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)

A case is described of retrobulbar optic neuritis in a 33-year-old female with acute type B hepatitis. The ocular distress, principally affecting the left eye, followed the normalisation of liver function tests and subsided after steroid therapy. At the onset of ocular symptomatology, complement activation, involving both classic and alternative pathways, and high levels of circulating immune complexes were present. HBsAg was positive. No relapse was observed during follow-up for 3 years. An association between HBV-infection, optic neuritis and an immune complexes-mediated neurotoxic activity are hypothetized.
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PMID:Retrobulbar optic neuritis in a patient with acute type B hepatitis. 371 33

A 28-year-old man ingested methylene dianilene in potassium carbonate and gamma-butyrolactone. He developed toxic optic neuritis, with severe visual dysfunction (not previously reported in humans), prolonged toxic hepatitis, with disturbed liver-function tests 18 months after the incident, and other more transient effects. The course of his illness is described and the literature on methylene dianilene toxicity is reviewed.
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PMID:Methylene dianilene: a new toxic cause of visual failure with hepatitis. 398 6

Reports of cases of primary and secondary syphilis are increasing in the United States, particularly in urban areas and among homosexual men. While primary syphilis poses little diagnostic difficulty, many physicians are unfamiliar with the multisystem nature of secondary lues. Patients who have secondary syphilis commonly present with systemic signs, skin rash, mucous membrane lesions and generalized adenopathy. Less commonly, secondary syphilis may occur as acute meningitis, sensorineural hearing loss, iritis, anterior uveitis, optic neuritis, Bell's palsy, gastropathy, proctitis, hepatitis, pulmonary infiltration, nephrotic syndrome, glomerulonephritis, periostitis, tenosynovitis and polyarthritis. The diagnosis of secondary syphilis is easily confirmed. Its various manifestations are readily treated with penicillin and, if treated early, are entirely reversible. Two recent cases of secondary syphilis, one presenting as nephrotic syndrome and one as chorioretinitis and ptosis, illustrate the usual and unusual features of this common infection.
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PMID:Secondary syphilis: uncommon manifestations of a common disease. 670 90

Optic neuritis occurred in three of our patients receiving treatment with alpha interferon-2b (Intron-A; 3MU thrice weekly) for chronic hepatitis. The complication appeared within, 1, 9 1/2 and 10 months of treatment, respectively. In all cases, blurred vision was the initial complaint and subsequent electrophysiologic investigation confirmed the presence of optic tract neuropathy. The patients had no other neurologic signs. Computerized tomography and magnetic resonance image of the brain were not remarkable. Psychiatric symptoms, in the form of an interferon-associated depressive reaction, were present in two of them; in one case, it was severe enough to require immediate discontinuation of treatment. In two patients the visual symptoms resolved and the parameters of neurophysiologic testing returned to normal within 1 month after stopping interferon. In one case, however, residual optic tract impairment associated with a unilateral central scotoma and a substantial decrease of visual acuity was present 2 years later, despite a course of methylprednizolone. In this patient the interferon treatment was continued for 3 months despite the visual symptoms, and he later received two additional interferon courses because of relapses of hepatitis. We conclude that clinically evident optic tract neuropathy may complicate interferon administration. Candidates for interferon treatment may need routine examination of optic fields and visual evoked potentials, before and during administration of the drug to avoid possibly permanent visual sequelae.
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PMID:Optic tract neuropathy complicating low-dose interferon treatment. 783 21

Prescribed since 1948 to control chronic alcoholism, disulfiram may cause severe toxicity as report in three cases of acute motive axonal polyneuritis. Disulfiram toxicity may present different clinical aspects: 1) Cytolytic hepatitis with fatal evolution in 30% of cases (fulminant hepatitis), and full recovery for the other 70%. The onset of the symptoms usually occurs as early as 15 days to a maximum of 6 months (most within 2 months) after initiation of treatment. 2) Severe optic neuritis with full recovery in 2 months. 3) Peripheral neuropathy usually dose dependent, with different clinical presentations: polyneuritis with sensory, motor, or both deficits, and few cases of tetraplegia. 4) Encephalopathy frequently associated with one of the precedent symptoms, having a favorable outcome (probably resulting in inhibition of dopamine-beta-hydroxylase by disulfiram). The mechanism of toxicity (direct or idiosyncractic) remain unclear. Disulfiram has been used safely in millions of people since 1948, and we have only few cases reports of severe toxicity. From a practical point of view, treated patients should benefit by a neurological examination once a month, ophtalmological examination every 2 months, and hepatic enzymes monitored twice a month during the 2 first months. This is the price to prevent and to detect side effects of disulfiram therapy.
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PMID:[Disulfiram (Esperal) toxicity. Apropos of 3 original cases]. 857 Sep 64

