Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of our study was to evaluate and compare the therapeutic efficacy & safety profile of three different antituberculous regimens for pulmonary tuberculosis. The study sample size included 90 newly diagnosed, sputum positive patients of pulmonary. tuberculosis. 30 each from different groups. The parameters studied were, therapeutic efficacy included weight gain, cough, sputum examination and safety profile: nausea, vomiting, anorexia, gastritis, hepatitis, jaundice diarrhoea, rashes, dizziness, tingling & numbness, flu like symptoms & joint aches. Group-I showed statistically significant weight gain when compared to Group-II. Improvement in cough and conversion to smear negative were seen in 100% of patients in Group-I, 83.3% of patients in Group-II and 93.3% of patients in Group-III. Therapeutic efficacy was highest with Group I regimen, followed by Group III and Group II which was least efficacious. Group II also registered; the maximum cost and highest incidence of adverse effects.
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PMID:Comparative evaluation of efficacy and safety profile of three anti-tuberculous regimens in Mangalore. 1264 66

We report about interesting case of treatment of pulmonary tuberculosis in 6-year old girl. Antituberculotic therapy induced toxic hepatitis (rise of transaminases, indirect hiperbilirubinemia). She was treated with streptomycin, etambutol, ciprofloxacyn and systemic corticosteroides. Two gallbladder stones and high-density sediment were diagnosed after ultrasound examination which could be a side effect of the therapy or previous findings.
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PMID:[Unusual therapeutic approach in treatment of pulmonary tuberculosis in six year old girl]. 1548 63

A retrospective study of the prevalence and pattern of tuberculosis among renal transplant patients in a single centre in southern China was performed. Twenty-three cases of tuberculosis were diagnosed among 440 patients between January 1991 and December 2002. There were 18 men and five women. The mean age of the patients was 39.3 +/- 13.4 yr. There were 13 living-related and 10 cadaveric renal transplants. The interval between renal transplantation and the development of tuberculosis ranged from 3 to 127 months with a median of 46 months. There were 18 cases of pulmonary tuberculosis, two cases of pulmonary plus laryngeal tuberculosis, two cases of disseminated tuberculosis, and one case of tuberculosis involving the urinary tract. Diagnosis was established by positive culture for Mycobacterium tuberculosis in 21 patients and response to empirical anti-tuberculosis treatment in two patients. The duration of symptoms before the diagnosis of tuberculosis was 27 +/- 12 d. The patients were treated with standard anti-tuberculosis drugs for 11 +/- 3 months. The anti-tuberculosis treatment was in general well-tolerated. Five patients developed transient hepatitis, three patients developed thrombocytopenia and five patients developed gouty arthritis. One patient died 2 months after initiation of anti-tuberculosis therapy. All other patients completed anti-tuberculosis treatment. No recurrence of tuberculosis was observed after a median follow-up of 90 months. We concluded that (i) tuberculosis is prevalent among southern Chinese renal transplant recipients; (ii) high index of suspicion for tuberculosis among renal transplant recipients is warranted to ensure early diagnosis and prompt initiation of treatment; and (iii) treatment with standard anti-tuberculosis drugs for an extended period of time is well-tolerated and is associated with favourable outcome.
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PMID:Tuberculous infection in southern Chinese renal transplant recipients. 1551 41

In 1996 a six-month short-course chemotherapy was adopted as a standard chemotherapy for pulmonary tuberculosis in Japan. The frequency of implementation of short course chemotherapy for smear positive new case was only sixty percent in 2003, although a short course chemotherapy was recommended all over the world for avoidance of acquiring a new resistance among new drug resistant tuberculosis. The reasons for the low adaptation of short course chemotherapy were speculated that high rate of elderly patients, and high frequency of drug-induced hepatitis. From our 14-year experience, the frequency of drug-induced hepatitis was 7.8% for all patients with standard 6-month or 9-month regimen, 7.2% in the patients with normal liver function tests at the start of chemotherapy, and 11.8% in the patients with any kinds of abnormality. The death rate was 0.04% among treated patients, and fatality was 0.49% among the patients with drug-induced hepatitis. Positive HCV antibody and less than 1,000 cells/microL of peripheral lymphocyte count at the beginning of treatment were independent risk factors for drug-induced hepatitis. The management of hepatitis during antituberculosis treatment was also referred.
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PMID:[Anti-tuberculosis drug-induced hepatitis]. 1624 92

