Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over a period of 18 months the development of hepatitis after intake of oxyphenisatin, a laxative, was established in 14 patients by re-exposure to the drug. The characteristic feature was nonspecific upper abdominal pain up to colic-like pain, lact of appetite, nausea or vomiting, and pruritus. The biochemical changes were those of chronic hepatitis with varying severity of biliary stasis and abnormal immunofluorescence. On re-exposure there was a particularly remarkable rise in GLDH activity. The histological picture showed acute inflammatory changes in the biliary passages on re-exposure, while the liver cells were clearly involved only secondarily. At a latter point the histological picture became non-specific. At laparoscopy there were different stages of minor periportal hepatic fibrosis to marked postnecrotic liver scars with portal hypertension and decompensation. Early diagnosis is difficult but crucial to the patient's fate, because this form of hepatitis regresses completely after oxyphenisatin has been stopped. Laxatives containing this drug should be withdrawn from the market.
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PMID:[Oxyphenisatin-induced liver disease (author's transl)]. 12 99

After a brief survey of the expected advantages of the early interruption of pregnancy by the Karman method, the author describes his own observations on immediate and early complications in 850 cases. In the course of intervention, 7.45% of the patients reacted with a vegetative manifestation of cervical shock--pallor, nausea, vomiting, colic-like pain in the lower part of the abdomen (mainly in nullipara). The aspirated amount of material did not surpass 50 ml in women with amenorrhea of 40-45 days duration. The mean duration of the aspiration was 1 minute, 57 seconds. There was menstruation-like bleeding from day 3 to days 10-12 in 86.3% of the women with interruption of pregnancy. Its occurrence in 2.49% of the patients was preceded by colic-like pain and shortlived elevation of axillary temperature up to 38oC. Inflammatory complications were registered up to the 2nd month in 2.49% of the 79.3% followed. The aspiration system with the hand vacuum extractor (Malstrom type) was used successfully for creating negative pressure and thus the special syringe (Karman type) was replaced.
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PMID:[Early artificial termination of pregnancy by Karman's method]. 65 60

One fatal and 1 nonfatal case of Japanese pieris (Pieris japonica) poisoning in goats prompted experimental feeding of the plant at 0.1% of a healthy goat's body weight. Clinical signs observed included colic and nausea. The principal necropsy finding was inhalation pneumonia.
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PMID:Japanese pieris poisoning in the goat. 67 56

A prospective double-blind study was performed to compare metoclopramide (Primperan) with morphatropin in the treatment of ureteral colic. Twenty-one patients (10 in the morphatropin group and 11 in the metoclopramide group) entered the study and diagnosis was confirmed radiologically. Using the Mann-Whitney rank sum test, no significant difference was found in the pain-relieving effect 10, 20, or 30 min after treatment with either 1 ml morphatropin s.c. or 20 mg metoclopramide i.v. Two patients in the morphatropin group developed nausea and giddiness, respectively, and 1 patient from this group was omitted due to the development of urticaria. No side effects occurred in the metoclopramide group. Thus metoclopramide seems to be an alternative to the traditional treatment of ureteral colic with morphia.
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PMID:Metoclopramide (Primperan) in the treatment of ureterolithiasis. A prospective double-blind study of metoclopramide compared with morphatropin on ureteral colic. 169 82

Treatment of different types of pain Type A: 1. Diflunisal 500 mg b.i.d./naproxen 500 mg b.i.d. or another NSAID. Satisfactory effect: Continue Partial effect: Continue, but add step 2 No effect: Proceed to step 2 2. Morphine. Conventional tablets/mixture or slow release morphine. Dosage as described above. Nausea is treated with haloperidol 1-5 mg at night. Some patients do better t.i.d. 3. Glucocorticosteroid, as described above 4. Epidural morphine/local anaesthetic Type B: 1. Amitriptyline. Starting dose: 10 mg at night. Increase by 10 mg every other night until the patient has pain relief or experiences unacceptable side effects 2. Nerve blocks, if possible 3. Glucocorticosteroids 4. Strong opioids 5. Epidural opioids/local anaesthetics Type C: 1. Carbamazepine in increasing doses to 200-400 mg t.i.d. 2. Proceed as described for type B Type D: 1. Urinary colic: flavoxolate (Urispadol) 200-400 mg t.i.d. or emepronium bromide (Cetiprin) 200-400 mg t.i.d. 2. Opioids perorally 3. Epidural local anaesthetic (sympathetic block)/opioids.
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PMID:Carcinoma of the prostate. Treatment of pain. 176 76

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

Gallstones are very common, but at least two thirds of detected stones are asymptomatic and a large number undoubtedly go undetected. The presence of symptoms or complications is the indication for surgery. It is important to accurately identify which symptoms are caused by gallstones, because removing the gallbladder will relieve only these symptoms. Making this determination is a challenge, however, because the classic picture of biliary colic may be inaccurate and the connection between gallstone disease and flatulent dyspepsia is questionable at best. Descriptions of both these conditions are based on anecdotal evidence or reports of uncontrolled surgical series. A review of recent controlled trials suggests that the pain of biliary colic is constant and infrequent, comes in episodes lasting 1 to 5 hours, is located in the epigastrium or right upper quadrant of the abdomen, and characteristically occurs at night. There are few additional symptoms other than nausea or vomiting, and colic is not induced by eating fatty meals. Flatulent dyspepsia--a symptom complex of vague pain in the right upper quadrant, fatty-food intolerance, and bloating--is probably not related to the presence of gallstones in the majority of patients.
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PMID:Gallstone symptoms. Myth and reality. 192

