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)

The physiopathology of malnutrition among AIDS, ARC and HIV infected children was reviewed. One-hundred eight-three newborns were studied, 152 of which were born at "La Fe" Maternity Hospital. Of these patients, 29% were LBW and 28% preterm. Transfused and hemophiliac patients were excluded from the study. Anorexia, vomiting, fever, infections of the respiratory and GI tracts and drug therapy were the most frequent factors affecting the nutritional status. Fifty-three newborns were infected with the HIV (29%). The children were classified into three groups (G). Group-I was formed by HIV+children > 18 months of age, G-II, P-2 class by children < 18 months of age and G-III was formed by those children that died of AIDS. The most common symptoms were chronic diarrhea and infections of the respiratory tract. Of the HIV+children > 18 months of age, 65% had a weight < the 10th percentile and 61% were < the 10th percentile for height. Of the children that died of AIDS, 80% were in the lower 10th percentile for both weight and height. Hemoglobin, T4/T8, total proteins, seroalbumin and calcium were also negatively affected. Those most severely affected were the dead patients, followed by P-2 < 18 months and finally the HIV+ > 18 months of age. The differences between G-I and G-II-G-III were statistically significant, p < 0.01. The biochemical quantification of the nutritional status was difficult due to the limited amount of blood available. HIV infected children require nutrition supplementation to maintain an adequate nutritional status. Among these patients, malnutrition is a multifactorial phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nutritional status in HIV infection in infancy]. 145 14

Foscarnet (Foscavir) is an antiviral drug for intravenous (i.v.) treatment of cytomegalovirus (CMV) retinitis in immunocompromised patients. The drug forms complexes with divalent metal ions such as Ca2+ and serum calcium levels may be affected during its i.v. infusion. In this study, the effect on calcium homeostasis was investigated during daily 8-hr infusions of foscarnet in dogs. After priming infusions of 40 or 80 mg/kg administered during 0.5 hr, maintenance infusion rates were 46 or 91 mg/kg/hr (total daily doses of 410 or 810 mg/kg). At the low infusion rate, foscarnet was administered for 5 consecutive days. The mean plateau serum concentration was 0.56 mmol/liter and the main clinical sign was vomiting. Total serum calcium was reduced from about 2.5 to 2.0 mmol/liter and ionized calcium from 1.3 to 0.9 mmol/liter. Parathyroid hormone (PTH) levels in serum were elevated three to six times while calcitriol (1,25-(OH)2D3) levels were unaffected. At the high infusion rate, treatment was discontinued after 1-2 days of dosing due to pronounced adverse clinical signs such as extensive vomitings, apathy, ataxia, and muscle spasms. The mean serum plateau concentration of foscarnet at this dose level was 1.2 mmol/liter. Total serum calcium was reduced from 2.5 to 1.6 mmol/liter and ionized calcium from 1.3 to 0.7 mmol/liter. PTH as well as 1,25-(OH)2D3 levels in serum were elevated. Total and ionized calcium levels were normalized within 16 hr after stopping drug treatment. The results showed that foscarnet infusion affects calcium homeostasis and that calcium monitoring might be considered in the clinical use of the drug.
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PMID:Hypocalcemia induced by foscarnet (Foscavir) infusion in dogs. 153 76

The drugs used in migraine therapy can be divided into two groups: agents that abort an established migraine attack and agents used prophylactically to reduce the number of migraine attacks. Both groups have drugs that are specific for migrainous headaches and that are non-specific, and are used to treat the accompanying headache (analgesics), vomiting (anti-emetics), anxiety (sedatives and anxiolytics), or depression (antidepressants). The main drugs with specific action on migraine include ergot alkaloids (ergotamine, dihydroergotamine), agonists (sumatriptan) or partial agonists (methysergide) at a specific subtype of 5-HT1-like receptors, beta-adrenoceptor antagonists (propranolol, metoprolol), calcium antagonists (flunarizine) and anti-inflammatory agents (indomethacin). The pharmacological basis of therapeutic action of several of these drugs is not well understood. In the case of the ergot alkaloids and 5-HT1-like receptor agonists, however, it is likely that the antimigraine effect is related to the potent and rather selective constriction of the large arteries and arteriovenous anastomoses in the scalp and dural regions. In addition, these drugs inhibit plasma extravasation into the dura in response to trigeminal ganglion stimulation, but it is possible that this effect is related to the selective vasoconstriction in the extracerebral vascular bed. The selectivity of the pharmacological effects of these antimigraine drugs (constriction of the extracerebral arteries and arteriovenous anastomoses, poor penetration into the central nervous system and the absence of an antinociceptive effect even after intrathecal administration) strongly suggests that excessive dilatation in the extracerebral cranial vasculature, probably initiated by a neuronal event, is an integral part of the pathophysiology of migraine.
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PMID:Pharmacology of antimigraine drugs. 164 88

A diagnosis of cholecalciferol toxicity in a young dog was made on the basis of adequate history and the finding of extremely elevated serum calcium levels. The traditional treatment of fluid therapy, diuresis and corticosteroids resulted in lowering the serum calcium levels over a 5-d period. The dog displayed clinical signs of severe depression, anorexia and intermittent vomiting during this time interval. Serum calcium levels rose on day 6 and remained elevated up until the dog was euthanized on day 9. Gross and histopathological examinations revealed diffuse metastatic mineralization throughout the body, particularly involving the lung, kidney, atria and stomach. The amount of cholecalciferol ingested was determined well below the lethal dose reported in dogs. This report indicates that young dogs may be much more susceptible to the lethal effects of this compound than initially believed.
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PMID:Accidental ingestion of a cholecalciferol-containing rodent bait in a dog. 165 54

