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)

Of 61 cases of ibuprofen overdosage reported consecutively to the Rocky Mountain Poison and Drug Center from September 1985 through April 1986, 16 were excluded because of incomplete follow-up or concurrent medication ingestion. A toxic reaction developed in 7 (16%) of the remaining 45 patients. Nausea, vomiting, abdominal cramps, mild central nervous system depression, coma, tachycardia, apnea, metabolic acidosis with or without respiratory alkalosis, hematemesis, and oliguric renal failure were noted. Two of six adults had a toxic reaction, and one died. Among pediatric patients, 5/39 (13%) had a toxic reaction. Of patients whose ibuprofen ingestion was less than 104 mg per kg, none became ill. All patients in whom the time of ingestion was known (six of seven) and who had a toxic reaction did so within four hours of ingestion. An ibuprofen overdose, although usually benign, can occasionally produce serious toxicity.
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PMID:Ibuprofen overdose--a prospective study. 317 71

In an effort to improve the treatment of patients with refractory or recurrent lymphoma, we developed a protocol using cis-platinum combined with two other agents of known efficacy in these disorders but with differing side effects: VP-16 and MGBG. Twenty-six eligible patients were treated with this regimen. There were 15 men and 11 women with a median age of 54 years (22-73), and performance status of 1 (0-3). Their diagnoses were Hodgkin's disease 5 and non-Hodgkin's lymphoma [NHL] 21 which included 11 with diffuse histocytic lymphoma [DHL]. The median number of chemotherapy regimens was 2 (1-5); 12 also received radiotherapy. Twenty patients are evaluable for response: 15 NHL and 5 Hodgkin's disease. Three patients, all of whom had DHL entered complete remission (20%) with a median time to treatment failure of 7 1/2 months. Six NHL (40%) and one Hodgkin's disease (20%) patients entered a partial remission. There were three early deaths: one due to progressive disease, one to acute respiratory failure, and one with disease status undocumented. Toxicity included leukopenia, thrombocytopenia, anorexia, nausea, vomiting, stomatitis, alopecia, renal failure, profound peripheral neuropathy, and hypersensitivity vasculitis. Treatment was stopped because of the latter two. These agents are non-crossresistant with doxorubicin-containing regimens. The drugs are possibly synergistic and modestly active with moderate to severe toxicity.
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PMID:Cisplatin, VP-16-213 and MGBG (methylglyoxal bis guanylhydrazone) combination chemotherapy in refractory lymphoma, a phase II study. 319 89

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.
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PMID:[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage]. 322 Oct 52

The management of the patient presenting to the Emergency Department with nephrolithiasis or renal colic should include evaluation of the patient for concurrent diseases, risk factors for stone formation, and possible etiologies for stones. Suspicion of ureterolithiasis is based on a cogent history and physical examination and reinforced by a finding of hematuria. Diagnosis should be based upon a promptly performed intravenous pyelogram, unless the patient is truly allergic to contrast media or has substantial risk of a contrast-induced renal failure. A solitary flat plate of the abdomen adds no useful information and is an unnecessary expense to the patient. Essential laboratory data include a urinalysis, CBC, and electrolyte, BUN, creatinine, and serum calcium levels. A urine culture should be obtained in all patients because urinalysis alone may not be sufficient to exlude a urinary tract infection. Initial treatment of the patient with an uncomplicated renal colic should include hydration, relief of pain, and reassurance. Evaluation by a consultant may be done as an outpatient on a nonemergent basis. If the colic has not resolved after 72 hours, hospitalization generally is recommended. If the patient has vomiting, dehydration, a complete obstruction, or a solitary kidney, hospitalization in indicated and urgent consultation recommended. If the patient has fever or other signs of infection, emergent consultation and immediate hospitalization are essential. Retained obstructing stones are generally managed by urologic consultants. It is in the care of the patient with the retained stone that greatest advances have been made in the past 10 years. Patients should be counseled that the retained stone no longer calls for extended hospitalization and convalescence.
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PMID:Nephrolithiasis. 329 30

Two years and 10 months after gastrectomy, a 38-year-old man was diagnosed as having carcinomatous peritonitis due to gastric cancer. He was treated by intra-abdominal administration of 100 mg CDDP three times in addition to UFT. After each administration of CDDP, the amount of ascites and the serum value of CEA were decreased. Subjective symptoms, such as epigastric pain or sensation of fullness, were also improved. Although one year and 8 months has passed since the first administration of CDDP, the performance status of the patient remains 0. Nausea or vomiting was noted within 2 days after each administration. However, severe complications, like renal failure or intra-abdominal hemorrhage, were not observed. These findings suggest that repeated intra-abdominal administration of CDDP may be a useful therapy for carcinomatous peritonitis due to gastric cancer.
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PMID:[Repeated intra-abdominal administration of CDDP in carcinomatous peritonitis due to gastric cancer--a case report]. 336 74

