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)

A 59-year-old man with a 30-year history of type 2 diabetes mellitus presented with fatigue, confusion, and weight loss over a 3-month period. He was found to be hypercalcemic (11.8 mg/dL) and dehydrated, and his hypercalcemia improved with intravenous fluids. While in the hospital, he developed hyponatremia, hypoglycemia, and hypotension. He was found to have a subnormal cortisol level of 2.3 microg/dL at baseline, which increased to only 5.6 microg/dL 60 minutes after a 250-microg corticotropin intravenous stimulation test. The patient developed pneumonia and adult respiratory distress syndrome and died of an acute myocardial infarction. During the autopsy, he was found to have lymphocytic hypophysitis with a severe reduction in corticotropin-producing anterior pituitary cells. No malignancy was identified at autopsy. He is the first male patient to be described in the literature who presented with hypercalcemia caused by lymphocytic hypophysitis.
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PMID:Lymphocytic hypophysitis in a man presenting with hypercalcemia. 1126

Tumor markers used in the diagnosis and follow-up of patients with neuroendocrine tumors are in most instances not specific for a given tumor and circulate under normal conditions in the serum, making their use as an early diagnostic tool difficult (low sensitivity). By combining hormone measurements with tissue responsiveness, demonstrations of inappropriate secretions of PTH, insulin, and gastrin during hypercalcemia, hypoglycemia, and hyperacidity, respectively, become highly sensitive and specific diagnostic tests. The application of polyclonal antibodies in RIAs of hormones, such as ACTH, insulin, and gastrin, increase the diagnostic level of hormone measurements in patients with neuroendocrine tumors. Other markers, such as chromogranin A, neuron-specific enolase, and alpha-subunit, as well as peptide receptor visualization, are of increasing importance in the diagnosis and follow-up of neuroendocrine and non-neuroendocrine tumors.
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PMID:Neuroendocrine tumor markers. 1158 55

Subcutaneous fat necrosis of the newborn is an uncommon, self-limited panniculitis of neonates. Rare complications such as hypercalcemia, thrombocytopenia, hypertriglyceridemia, and hypoglycemia have been reported. We describe the first case where all of the above complications were encountered in the same infant. Physicians caring for infants with subcutaneous fat necrosis of the newborn should be aware of the above associations in order to provide prompt and appropriate treatment to prevent associated, undesirable sequelae.
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PMID:Complications of subcutaneous fat necrosis of the newborn: a case report and review of the literature. 1278 78

Cancer has many effects on the veterinary patient. One group of syndromes that must be paid particular attention to is the paraneoplastic diseases. These are a group of changes that occur in the body at sites distant from the actual tumor. Paraneoplastic syndromes can affect many different body systems. Paraneoplastic diseases are important to recognize for many reasons. Often the paraneoplastic change is the earliest indication of cancer and, thus, neoplasia must be included on any differential list when typical paraneoplastic changes are found in the routine medical work-up. Paraneoplastic syndromes can also be used as markers of remission. Many of the paraneoplastic changes will disappear when remission is achieved, and will reappear once the period of remission had come to an end. Identification of paraneoplastic changes is also important in that often they must be treated before treatment of the primary disease can occur. Treating the remote effects of cancer will increase quality of life. Although many different paraneoplastic syndromes exist, hypercalcemia, hypoglycemia, cachexia and anemia are the most clinically significant in the veterinary patient. Chronic treatment most commonly involves removal or treatment of the primary or inciting neoplastic process. The acute treatment of these syndromes can occur quickly. Rapid identification and treatment will allow the patient to have a better prognosis and will help to improve quality of life.
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PMID:Common paraneoplastic syndromes. 1283 Oct 75

Clinical syndromes occasionally associated with or heralding cancer are summarized and classified.Some tumours present with manifestations of an endocrine or endocrine-like action; included in this group are thymomas, non-beta-cell tumours of the pancreas and carcinoids. Cushing's syndrome, hypoglycemia, hypercalcemia, polycythemia and gynecomastia have been produced by a wide variety of tumours. Tumour emboli, non-bacterial thromboendocarditis and thrombophlebitis occasionally occur, but thrombophlebitis is not so frequent as was previously considered. Neurological syndromes are rare and show a great variety of presentations. Other occult manifestations of cancer include hypertrophic pulmonary osteoarthropathy, various skin diseases, obscure pyrexias and, in Hodgkin's disease, pain secondary to alcohol consumption.
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PMID:Occult manifestations of cancer. 1395 5

Tumours of non-endocrine origin may exert deleterious effects by elaborating active principles which disturb body regulation. Systemic manifestations are fairly common with neoplasms of the lung, kidney, gastro-intestinal tract and thymus. The secretion of these tumours may have a known chemical structure (serotonin), may present hormone-like action (parathormone, antidiuretic hormone, insulinoid), or have well-defined biological properties (erythropoietin, gastrin-like principle). Tumours may stimulate endocrine glands by an unknown mechanism, producing disorders such as Cushing's syndrome, hypercalcemia, gynecomastia and hypoglycemia. Thymomas may be associated with autoimmune diseases. Tumours may extensively utilize or excrete some metabolite (glucose) or electrolyte (Na or K). Awareness of the systemic effects of various neoplasms may lead to an early diagnosis and proper treatment of these manifestations.
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PMID:SYSTEMIC EFFECTS OF NON-ENDOCRINE TUMOURS. 1420 55

