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)

We reviewed reactions previously reported in patients treated with isoniazid, who ate certain fish and cheeses. We observed similar reactions in two patients after they ingested cheese and wine. Isoniazid is an inhibitor of both monoamine and diamine oxidases, which contribute to the metabolism of histamine that may be present in some fish and cheeses. Monoamine oxidase also acts in the metabolism of tyramine, present in some cheeses and wines. Reactions reported after eating fish or cheese, in patients treated with isoniazid, are similar in that both are characterized by headache, palpitations, skin flushing, nausea, vomiting, and pruritus. Reactions after fish have not been associated with increased blood pressure, whereas those following cheese ingestion frequently result in modest increases in blood pressure. Patients treated with isoniazid should be alerted to the possibility of reactions after eating certain foods.
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PMID:Interactions of isoniazid with foods. 710 82

In order to determine the efficacy of short course chemotherapy (SCC) for tuberculosis in children, 83 newly diagnosed cases in children < 12 years old were given SCC and were prospectively followed for 1-3 years. Seventy-one cases were treated for 6-9 months as they had mild to moderate involvement. Twelve cases were treated for 12 months as they had meningitis (7), disseminated tuberculosis (2), or miliary tuberculosis (3). The results showed that none of the children, at the end of follow up, showed evidence of active tuberculosis. All children tolerated the drugs well, with side effects noticed being mild, namely transient hepatitis (4), vomiting (1), and skin rash (1). It is suggested that SCC for 6-9 months using isoniazid (INH) and rifampicin along with other drugs when necessary is highly effective in most cases of tuberculosis in children and has several advantages over conventional chemotherapy of 18 months or longer duration.
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PMID:Short course chemotherapy for tuberculosis in children. 813 59

We report the case of a 28-year-old-prostitute from Thailand with HIV infection stage B2 associated with retroperitoneal lymph node tuberculosis. 6 days after the beginning of anti-tuberculous therapy (isoniazid, rifampicin, pyrazinamid and ethambutol) the temperature rose to 40.5 degrees C, diarrhea, vomiting, and tachycardia developed and systolic blood pressure fell to 80 mm Hg. Liver function tests revealed acute hepatic failure (ALT 800 IU/l rising to 1500; serum bilirubin 89 mumol/l rising to 238.0; alkaline phosphatase 199 IU/l; glucose 1.8 mmol/l; prothrombin time 20%). Isoniazid, rifampicin, and pyrazinamid were replaced by streptomycin and PAS. A few days after withdrawal the liver profile returned to normal. Hours after the reintroduction of rifampicin total body erythema, pruritus, vomiting and severe hypotension developed, requiring saline methylprednisolone and epinephrine administration. The next reexposure to intravenous rifampicin produced a rash and was rapidly discontinued. Liver function tests remained normal. Later mild adverse reactions to streptomycin and pyrazinamid occurred, two drugs which had been well tolerated before. Subsequently the diagnosis of adrenal insufficiency was established. After initiation of steroid replacement (50 mg prednisolone) the antituberculous therapy with isoniazid, pyrazinamid and ethambutol was well tolerated. We conclude that the shock in this HIV-infected patient was either due to severe anaphylaxis to rifampicin or acute adrenal insufficiency ensuing on this drug. The reversible fulminant acute hepatic failure represents either an adverse effect of antituberculous drugs, especially hepatotoxic interactions of drug combinations, or an ischemic liver injury during hypotension caused by anaphylaxis. The case illustrates the complex nature of side effects of antituberculous drugs in HIV patients and their aggravation by adrenal insufficiency.
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PMID:[Fulminant, rapidly reversible hepatitis and life-threatening anaphylaxis following rifampicin in an HIV-positive female patient with latent adrenal cortex insufficiency]. 864 39

Since isoniazid is increasingly being used to control the spread of tuberculosis, physicians must be aware of its potentially fatal effects. The ingestion of toxic amounts of isoniazid causes recurrent seizures, profound metabolic acidosis, coma and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5 g of isoniazid. Doses larger than 30 mg per kg often produce seizures. When ingested in amounts of 80 to 150 mg per kg or more, isoniazid can be rapidly fatal. The first signs and symptoms of isoniazid toxicity usually appear 30 minutes to two hours after ingestion and include nausea, vomiting, slurred speech, dizziness, tachycardia and urinary retention, followed by stupor, coma and recurrent grand mal seizures. The seizures produced by isoniazid toxicity are often refractory to anticonvulsant therapy. Given in gram-per-gram amounts of the isoniazid ingested, pyridoxine (vitamin B6) usually eliminates seizure activity and helps to correct the patient's metabolic acidosis. Isoniazid toxicity should be suspected in any patient who presents with refractory seizures and metabolic acidosis.
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PMID:Isoniazid overdose: recognition and management. 949 Sep 97