Disulfiram is known to cause hepatitis, which is sometimes fatal. The best estimate of the frequency of disulfiram-induced fatal hepatitis is 1 case in 30,000 patients treated/year. Its appears to be more common in patients given disulfiram for the treatment of nickel sensitivity. Frequent blood testing for liver function is probably not necessary, but patients taking disulfiram should be in regular contact with a physician. There are rare reports of psychosis and confusional states in conjunction with disulfiram treatment and peripheral neuropathy and optic neuritis have been reported; these effects are dose-related. Psychiatric complications appear to be more common with the use of disulfiram in India than in Western countries. Of the less serious adverse effects, tiredness, headache and sleepiness are the most common. Deaths from the disulfiram-alcohol (ethanol) interaction have not been reported in recent years, possibly because the dosages used are lower than those used 40 years ago, and patients with cardiac disease are now excluded from treatment. There is no evidence to suggest that disulfiram causes cancer. Of note, there are drug interactions with compounds that utilise the cytochrome P450 enzyme system. Disulfiram can be viewed as a drug with a moderate record of adverse effects. Alcohol dependence, for which it can be a helpful treatment, is associated with a high morbidity and mortality.
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PMID:Safety issues concerning the use of disulfiram in treating alcohol dependence. 1034 93

By presenting this case report describing Parinaud's oculoglandular syndrome, we review the medical literature on its most frequent etiology: catscratch disease, a self-limited, systemic illness caused by a Gram-negative bacillus, Bartonella henselae, principally affecting children under 15 years of age. Typical symptoms include regional lymphadenopathy, fever, malaise, and fatigue, possibly with more severe complications such as splenomegaly, granulomatous hepatitis, and encephalopathy. Ocular manifestations may include follicular conjunctivitis, Parinaud's oculoglandular syndrome, neuroretinitis, optic neuritis, and chorioretinitis. Diagnosis is based on serologic tests, and when necessary, antimicrobial treatment can be considered.
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PMID:[Cat's cratch disease and Parinaud's oculoglandular syndrome]. 1502 49

A 24-year-old Vietnamese woman presented with a 3-month history of non-itchy erythematous plaques on the face, trunk and limbs. Borderline lepromatous leprosy was confirmed by clinical findings, acid-fast bacilli on skin biopsy specimen and skin smear and a history of exposure. Around the twentieth day of World Health Organization (WHO) multibacillary standard treatment (rifampin 600 mg per month, dapsone 100 mg per day, clofazimine 300 mg per month and 50 mg per day for 1 year), she developed fever, general malaise, blurred vision, cough, nausea, epigastric pain, and arthralgia. The skin lesions also became swollen. During hospitalization, her illness was complicated by retrobulbar optic neuritis, secondary bacterial pneumonia, pleuritis, ascites, hepatitis, antral gastritis, progressive normocytic anemia, and peripheral sensory loss. The patient recovered after receiving systemic steroid pulse therapy (prednisolone equivalent dose 1250 mg) with systemic antibiotics (cefuroxime), adjustment of her anti-lepromatous therapy, and supportive care. She resumed the WHO multibacillary regimen uneventfully. This patient presented with a diverse type 1 reaction, which is a complex immune response in leprosy. We found that the judicious use of high dose steroids followed by a slow tapering course is beneficial in managing patients with a severe type 1 reaction. At the 1-year follow up, the patient had generalized skin hyperpigmentation resulted from long-term clofazamine use and numbness on feet without other systemic sequelae.
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PMID:Corticosteroid pulse therapy for leprosy complicated by a severe type 1 reaction. 1856 21

Optic neuritis (ON), an inflammatory demyelinating optic nerve disease, occurs in multiple sclerosis (MS). Pathological mechanisms and potential treatments for ON have been studied via experimental autoimmune MS models. However, evidence suggests that virus-induced inflammation is a likely etiology triggering MS and ON; experimental virus-induced ON models are therefore required. We demonstrate that MHV-A59, a mouse hepatitis virus (MHV) strain that causes brain and spinal cord inflammation and demyelination, induces ON by promoting mixed inflammatory cell infiltration. In contrast, MHV-2, a nondemyelinating MHV strain, does not induce ON. Results reveal a reproducible virus-induced ON model important for the evaluation of novel therapies.
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PMID:Experimental optic neuritis induced by a demyelinating strain of mouse hepatitis virus. 1857 91

A 34-year-old woman developed bilateral optic neuritis 2 weeks after the onset of acute hepatitis C. The strong temporal relationship between the initial clinical manifestations of hepatitis C and the development of optic neuritis provides a basis for thinking that the hepatitis caused the optic neuritis After corticosteroid treatment, the optic neuropathy markedly improved but left behind retinal nerve fiber thinning, as measured by optical coherence tomography, and optic disc pallor. Optic neuritis has been reported in conjunction with hepatitis A and B but not with hepatitis C.
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PMID:Bilateral optic neuritis in acute hepatitis C. 1949 36


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