Isolated segments of the guinea-pig small intestine were vascularly perfused and the release of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) into the portal venous effluent determined by high pressure liquid chromatography with electrochemical detection. Release of acetylcholine from isolated superfused intestinal segments was determined as outflow of [3H]radioactivity from preparations preincubated with [3H]choline. Cisplatin (3 microM) increased the outflow of 5-HT and 5-HIAA by about 90%. At 30 and 100 microM cisplatin decreased the outflow of 5-HT and its metabolite by 40%-50%. The stimulatory effect of cisplatin was consistently observed only when the bicarbonate-phosphate buffer of the Tyrode's solution was replaced by HEPES-buffer. The stimulatory effect of cisplatin was abolished in the absence of extracellular calcium or presence of tetrodotoxin (1 microM). The stimulatory effect of cisplatin was also prevented by hexamethonium (100 microM) or scopolamine (100 nM). The 5-HT3 receptor antagonists ondansetron and ICS 205-930 in concentrations as low as 1 pM also abolished the stimulatory effect of cisplatin. The 5-HT3 receptor antagonist MDL 72222 prevented the stimulatory effect of cisplatin only at a concentration of 1 microM. None of the 5-HT3 receptor antagonists alone significantly altered the outflow of 5-HT and 5-HIAA. Cisplatin (3 microM) enhanced the outflow of [3H]radioactivity from intestinal segments and caused longitudinal muscle contractions that were abolished by 100 nM scopolamine. In conclusion, cisplatin, at concentrations which occur during anti-cancer therapy in humans and induce emesis, increases the release of 5-HT from the enterochromaffin cells of the small intestine of the guinea-pig.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cisplatin increases the release of 5-hydroxytryptamine (5-HT) from the isolated vascularly perfused small intestine of the guinea-pig: involvement of 5-HT3 receptors. 171 32

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

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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PMID:Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs. 188 58

Survival following attempted suicide in a 50-year-old man by ingestion of 12.4 g of mexiletine, 620 mg of nifedipine and 50 to 100 tablets of sublingual nitroglycerine 1:150 is reported. Initial presentation was that of mental obtundation, vomiting, tonic-clonic seizure, high-degree atrioventricular block, profound vasodilation and cardiovascular collapse. Treatment consisted of intravenous calcium gluconate and aggressive fluid management. Maintenance of cardiovascular stability required continuous infusion phenylephrine, dopamine and epinephrine. The patient made a full recovery and was medically discharged on the fourth hospital day. This case represents the largest overdose of mexiletine to date to end in patient survival.
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PMID:Survival following severe overdose with mexiletene, nifedipine, and nitroglycerine. 189 1

A 36-year-old woman had for two months experienced progressively more marked diffuse abdominal pain, at times colicky, as well as nausea, vomiting and severe constipation. In addition, paraesthesias and motor weakness developed in the thighs. This was accompanied by a normochromic, normocytic anaemia with a haemoglobin concentration of 9.6 g/l. A short time later her mother and daughter also fell ill with similar symptoms. After symptomatic treatment had failed, secondary coproporphyria due to lead poisoning was found. The poisoning had resulted from criminal contamination of food, especially of cocoa powder, with lead acetate. Raised lead concentrations in serum were found in two other members of the family. In all the patients treatment was undertaken with sodium calcium edetate (20 mg/kg body-weight) in several three-day cycles, achieving a gradual fall in serum lead concentration. When the level had fallen to below 4 mumol/l the symptoms disappeared. Below 3 mumol/l porphyria was no longer demonstrable and the anaemia regressed. It is pointed out that, as lead poisoning may be fatal, it should be considered in the differential diagnosis of acute abdominal colic of unclear cause.
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PMID:[Acute lead poisoning]. 189 43

The clinical suitability of conventional glyceromonooctanoin (GMOC) and ethylenediaminetetraacetic acid (EDTA) containing solvents for the dissolution of common bile duct stones is questionable. To improve the solvent-stone contact and the miscibility with bile, GMOC was hydrophilized by the addition of polyethyleneglycol-caprylglyceride, polyethyleneglycol-sorbitan-etheroleyl-ester, and polyethyleneglycol-sorbitanlauryl-ester (PEG-GMOC). This product was mixed with a bile acid-EDTA (BA-EDTA) solution in a ratio of 1:2 (v/v) for cholesterol solubilizing and calcium complexing capacities. To determine clinical efficiency, the new solvent was infused via a nasobiliary tube in 16 patients with endoscopically nonextractable common bile duct stones and compared with a group of 16 patients treated with an alternating GMOC/BA-EDTA regimen. Continuous perfusion with PEG-GMOC-BA-EDTA led to a total (12 patients) or partial (3 patients) disappearance of the stones within 2-15 days. Similarly, alternating GMOC and BA-EDTA treatment dissolved the stones in 12 patients. The average volume of PEG-GMOC-BA-EDTA infused contained only 27% of the GMOC applied during the alternating therapeutic regime. This reduction of the GMOC dose was associated with a significant reduction of adverse effects such as emesis, diarrhea and biliary pain. We concluded that GMOC is equally efficient in the new hydrophilized form but it is clearly superior as far as side effects are concerned. In all, this supports its clinical suitability for the dissolution treatment of common bile duct stones.
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PMID:Dissolution of bile duct stones by a hydrophilized glyceromonooctanoin-bile-acid-EDTA emulsion. 190 80


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