare, constituting less than 2% of all gynecologic malignancies. It occurs most frequently in the cervix but can also occur in the endometrium, ovary, fallopian tube, vagina, and vulva. SCC of the genital tract is microscopically indistinguishable from that of the lung. Neuroendocrine differentiation is often manifested by a histologic growth pattern, argyrophilia, ultrastructural demonstration of secretory granules, and expression of neuroendocrine markers. Patients with SCC of the female genital tract may be asymptomatic but usually present with localized pain, vaginal bleeding, abdominal bloating or a mass, or symptoms of metastasis disease to the liver, bone, lung, or regional lymph nodes. Ectopic Cushing's syndrome has been reported in SCC of the vagina, and hypercalcemia and inappropriate secretion of antidiuretic hormone have been noted with SCC of the ovary. In general, these tumors have an aggressive clinical course with a propensity for extensive local invasion and distant metastases. Therapy has included surgery, radiation, and chemotherapy akin to those regimens used for SCC of the lung. Although there are no randomized clinical trials, it appears that multimodality therapy is associated with the best results and is the treatment of choice for most patients. Despite aggressive therapy, however, the prognosis for SCC of the female genital tract is poor, with only a minority of patients enjoying a prolonged survival. Indeed, the majority of patients have an early demise with extensive distant disease. We review the clinical features, evaluation, and management of SCC of the female genital tract based on a comprehensive review of the literature.
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PMID:Small cell carcinoma of the female genital tract. 1727 Jun 67

Male rats exposed to 500 R of whole-body x-irradiation were allowed food and water ad libitum and housed in metabolism cages; water and food intake and urinary and fecal excretion were recorded daily. Urine output increased 200% during the first 24 hours after irradiation. No significant changes occurred in daily sodium, potassium, urea, or total solute excretion, although calcium excretion approximately doubled after irradiation. The marked increase in free water excretion implicates antidiuretic hormone (ADH) in this phenomenon. Application of a sensitive bioassay for ADH permitted measurement of plasma ADH concentrations in undisturbed, unanesthetized rats before and after irradiation. ADH levels were lower and frequently not detectable 24 hours after exposure. High ADH levels, however, could be provoked in irradiated rats by hemorrhage, indicating that the receptor cells and secretory ability of the posterior pituitary remained intact. Furthermore, irradiated rats responded normally to small intravenous injections (4 to 8 microU) of exogenous ADH. Rats with congenital diabetes insipidus given daily injections of Pitressin showed no postirradiation diuresis. Lastly, increased urinary calcium excretion may result from hypercalcemia which is known to induce diuresis through calcium-vasopressin antagonism. These results further suggest that the diuretic response is due to decreased circulating ADH.
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PMID:Circulating antidiuretic hormone in the X-irradiated rat. 1738 77

Paraneoplastic syndromes are frequently detected in many small cell lung cancer (SCLC) patients. In the present paper we report 2 cases of patients diagnosed with SCLC, in whom 2 distinct endocrine paraneoplastic syndromes were identified during diagnosis. In the first patient, severe hyponatremia and renal sodium loss with inappropriate antidiuresis was found during routine laboratory tests. Serum antidiuretic hormone (ADH) level was within normal limits, but the atrial natriuretic peptide (ANP) level was elevated. The second case presented with severe hypercalcemia secondary to an excessive parathormone (PTH) secretion. We discuss the 2 cases and review the literature.
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PMID:Endocrine paraneoplastic syndromes in small cell lung carcinoma. Two case reports. 1791 99

