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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty to ninety percent of pediatric AIDS cases are complicated by neurologic dysfunction. We present a case of a 5-year-old black female with AIDS encephalopathy and Mycobacterium avium intracellulare. Her initial presentation was that of neuroencephalopathy with loss of developmental milestones, pyramidal tract signs, and subsequent evidence of cortical atrophy. Her initial CT scan at the time of frank encephalopathy was normal, whereas 18 months into the clinical course of her encephalopathy, her CT scan of the head demonstrated typical ventricular dilatation and severe cortical atrophy consonant with her clinical picture. She subsequently developed Mycobacterium avium intracellulare documented by gastric aspirate culture and other opportunistic infections including Candida esophagitis. Her neuroencephalopathy plateaued with continued evidence of immune dysfunction and mycobacterium by gastric aspirate, despite triple antibiotic therapy with INH, streptomycin, Pyrazinamide with later addition of Rifampin and final substitution of the investigational congener Rifabutin. AIDS encephalopathy and Mycobacterium intracellulare are discussed in terms of their prognosis and therapy, particularly in view of new reports of the application of AZT and immunoglobulin therapy.
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PMID:Encephalopathy as a presentation of pediatric AIDS: case report. 255 69

Isoniazid and pyrazinamide are well-known hepatotoxic drugs, often used in combination. The aim of this study was to assess the prognostic influence of pyrazinamide on the outcome of fulminant or subfulminant liver failure caused by antituberculous therapy. Eighteen patients with fulminant or subfulminant liver failure due to antituberculous therapy were studied. Nine patients received isoniazid and rifampicin without pyrazinamide (group 1), and nine patients received isoniazid and rifampicin together with pyrazinamide (group 2). The severity of fulminant and subfulminant liver failure, as judged by the prevalence of coma and the lowest level of factor V, was similar in the two groups. Spontaneous survival was greater in group 1 (eight of nine) than in group 2 (two of nine) (P < .02). The authors conclude that pyrazinamide co-administration was associated with an increased mortality in patients with fulminant or subfulminant hepatitis occurring during antituberculous therapy. In these patients, pyrazinamide administration and an interval of more than 15 days between the onset of antituberculous treatment and jaundice, combined with grade III encephalopathy and factor V below 20%, predicted death without liver transplantation.
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PMID:Deleterious influence of pyrazinamide on the outcome of patients with fulminant or subfulminant liver failure during antituberculous treatment including isoniazid. 770 2

ALF is characterized by sudden onset, impaired liver function, jaundice and encephalopathy, without previous liver disease. We analyzed the patients who underwent LT due to toxic agent induced ALF to raise community awareness about preventing the toxic agent induced ALF. Five children (three boys, two girls) underwent LT due to toxic agent ingestion. Toxic agents were mushroom poisoning (n = 2), Datura stramonium (n = 1), yellow phosphorous (n = 1) and INH (n = 1). On admission, one patient had stage IV, two had stage III and two had stage II hepatic encephalopathy but worsened during the follow-up. One patient had renal failure, and three patients required mechanical ventilation. Three patients underwent LRLT and others from a DD. Post-operative complications were managed by supportive managements successfully, and overall all the patients are alive (100% survival) without any organ sequelae. Although outcome of these patients are excellent, ALF may be prevented in these cases by educating the public about consuming mushrooms and toxic effects of wild plants, prohibiting fireworks and serial liver enzyme measurements after initiating INH.
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PMID:Liver transplantation for acute liver failure due to toxic agent ingestion in children. 1921 Feb 66

The causative agent of Tuberculosis meningitis is Mycobacterium tuberculosis, which is the bacteria that causes pulmonary tuberculosis. Proliferating into the central nervous system occurs from other sites of infection within the body. Brain damage can result from the infection that may lead to abnormal behavior, mental impairments, motor type paralysis, and seizures. Tuberculosis infections of the central nervous system are a serious and often fatal disease predominantly impacting young children, and is thought to be the most devastating form of the disease. Isoniazid is the only first line bactericidal agent that easily crosses the blood-brain barrier and achieves concentrations in cerebrospinal fluid similar to those in serum. Rifampicin, ethambutol, and streptomycin all penetrate into the cerebrospinal fluid poorly, and even in the setting of meningeal inflammation. As much as one-third of the current world's population may be infected with tuberculosis. Tuberculosis infection of the central nervous system is a serious type of extrapulmonary proliferation of this disease . In developing countries, it has high predominance in children. Pathological manifestations of cerebral tuberculosis occur, of which the most common is tuberculous meningitis, followed by tuberculoma, tuberculous abscess, cerebral miliary tuberculosis, tuberculous encephalopathy, tuberculous encephalitis, and tuberculous arteritis. Brain abscesses of Mycobacterium tuberculosis can induce seizures and coma leading to death and complicated due to multiorgan failure. Rapid diagnosis and early intervention is vital for successful outcome for patients. Further studies are required to understand the proliferation of tuberculosis meningitis in addition to the elucidation of new therapeutic drugs for the successful clinical treatment of this deadly disease.
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PMID:Tuberculosis infections of the central nervous system. 2238 92

We report isoniazid (INH)-induced encephalopathy in two male patients on hemodialysis. One of them had tuberculous adenitis, and the other had pulmonary tuberculosis. Both were given rifampicin, INH, pyrazinamide, and ethambutol with pyridoxine 40 mg/day. Two patients developed disturbances in consciousness. After excluding other causes, INH-induced encephalopathy was suspected so the drug was stopped and dose of pyridoxine increased. Both patients retained their consciousness within 1 week and were discharged.
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PMID:Encephalopathy secondary to isoniazid in patients on hemodialysis. 2358 Aug 7

A high proportion of HIV-positive patients in South Africa receive concomitant efavirenz (EFV) and isoniazid (INH) therapy. EFV is metabolised in the liver via CYP2B6, and genetic polymorphism of CYP2B6 is known to result in slowed metabolism of the drug. INH is also metabolised in the liver, causing inhibition of a pathway that plays an important role in slow EFV metabolisers. Concomitant INH use therefore affects plasma levels of EFV. EFV is well known to cause neuropsychiatric side-effects on initiation, and a recent adult case series described late-onset neurotoxicity in the form of subacute ataxia and encephalopathy in patients treated with EFV for a median of 2 years, in association with toxic plasma levels of the drug. We have seen an increase in cases of EFV toxicity presenting to our neurology referral unit. All cases have been in the context of recent initiation of concomitant INH. We therefore conducted a retrospective case record audit to describe these seven cases with the additional advantage of tertiary-level assessment. We outline the clinical features and investigation results, as well as outcomes after EFV was stopped. Our main objectives are to highlight the probable role of concomitant INH use in the development of this syndrome, and to suggest that only limited work-up may be warranted in suspected cases.
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PMID:A proposed management algorithm for late-onset efavirenz neurotoxicity. 2962 76