Acute barium salt poisoning may cause acute hypokalemia and result in respiratory paralysis and ventricular tachyarrhythmias. The early nonspecific gastrointestinal symptoms of barium poisoning due to food contamination could be confused with other benign food poisonings. Early diagnosis and initiation of intensive supportive care is essential. We report an outbreak of acute barium carbonate poisoning, occurring at a family reunion party, which resulted in 9 hospital admissions. All of the victims initially developed nausea, vomiting, abdominal colic, dizziness and watery diarrhea followed by numbness of the face and distal extremities 1-2 h after ingesting fried flour-coated sweet potatoes. The flour was later confirmed to be contaminated with barium carbonate. One person died in the emergency room with a serum potassium level of 0.8 mEq/L. Two other victims developed ventricular tachycardia and respiratory paralysis but completely recovered with the treatment advice provided by the poison center. The poison center was successful in helping to make the correct diagnosis in a timely manner, immediately distribute the treatment protocol, and coordinate the laboratory confirmation of barium carbonate poisoning.
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PMID:The essential role of a poison center in handling an outbreak of barium carbonate poisoning. 203 49

For studying the side effects of praziquantel in children with active intestinal bilharziasis 6 groups of children were followed: group P-1 (active intestinal bilharziasis +/- hepatosplenomegaly). They were treated with praziquantel (40 mg/Kg b.w. orally every 6 months). group P-2 (children with active mansoniasis +/- hepatosplenomegaly. They were treated with an initial full dose of praziquantel (40 mg/kg) to be followed by suppressive dose (20 mg/kg) at 3-months intervals, group P-3 (school children with active mansoniasis +/- hepatosplenomegaly). Initial loading praziquantel dose was followed by suppressive dose at monthly intervals, group N-1 (non-bilharzial children given an oral monthly praziquantel prophylactic dose of 20 mg/kg, group N-2 (non-bilharzial children given an oral 3-monthly praziquantel prophylactic dose of 20 mg/kg), group N-3 (non-bilharzial school children given an oral placebo in the form of vitamin B complex tablets at 3-monthly intervals. Surveillance for praziquantel adverse reactions for all these groups was done. It revealed that the adverse reactions were nausea, vomiting, abdominal colic, diarrhea, dizziness, headache and pyrexia. These were noticed more after full therapeutic praziquantel dose than half doses (subcurative or prophylactic) & among bilharzial children than non-bilharzial cases. As regards school children with active urinary hematobiasis 3 groups were followed: Group 1 (school children with active urinary hematobiasis treated with praziquantel orally 40 mg/kg b.w. every 6 months). Group 2 (non-bilharzial school children given oral monthly prophylactic dose of 20 mg/kg b.w. praziquantel). Group 3 (non-bilharzial school children given oral placebo in the form of two vitamin B-complex tablets monthly).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Side effects of praziquantel in bilharzial children on a field level. 212 46

Knowledge of side effects associated with different cephalosporins may be of help to prescribers. There are several side effects that are common to all cephalosporins, but overall, cefotaxime and ceftizoxime cause the fewest adverse reactions. Bleeding is probably the most common serious side effect of cephalosporins. Moxalactam causes coagulopathy and bleeding more often than do other cephalosporins, probably because it is carboxylated and has a methylthiotetrazole side chain. Cefoperazone also has a methylthiotetrazole side chain and may cause bleeding, particularly when used in doses greater than 4 g per day. Ceftriaxone has a similar side chain and there is some evidence that it can induce a coagulopathy. Coagulation tests should be monitored when any of the third-generation cephalosporins are given to patients with a high risk of bleeding. Disulfiram-like reactions are also related to the side chains associated with coagulation defects and have been reported when patients receiving cefoperazone, moxalactam, or ceftriaxone have ingested alcohol. Seizures have been reported with ceftazidime, but are uncommon. Hematologic reactions are rare with all third-generation cephalosporins. Benign diarrhea and Clostridium difficile colitis probably occur most often with moxalactam, cefoperazone, ceftazidime, and ceftriaxone, but there are few good data on this issue. Ceftriaxone has the unique ability to cause sludge (also referred to as pseudolithiasis) to form in the gallbladder, particularly in children. This may be associated with nausea, anorexia, epigastric distress, and colic, and is usually detected using ultrasonography. The sludge dissolves and symptoms subside after therapy is discontinued. None of the third-generation cephalosporins is clearly significantly nephrotoxic, even when combined with aminoglycosides. Most of the third-generation cephalosporins have surprisingly few serious side effects, which make them attractive for use in the treatment of a wide variety of serious infections.
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PMID:Safety of parenteral third-generation cephalosporins. 218 9


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