The most frequent electrolytic disorders associating with tumors are hypercalcemia and hyponatremia, which should often be dealt with on an emergency basis. Hypercalcemia is observed in around 10% of metastatic solid tumors including lung, breast, head and neck and renal cancers. In hematological malignancies, hypercalcemia is observed with a relatively high incidence in malignant lymphoma. Hypercalcemia is caused by bone metastasis or PTH-rP secreted from tumors. In other cases, it is induced by calcitriol produced from tumor. Hypercalcemia sometimes results in a fatal outcome, and should be carefully monitored. Hyponatremia presented as SIADH is sometimes caused by arginine vasopressin derived from tumors. In other cases, SIADH is induced with chemotherapeutic drugs such as cyclophosphamide and cisplatin. Neither hypercalcemia nor hyponatremia has any specific symptoms. Delayed treatment often results in severe condition, such as unconsciousness or even death. Therapy for hypercalcemia is started by infusion of normal saline, and a patient with severe hypercalcemia should be treated with bisphosphonates. Zoledronic acid is the best bisphosphonate among them at this present. Treatment of SIADH is started by water restriction. In an emergency, treatment with hypertonic saline(3-5%)should be considered together with loop diuretics. Demethyl chlorotetracycline is considerable in poor response cases, and mozavaptan hydrochloride is applicable in case of vasopressin-producing tumors. In any case, inappropriate rapid correction of hyponatremia could induce severe brain damage called CPM without careful management.
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PMID:[Treatment for the electrolytic disorders in cancer patients]. 1909

In the present paper, the authors reviews the endocrine and metabolic manifestations in tuberculosis. Disorders as adrenal insufficiency, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypercalcemia, endocrine effects of antituberculous drugs, hypopituitarism, tuberculous involvement of the thyroid gland and pancreas and chest radiograph presentation in diabetes mellitus are discussed. In the literature, several reports support the presence of abnormal calcium metabolism in tuberculosis.
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PMID:[Endocrine and metabolic manifestations in tuberculosis]. 1977 92

The aim of this study was to review all the paraneoplastic syndromes of primary tumours of the oral cavity. Metastatic tumours of the mouth and primary tumours of the oropharynx (including tonsils), and major salivary glands were excluded. The primary search was conducted on PubMed, Scopus and EMBASE, and included every paraneoplastic syndrome from a primary oral tumour described in English, French, or German papers during the last 20 years. The secondary search was conducted by handpicking articles from reviews on paraneoplastic syndromes of the head and neck. The aim of the tertiary search was to identify conditions that had been reported only rarely. We then cross-referenced "mouth neoplasm" with every paraneoplastic condition cited in relevant review articles. We classified the paraneoplastic syndromes that arose from tumours of the head and neck into six categories: endocrine, dermatological, vascular and haematological, rheumatoid, ocular, and neurological. The following conditions are described in this review: syndrome of inappropriate antidiuretic hormone production, hypercalcaemia, hypercalcaemia-leucocytosis syndrome, ectopic production of beta-human chorionic gonadotrophin, Bazex syndrome, Sweet syndrome, tripe palm syndrome, pemphigus, pityriasis rotunda, neutrophilic leukemoid reaction, cerebral venous sinus thrombophlebitis, digital ischaemia, dermatomyositis, necrotising myopathy, autoimmune retinal degeneration, and subacute cerebellar degeneration. Paraneoplastic syndromes of the oral cavity are a heterogeneous group. Most syndromes occur from squamous cell carcinoma and their aetiology is poorly understood. They are important to recognise as they can be the presenting complaint of a malignant tumour, change the prognosis, and considerably reduce the quality of life.
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PMID:Paraneoplastic syndromes in patients with primary oral cancers: a systematic review. 1983 19

A paraneoplastic syndrome is defined as a group of symptoms that develop when substances released by some cancer cells disrupt the normal function of the surrounding cells and tissue. Paraneoplastic renal syndromes are diseases that indirectly compromise tubular and glomerular function by electrolyte imbalance, hormone-producing tumors or deposition of antigen-antibody complexes in the glomeruli. In order to describe the most common paraneoplastic syndromes, which may compromise the renal function, an extensive review was performed of papers, including case reports, guidelines, meta-analysis and other scientific publications. Renal function can be affected by many paraneoplactic syndromes: hypercalcemia in malignancies, syndrome of inappropriate secretion of antidiuretic hormone, tumor lysis syndrome, renin-producing tumors and paraneoplastic glomerulopathies. An early diagnosis and effective treatment might improve quality of life and alter prognosis of these patients.
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PMID:Paraneoplastic syndromes and the kidney. 2022 4


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