Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two children, ages 13 2/12 and 6 6/12 years, with osteogenesis imperfecta were treated with salmon calcitonin. During the course of therapy the older child developed calcitonin dose-related hypomagnesemia on two occasions. The younger child, coincident with otitis media and vomiting, developed hypomagnesemia, hypophosphatemia, hyponatremia, and hypokalemia. Since rib biopsies obtained before and after one year of treatment with salmon calcitonin failed to demonstrate any histologic changes, therapy was discontinued because of the induced metabolic consequences of calcitonin therapy.
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PMID:Calcitonin therapy of children with osteogenesis imperfecta. 56 30

Possible local and systemic adverse effects following administration of salmon (sCT) and human (hCT) calcitonin (CT) have been evaluated in a double-blind, within-subject, comparative trial in 30 young, healthy volunteers. Each subject received 0.25 and 0.5 mg hCT and 100 IU sCT s.c.. Adverse effects and hypocalcaemia were recorded 1, 3 and 6 h after each injection. Significantly fewer local adverse reactions were observed after hCT (20 or 33%) than after sCT (80%), possibly due to the different vehicles employed (mannitol solution and acetic acid). The most frequent systemic adverse effects were gastrointestinal (nausea, vomiting), which occurred in 80% after 1 h, independently of the CT--preparation used. Hypocalcaemic changes were generally small and lasted longer after sCT. It is concluded that the hCT preparations were better tolerated locally than sCT in young, healthy volunteers, and that there were no differences in the systemic side effects or hypocalcaemic activity.
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PMID:Superior local tolerability of human versus salmon calcitonin preparations in young healthy volunteers. 174 38

We report our experience of the presentation and management of symptomatic hypercalcaemia in advanced lung cancer. Between 1981 and 1987, 55 patients required urgent admission due to rapid clinical deterioration accompanied by significant hypercalcaemia (greater than 2.75 mmol l-1). Forty patients (72%) had squamous cell cancer, five small cell, three large cell, two adenocarcinoma and five unclassified. Thirty-five had evidence of bony metastases. Symptoms were categorized for each patient on the basis of being either potentially attributable to hypercalcaemia or not. All patients were rehydrated but specific treatment schedules over the period varied [1981-1985: steroids, calcitonin, mithramycin; 1985-1987: aminohydroxypropylidene bisphosphonate (APD)]. Treatment resulted in a significant reduction in the prevalence of all systems except for pain and nausea/vomiting; the greatest effect being seen on central nervous system and renal tract symptoms (75 and 80% reduction respectively; P less than 0.005 pre- versus post-treatment). Overall, 45 patients (82%) had a biochemical response; serum calcium fell from 3.28 +/- 0.33 mmol l-1 (mean +/- SE) to a nadir of 2.54 +/- 0.36 mmol l-1 (P less than 0.001). Twenty-five (49%) patients were discharged home. We conclude that despite the poor life expectancy of this group of patients (median survival 42 days) treatment of hypercalcaemia is worthwhile as it results in a significant symptomatic improvement.
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PMID:Symptomatic hypercalcaemia in lung cancer. 183 17

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

Although the incidence of obesity in the domesticated dog is high, few studies have investigated the regulation of food intake in this species. In the present study we investigated the response of the dog to a number of putative satiety agents including cholecystokinin (CCK), bombesin, calcitonin and naloxone. CCK significantly suppressed food intake during a scheduled fifteen minute meal in intact dogs and in dogs receiving total subdiaphragmatic vagotomies. Emesis occurred following injection of higher doses of CCK in most dogs. Bombesin and calcitonin reduced intake in both normal and vagotomized dogs, although higher doses of calcitonin were needed to significantly suppress feeding in vagotomized dogs compared with intact animals. Naloxone reduced feeding by as much as 60% in intact and vagotomized animals. Glucagon suppressed feeding in intact dogs, but not in vagotomized animals. Somatostatin and pancreatic polypeptide did not alter food intake. Thus the domesticated dog responds somewhat differently to some neuropeptides compared with the laboratory rat stressing the importance of examining the regulation of food intake across species.
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PMID:Peptidergic regulation of feeding in the dog (Canis familiaris). 614 23

Synthetic human calcitonin was used in the treatment of 26 patients over a period of 1-14 months. 17 patients had Paget's disease of the bone, 6 postmenopausal osteoporosis and 3 Sudeck's syndrome. Subjective improvement (reduction of pain, improvement of mobility) was found in 15 patients with Paget's disease, in 4 females with postmenopausal osteoporosis and in all 3 patients with Sudeck's syndrome. Radiographic improvement of bone changes developed only very slowly. These results were confirmed by diminution of the exchangeable calcium pool indicating reduction of rates of osseous degradation. Calcitonin tolerance was acceptable. Transitory nausea and occasional vomiting occurred in 3 patients.
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PMID:[Synthetic human calcitonin in Paget's disease of bone and osteoporosis (author's transl)]. 616 31

In a 32-year-old woman presenting with fever, vomiting and right upper abdominal pain a tumor of the papilla of Vater was detected endoscopically and removed surgically. Histologically it was a carcinoid shown immunohistochemically to produce calcitonin. The tumor had metastasized to a lymph node in the hepatoduodenal ligament. Clinically the patient showed typical signs of von Recklinghausen neurofibromatosis. A survey of the literature suggests that carcinoid of the papilla of Vater may be more frequent in patients with neurofibromatosis. Possible relationships between neurofibromatosis and carcinoid are discussed in the light of the pertinent literature.
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PMID:[Calcitonin-producing duodenal carcinoid in Recklinghausen's neurofibromatosis. Clinical case report and review of the literature]. 641 May 2

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Effects of synthetic eel (E-), salmon (S-), and human (H-) calcitonin (CT) on gastrointestinal motility were studied in conscious beagle dogs, which had been implanted with strain gauge force transducers. Intramuscular administration of E-, S-, or H-CT interrupted gastric migrating motor complexes, digestive pattern, and gastric emptying. The order of potency was E-CT = S-CT > H-CT. Motor inhibition induced by CT occurred independently of plasma immunoreactive motilin levels or hypocalcemia. In addition, E-CT and S-CT induced vomiting without a retrograde giant contraction (RGC) during the postprandial state. Apomorphine or CuSO4 initiated RGC prior to vomiting. RGC induced by apomorphine was inhibited by pretreatment with E-CT as well as hexamethonium, atropine, or surgical vagotomy. E-CT showed no inhibitory effect on nicotine stimulated contraction of isolated guinea-pig ileum. These results suggest that peripherally administered CT inhibits canine gastrointestinal motility at the central nervous system level by lowering vagal activity.
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PMID:Gastrointestinal motor inhibition by exogenous human, salmon, and eel calcitonin in conscious dogs. 760 Apr 51


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