An 89-year-old male patient on hemodialysis presented clouding of consciousness caused by hypoglycemia during taking an anti-diabetic agent. His somnolent state continued in spite of glucose dispensation, and parental nutrition was started by a nasogastric tube because he couldn't have peroral ingestion. Though his blood glucose level recovered normal, his consciousness disorder was suspended, and he showed remarkable hypercalcemia. He was dosed with elcatonin, and the parental nutrient was changed to the other one that contained less vitamin D and calcium, and so his serum calcium level diminished slowly but he showed drowsiness about a month long. After resumption of peroral ingestion, his consciousness restored to the former condition rapidly. This case suggests that careful observation is needed in less active dialysis patients with parental nutrition because nutrient-contained vitamin D and calcium, which doesn't harm patients without renal insufficiency, may cause hypercalcemia.
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PMID:[Hypercalcemia complicated with status nervosus in an elderly patient on hemodialysis during parental nutrition]. 1574 2

We can define paraneoplastic syndromes as a combination of effects occurring far from the original location of the tumour and independently from the local repercussion of its metastases. Paraneoplastic hormonal syndromes depend on the secretion of hormonal peptides or their precursors, cytokines and, more rarely, thyroidal hormones and Vitamin D, which act in an endocrine, paracrine or autocrine way. Sometimes, paraneoplastic syndromes can be more serious than the consequences of the primary tumour itself and can precede, develop in parallel, or follow the manifestations of this tumour. It is important to recognise a paraneoplastic hormonal syndrome for several reasons, amongst which we would draw attention to three: 1) It can lead to the diagnosis of a previously undetected, underlying malign or benign neoplasia; 2) It can dominate the clinical picture and thus lead to errors with respect to the origin and type of primary tumour; and 3) It can follow the clinical course of the underlying tumour and thus be useful for monitoring its evolution. The molecular mechanisms responsible for the development of these syndromes are not well-known, but it is believed that they might be inherent to the mutations responsible for the primary tumour or depend on epigenetic factors such as methylation. In this review, we consider the following paraneoplastic hormonal syndromes: malign hypercalcaemia, hyponatraemia (inappropiate secretion of the antidiuretic hormone), ectopic Cushing's syndrome, ectopic acromegaly, hypoglycaemia due to tumours different from those of the islet cells and paraneoplastic gynaecomastia; we make a brief final reference to other hormones (calcitonin, somatostatin, and VIP).
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PMID:[Paraneoplastic hormonal syndromes]. 1615 18

233 SD rats weighing 100 approximately 120 g were divided randomly into 6 groups. The animals in group I and group II received 0.1 mg/kg selenium in the form of sodium selenite only and served as the negative control and positive control, respectively. Animals in groups III, IV and V were fed with selenium as Se-enriched malt supplemented diets (0.3, 1 and 3 mg/kg), and group VI with selenium by using sodium selenite supplemented diets (3 mg/kg). Animals of groups II approximately VI were induced hepatoma by diethylnitrosamine (100 mg/l) for 16 weeks, then drunk with sterilized water for 2 more weeks. Subsequently, the effects of Se-enriched malt and sodium selenite on hepatoma nodules, relative liver weight, the liver function indices including alanine aminotransferase (ALT), alkaline phosphatase (ALP), albumin (ALB), total bilirubin (TBIL), and the tumor markers, named as gamma-glutamyltranspeptidase (GGT), alpha-fetoprotein (AFP), insulin-like growth factor-II (IGF-II) were recorded. The calcium concentration, glucose content in plasma and values of the hormones regulating blood glucose, such as insulin, glucagons and thyroid hormones (3,5,3'-tetraiodothyronine, T(3); 3,5,3'5'-tetraiodothyronine, T(4)) were observed as well. At the same time, the correlations between the concentration of plasma glucose and related hormones were also analyzed. The results indicated that Se-enriched malt showed a better chemopreventive efficiency in decreasing the number of hepatoma nodules, relative liver weight and the contents of AFP, GGT, IGF-II, ALT, ALP and TBIL in the plasma, and delaying the descent of hormones in the serum, names as insulin, glucagons, T(3) and T(4) than those feeding with sodium selenite. Effect of Se-enriched malt excelled sodium selenite in the aspects of deadening the descent of glucose concentration in the plasma and the rise of calcium concentration in the serum of the rats with hepatoma induced by diethylnitrosamine. The values of glucose and calcium were significantly related to those items fore-named. In conclusion, the function of Se-enriched malt in deadening the lesion and delaying the development of hepatoma of rats induced by diethylnitrosamine was better than that of sodium selenite. Hypoglycemia and hypercalcemia were significantly correlated with the multifactors mentioned above.
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PMID:Effect of selenium-enriched malt on hepatocarcinogenesis, paraneoplastic syndrome and the hormones regulating blood glucose in rats treated by diethylnitrosamine. 1626 26

Life-threatening metabolic complications observed in cancer patients are: hypercalcaemia, hyponatremia, hyperurcaemia, tumour lysis syndrome, hypoglycaemia, hyperuremia and hypercreatininemia secondary to renal failure, hyperammoniemia, lactic acidosis and adrenal failure. They may be associated with any kind of neoplastic disease causing dysfunction of vital organs, which can be determined by neoplastic spread, anti-cancer treatment or, more rarely, by paraneoplastic phenomena. The clinical presentation of metabolic complications is typically aspecific. Encephalopathy, raging from mild confusion to coma, is the most common and clinically most severe symptom. The severity of consciousness impairment is related to both the rate of onset and the magnitude of the metabolic disorder. The definitive diagnosis will be established by laboratory examination and radiological work-up. Cancer patients presenting metabolic should be referred to oncologic departments or intensive care units. The treatment of metabolic disorders include: prophylactic measures, emergency measures to preserve vital functions and to restore biological parameters and the treatment of the underlying primary.
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PMID:Metabolic emergencies. 1633 7


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