Examination was made in 155 patients, including 60 patients were diagnosed as having hepatitis, hepatic lesion being first detected by a screening survey for markers of hepatitis. The antipyrine test was carried out. Patients with slow and rapid hydroxylation were identified. No changes were found in the biotransformation functions of the liver in patients with pulmonary tuberculosis 6 months after intravenous intermittent chemotherapy twice a week from the beginning of therapy; however, there was inhibition of the activity of monooxygenases and a two-fold increase in the number of patients with slow hydroxylation among patients with concomitant chronic hepatitis B and/or C. The best results of chemotherapy were found in tuberculous patients with slow hydroxylation: they less frequently underwent surgical interventions since decay cavities were therapeutically closed.
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PMID:[The clinicobiological status of patients with pulmonary tuberculosis concurrent with chronic hepatitis B and/or C]. 1681 60

Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) syndrome reflects a serious hypersensitivity reaction to drugs, characterized by skin rash, fever, lymph node enlargement, and internal organ involvement. So far, numerous drugs such as sulfonamides, phenobarbital, sulfasalazine, carbamazepine, and phenytoin have been reported to cause the DRESS syndrome. We report a case in a 29-yr-old female patient who had been on celecoxib and anti-tuberculosis drugs for one month to treat knee joint pain and pulmonary tuberculosis. Our patient's clinical manifestations included fever, lymphadenopathy, rash, hypereosinophilia, and visceral involvement (hepatitis and pneumonitis). During the corticosteroid administration for DRESS syndrome, swallowing difficulty with profound muscle weakness had developed. Our patient was diagnosed as DRESS syndrome with eosinophilic polymyositis by a histopathologic study. After complete resolution of all symptoms, patch tests were positive for both celecoxib and ethambutol. Although further investigations might be needed to confirm the causality, celecoxib and ethambutol can be added to the list of drugs as having the possibility of DRESS syndrome.
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PMID:Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) syndrome induced by celecoxib and anti-tuberculosis drugs. 1858 92

This retrospective review presented the prevalence and manifestations of tuberculosis among renal transplant recipients in our center between 1987 and mid 2007. The prevalence of tuberculosis was 5/151 (3.3%) recipients with a median age of 49 years (range = 38-55). The median time of diagnosis after transplantation was 23 months (range = 1-47). All five patients had pulmonary tuberculosis. None developed extrapulmonary infection. Presenting symptoms were fever (60%), productive cough (80%), weight loss (40%), and hemoptysis (20%). One patient had non-parathyroid-related hypercalcemia. Cyclosporine dosage needed to be increased in all patients. Two subjects who experienced side effects of hepatitis and/or jaundice from rifampicin were switched to second-line drugs. Infection with Mycobacterial tuberculosis is a not uncommon problem in renal transplant recipients especially in endemic areas. Tuberculosis must be excluded for immunosuppressed patients with clinical or radiological suspicion.
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PMID:Prevalence and manifestations of tuberculosis in renal transplant recipients: a single-center experience in Thailand. 1879 Feb 40

Several cases of Polygonum multiflorum Thunb-induced hepatitis have been reported worldwide. Anthraquinone is an active ingredient of P. multiflorum Thunb. that has been thought to play a role in its hepatotoxicity. Here we report the case of a 34-year-old Korean man who had P. multiflorum Thunb-induced hepatitis and reactivation of pulmonary tuberculosis caused by bone marrow suppression, which developed simultaneously. He was admitted to our hospital with recently developed fatigue and aggravated jaundice. He was a previously healthy man except for the sequelae of pulmonary tuberculosis seen on chest X-ray. He had a 30-day history of ingesting the root of P. multiflorum as a form of liquor and tea. The patient was diagnosed with P. multiflorum Thunb-induced hepatitis after excluding all other potential causes of acute hepatitis. Liver function gradually improved following the total cessation of the consumption of the material. However, he suffered from spiking fever with progressive pancytopenia during the hospital stay. A bone marrow biopsy showed markedly hypocellular marrow, suggesting transient bone marrow suppression, which was probably caused by extrinsic factors such as drugs, toxins, and viral infection. Although he began to complain of a dry cough, repeated sputum investigations revealed positive acid-fast bacillus staining. The fever subsided and pancytopenia improved after treatment for pulmonary tuberculosis. These observations suggest that P. multiflorum Thunb induces both bone marrow suppression and hepatotoxicity.
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PMID:Reactivation of Pulmonary Tuberculosis in a Patient with Polygonum multiflorum Thunb-Induced Hepatitis. 2047 2