The records of 147 cancer patients who received at least three courses of cisplatin-containing chemotherapy in the Arizona Cancer Center clinic between 1982 and 1985 were reviewed to determine the safety and tolerance of cisplatin administered in the outpatient setting. Cisplatin was administered at doses of 50-120 mg/m2 every 3-4 weeks. The drug was added to 400 ml of 10% mannitol, was brought up to 1-L volume with normal saline containing 3 g of magnesium sulfate, and was administered iv over 1 hour. An additional liter of normal saline was administered over approximately 1 hour in patients who received cisplatin doses of 70-120 mg/m2. Courses were interrupted if the serum creatinine was greater than 1.5 mg/dl just prior to the next scheduled dose. The median total doses of cisplatin per patient were 487, 595, and 683 mg/m2 and complete plus partial response rates were 64%, 71%, and 78% for those patients who received 50-60, 70-90, and 100-120 mg/m2/course, respectively. Cisplatin-containing therapy was tolerated without evidence of renal failure and with only moderate to severe emesis in 25% of the patients. Calculated creatinine clearances dropped only 4.9%, 13.9%, and 14.9% between Courses 1 and 6 in patients receiving cisplatin doses of 50-60, 70-90, and 100-120 mg/m2, respectively. We conclude that cisplatin doses of 50-120 mg/m2 can be administered safely and with acceptable tolerance in the outpatient setting.
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PMID:Safe, rapid administration of cisplatin in the outpatient clinic. 353 27

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

Acute fatty liver of pregnancy, or Sheehan's syndrome, is a rare complication of pregnancy, occurring in about 0.5% cases of jaundice in pregnancy. The anatomo-clinical picture and the biology of the condition is described using as basis a personal case history and the 28 cases to be found in the French literature. The condition shows, vomiting, abdominal pain and tachycardia in an apyrexial patient in the 3rd trimester of the pregnancy in which the disease occurs. The date shows itself a few days after the prodromal symptoms and is characterised by the triad of pruritus, jaundice and encephalopathy. All cases show an increased white blood count and hyperbilirubinaemia. If the condition goes on to become very serious one has to look for signs of haemorrhage and of liver and renal failure. Liver biopsy confirms the diagnosis. Prognosis will be improved if moderate forms are recognized early and if the condition is watched carefully. It may be necessary to stop the pregnancy before the serious conditions of the illness show up. Labour induced at the 37th week after checks had been made for fetal pulmonary maturity seemed to be a good way of treating the condition even if it has not yet become desperate. The final prognosis for the mother and the baby is always favourable if the baby is born alive.
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PMID:[Acute hepatic steatosis of pregnancy. Apropos of a case and review of the French literature]. 359 1

A patient with longstanding diabetes and renal failure presented with painless vomiting due to duodenal obstruction was found to have an annular pancreas. Initial operative evaluation, later pathologically confirmed, demonstrated involvement of not only the annulus, but also the entire gland by diffuse atrophic chronic pancreatitis. We speculate on the possible influence of the underlying diabetes and renal disease on the pathogenesis of the unusual generalized chronic inflammatory changes and the precipitation of duodenal obstruction in this patient.
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PMID:Annular pancreas associated with diffuse chronic pancreatitis. 360 30

In the second part of this review of mushroom poisonings, the syndromes with intermediate and long lag-times are discussed. They include the coprinus-, phalloides-, gyromitrin- and the orellanus syndrome. The coprinus syndrome occurs whenever alcohol is consumed after a meal containing coprine. The lag-time varies according to the amount and time of alcohol intake. It is very similar to the disulfiram syndrome which is known from the adverse therapy of alcoholism. The lag-time of the phalloides syndrome varies between 7 and 24 hours. It starts with massive gastroenteritis followed by hepatopathia which can lead to hepatic coma and kidney failure. The phalloides syndrome is caused by the amatoxins of the death caps, which inhibit the RNA Polymerase B in the nucleus of the liver cell. The gyromitrin syndrome exhibits also a delayed onset. The hepatotoxicity and the nephrotoxicity are less severe than in the phalloides syndrome. The first metabolite of gyromitrin monomethylhydrazin is responsible for CNS-symptoms such as delirium and convulsions. In contrast to the phalloides syndrome vomiting can be the only leading symptom in gyromitrin poisoning. The orellanus syndrome has the most delayed onset of all mushroom poisonings with 1-3 weeks. It should be thought of in all cases of kidney insufficiency of unknown origin. The orellanines damage the kidney and induce all degrees of kidney insufficiency according to the amount of ingested poison. Terminal kidney failure which requires hemodialysis treatment can occur in severe cases.
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PMID:[Diagnosis and therapy of mushroom poisoning (II)]. 361 14


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