The notification rate of tuberculosis in Japan was 31.0 per 100,000 in 2000. The rate was especially high among the elderly population, reaching 85.5 per 100,000 among those over 65 years of age. We conducted a study of preventive therapy in middle-aged and elderly persons selected from the population-based screening by the mass miniature radiography. The eligible criteria were 50-79 years of age, fibrous lesion which were compatible with healed tuberculosis and showed no change for at least one year, no previous treatment for tuberculosis, normal liver function tests, and no serious disease at the time of study. The eligible criteria for liver function tests in this study was less than 50 IU/L of AST and ALT value, and less than 1.5 mg/dl of T-bil level. A total of 13,219 people underwent TB screening in 4 cities in 1997 and 2 cities in 1998. Among them, 440 persons fulfilled the above criteria based on the screening records and chest X-ray films. The municipal offices sent letters to 418 people, except 22 whose addresses were unknown, to obtain permission to use their addresses and results of screening in our study. Permission was obtained from 137 persons and we sent them invitation letters for cost-free physical checkup service. Ninety-five persons visited us, and we offered them physical checkup and explained about our study. After obtaining the informed consent, we performed chest X-ray and sputum examination for 3 consecutive days. Finally 29 people were enrolled in the study. They were divided into 4 groups by sex and age, and were randomly assigned to one of two treatment groups. One group took 300 mg of INH per day for 6 months and the other group was only followed up by chest X-ray. Fourteen out of 29 persons began to take INH and received monthly liver function test. All the subjects were scheduled to follow by medical checkup every 6 months for 5 years. The proportion of taking INH tablets was estimated to range from 94% to 100%, based on the calendar for record of taking medication and the number of remaining tablets each month. Six (42.9%) of 14 persons reported adverse reactions. Two of 6 persons complained some of diarrhea, vomiting and gastrointestinal disturbance within 2 weeks, and discontinued taking INH, although none of them showed abnormal liver function tests. Two of 6 persons who reported some kinds of symptoms and 2 of 8 persons who did not complain of any symptoms showed abnormal liver function tests. The abnormal liver function tests had developed from 2 months after the beginning of INH taking in most of the persons and the abnormality improved after the completion of 6-month treatment. We have followed them for a maximum duration of 2.5 years, and 3 cases dropped out from the study. These defaulted cases had completed 6 months of INH. One person (69 y.o. male) was diagnosed as active TB by his chest X-ray film at the 6th month medical checkup, although it was not confirmed bacteriologically. One person (62 y.o. female) had the mastectomy for breast cancer 7 months before the entry to this study and relapsed at the 8th month after the entry. One person (73 y.o. female) was diagnosed as lung cancer at the medical checkup on 2.5 years. Besides them, 4 persons were suspected of worsening the abnormal shadows on chest X-ray films; one was from the INH group and three were from the follow-up group. However none of them was diagnosed clinically and bacteriologically as active tuberculosis.
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PMID:[Preventive therapy in middle-aged and elderly persons selected from the population-based screening by mass miniature radiography--methodological aspect and adverse reactions]. 1244 Jan 39

To investigate the association between NAT2 genotypes and the incidence of isoniazid (INH)-induced adverse reactions, in the hope of identifying a pharmacogenetic approach that could be useful in the prediction and prevention of adverse reactions in Japanese patients, we retrospectively studied the genotypes of NAT2 in 102 Japanese patients treated with INH (without rifampicin co-administration). The subjects were classified into three groups according to their genotypes: rapid-type, intermediate-type, and slow-type. The clinical conditions of the patients were followed-up in order to evaluate the development of any adverse drug reactions (ADRs) and correlate them with patient genotypes. Six out of the 102 patients (5.9%) developed various ADRs following INH treatment. These reactions included nausea/vomiting, fever, visual impairment, and peripheral neuritis. We found a statistically significant difference between the incidence of ADRs and NAT2 genotype. The incidence of ADRs was significantly higher in the slow type than in the other two types, as 5 out of the 6 ADR patients were of the slow-type, and the other one was of the intermediate-type, while no patients of the rapid-type developed any ADRs. The results indicated that the genes coding for slow acetylation were associated with the incidence of serious ADRs following INH treatment. Our findings suggest that determination of NAT2 genotype might be clinically useful in the evaluation of patients at high risk of developing ADRs induced by INH.
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PMID:Genotyping of the N-acetyltransferase2 polymorphism in the prediction of adverse drug reactions to isoniazid in Japanese patients. 1561 86