Proton pump inhibitors (PPIs) are widely used drugs in the treatment or prophylaxis of peptic ulcer and gastro-oesophageal reflux disease. In addition to their well documented efficacy, these drugs are generally well tolerated with only rare serious adverse effects having been reported. Neutropenia and agranulocytosis are rare adverse events associated with PPI treatment. All previously published cases of isolated neutropenia have involved omeprazole, but leukopenia is labelled as a possible adverse effect in the summary of product characteristics of the other PPIs. In this report, we describe a case of omeprazole-induced neutropenia with further recurrence upon pantoprazole treatment. A 60-year-old man with chronic alcoholism and a medical history of pulmonary tuberculosis, untreated chronic C hepatitis, peripheral artery disease, chronic obstructive pulmonary disease and stable stage 3 chronic kidney disease was admitted with dehydration and malnutrition. Omeprazole 20 mg/day and sucralfate 3 g/day were started for diffuse gastritis on gastric endoscopy. While the patient's blood cell count had been within the normal range before this treatment, routine laboratory examination revealed moderate neutropenia (0.9 x 109/L) after 9 days of treatment. His blood cell count returned to the normal range after discontinuation of omeprazole and no further episodes of neutropenia were noted in the following months. One year later, oesophago-gastroscopy revealed a hiatal hernia with an extensive zone of Barrett's oesophagus. As the lesions did not improve with ranitidine and sucralfate therapy, the patient was started on pantoprazole 40 mg/day. His initial white blood cell count was normal, but moderate neutropenia (0.8 x 109/L) was again noted after only 2 days of pantoprazole treatment. Complete and further stable normalization was obtained within 3 days after replacement of pantoprazole with ranitidine. Toxic and immune-mediated mechanisms are the two commonly proposed mechanisms to explain the pathogenesis of drug-induced neutropenia. This report suggests that PPI-induced neutropenia is immune mediated and argues for a possible cross-reactivity between the two PPIs, as has already been described for PPI-induced hypersensitivity reactions. The report also indicates that patients with a history of neutropenia induced by one PPI may be at risk of recurrence of neutropenia if given another member of this drug class. In these patients, close haematological monitoring is proposed.
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PMID:Proton pump inhibitor-induced neutropenia: possible cross-reactivity between omeprazole and pantoprazole. 2058 18

Tuberculosis is one of the most common diseases in India and has attained epidemic proportions. Tuberculosis and liver are related in many ways. Liver disease can occur due to hepatic tuberculosis or the treatment with various anti-tubercular drugs may precipitate hepatic injury or patients with chronic liver disease may develop tuberculosis and pose special management problems. Tuberculosis per se can affect liver in three forms. The most common form is the diffuse hepatic involvement, seen along with pulmonary or miliary tuberculosis. The second is granulomatous hepatitis and the third, much rarer form presents as focal/local tuberculoma or abscess. Tubercular disease of liver occurring along with pulmonary involvement as in disseminated tuberculosis is treated with standard regimen for pulmonary tuberculosis. Granulomatous hepatitis and tubercular liver abscess are treated like any other extra-pulmonary tubercular lesions without any extra risk of hepatotoxicity by anti-tubercular drugs. Treatment of tuberculosis in patients who already have a chronic liver disease poses various clinical challenges. There is an increased risk of drug induced hepatitis in these patients and its implications are potentially more serious in these patients as their hepatic reserve is already depleted. However, hepatotoxic anti-tubercular drugs can be safely used in these patients if the number of drugs used is adjusted appropriately. Thus, the main principle is to closely monitor the patient for signs of worsening liver disease and to reduce the number of hepatotoxic drugs in the anti-tubercular regimen according to the severity of underlying liver disease.
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PMID:Tuberculosis and liver disease: management issues. 2302 55


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