A 44-year-old man consulted medical clinic, complaining of cough and sputum. Then he was admitted to our hospital, because of positive acid-fast bacilli in his sputum and positive PCR (polymerase chain reaction) for Mycobacterium tuberculosis. Combined use of isoniazid (INH), rifampicin (RFP), ethambutol (EB) and pyrazinamide (PZA) was started. But 4 days after starting treatment, we had to suspend tuberculosis chemotherapy because of hepatopathy. Since then he started to complain epigastralgia and vomiting. Plain abdominal X-ray and abdominal computed tomography (CT) led to a diagnosis of ileus. Inspite of insertion of ileus tube symptoms of ileus did not improve. Small bowl series showed severe stenosis at ileum end, necessitating jejunectomy. Macroscopic study revealed a ring ulcer and multiple epithelioid cell granuloma with Langhans' giant cells was detected histopathologically. PCR for M. tuberculosis of extracts from ileum was positive. Therefore the patient was diagnosed small intestinal tuberculosis. Treatment was continued by the combination of INH, RFP, EB, and the symptoms markedly improved. There have been no sign of recurrence since the end of the 6-month treatment for tuberculosis.
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PMID:[A surgically treated case of ileus caused by small intestinal tuberculosis during treatment for pulmonary tuberculosis]. 1818 80

Splenic abscess is a rare clinical condition and yet rarer is a tubercular splenic abscess. Here we report a case of tubercular splenic abscess. A forty years old male patient was admitted in Medicine unit of Mymensingh Medical College Hospital (MMCH) on 09-08-2006 with the complaints of Left upper quadrant abdominal pain and fever for 15 days and Respiratory difficulty for 2 days. Two days after admission he developed generalized abdominal pain and distension. Pain was not associated with vomiting. Patient was transferred to surgical unit for features of peritonitis. Ultrasonogram of whole abdomen revealed moderately enlarged spleen showing 8.8 x 9.7 cm semicystic mass, which may represent an abscess. There was mild free fluid collection in the lower abdomen. X-ray chest P/A view showed bilateral pleural effusion. On laparotomy huge amount of free pus was found in the peritoneal cavity and the spleen was hugely enlarged with a burst abscess cavity in it. Splenectomy and thorough peritoneal toileting was done. Postoperative recovery was uneventful except few stitch infections. Pus culture revealed no growth but histopathology of spleen confirmed Tubercular Splenic Abscess. Patient was given an antitubercular regimen with Rifampicin, Isoniazid, Ethambutol and Pyrazinamide for initial two month which to be followed by Rifampicin and Isoniazid for another ten months.
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PMID:Tubercular splenic abscess. 1828 36

A 42-year-old Indian man received 450 mg rifampicin (RIF) and 150 mg isoniazid (INH) daily after being diagnosed of a latent tuberculosis infection. Baseline serum aminotransferase and total bilirubin levels were within normal limits. On day 31 of treatment, the patient experienced epigastric discomfort and general malaise and one week later he developed nausea and episodic vomiting. The patient missed his first scheduled clinic appointment and he continued taking RIF-INH despite his symptoms. He visited the tuberculosis clinic on day 47 of treatment where he was found to be jaundiced and his liver enzymes were elevated. RIF-INH was stopped and the patient was admitted to our hospital as a case of RIF-INH induced hepatitis. On the 7th day of hospitalization, the patient developed consciousness disturbance with flapping tremor and high ammonia level. The patient was diagnosed with fulminant hepatic failure and transferred immediately to the medical intensive care unit, where he died 4 days later.
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PMID:Rifampicin-isoniazid induced fatal fulminant hepatitis during treatment of latent tuberculosis: A case report and literature review. 2085 96

Hereditary angioedema (HAE) is a rare, autosomal dominant disease due to functional deficiency of C1-esterase inhibitor (C1-INH). In this observational study anamnestic, clinical and treatment data from forty patients were retrospectively analysed. Thirty nine of the patients suffered from type I of HAE and one patient from type II. Between first manifestation of the disease and correct diagnosis a median time lag of 10 years was observed. Two C1-INH deficient individuals had no symptoms so far; 36 patients suffered from recurrent, self-limiting abdominal attacks (convulsion, vomiting and diarrhea); 32 patients presented with edema of the (sub-) cutis. Thirty percent of swelling attacks involved the upper respiratory tract and two larynx attacks needed intubation. Hormonal changes in 25% of the female patients were associated with an aggravation of the attacks. Long-term therapy was established in 19 patients; treatment of acute attacks was performed in 10 patients and 11 patients needed no therapy.
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PMID:[Clinical facets of hereditary angioedema among Swiss patients]. 2085 77


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