Filter by keywords:



Filtering documents. Please wait...

1/50. Neurological manifestations of chronic hepatitis c.

    hepatitis c virus (HCV) infection is often associated with abnormal immunological responses. We describe four patients with vasculitic neurological signs and symptoms following HCV infection. A 56-year-old woman with HCV infection developed peripheral neuropathy characterized by asymmetric distal painful hypesthesia, dysesthesia and moderate motor weakness of the lower limbs. Serological examinations revealed cryoglobulinemia and low levels of complement c4. A biopsy of the sural nerve revealed vasculitic neuropathy. HCV infection associated immunomediated vasculitis was diagnosed. While steroid therapy was ineffective, treatment with interferon-alpha improved the neuropathy considerably without, however, eliminating HCV infection. A 62-year-old man with HCV infection developed peripheral sensory neuropathy. complement c3 was slightly diminished. Nerve biopsy revealed vasculitic neuropathy. A 71-year-old woman developed chronic symmetric sensomotor polyneuropathy. HCV hepatitis followed blood transfusions. cryoglobulins tested positive, consistent with type II cryoglobulinemia. Complements C3 and C4 were diminished. Inflammatory infiltrates in the sural nerve biopsy specimen led to the diagnosis of chronic vasculitic disorder. A 55-year-old woman with HCV infection developed vasculitis of the skin, connective tissue, visceral organs, and kidney, leading to hemodialysis. Neurologically she developed severe apathy and drowsiness, myoclonic jerks, exaggerated deep tendon reflexes, and positive pyramidal signs. magnetic resonance imaging of the brain showed diffuse increased signal abnormalities involving supra- and infratentorial white matter suggesting cerebral vasculitis. cryoglobulins were positive, complements C3 and C4 slightly diminished (54 mg/dl, 4.3 mg/dl). Supportive therapy resulted in neurological improvement. Treatment with interferon-alpha was discontinued because of agranulocytosis. In patients with peripheral neuropathy or signs of leucencephalopathy, a hepatitis c associated vasculitis should be considered in the differential diagnosis.
- - - - - - - - - -
ranking = 1
keywords = hepatitis
(Clic here for more details about this article)

2/50. Reversible pancreatitis, hepatitis, and peripheral polyneuropathy associated with parenteral gold therapy.

    A 63-year-old man with seronegative rheumatoid arthritis developed acute pancreatitis, severe hepatitis, and sensorimotor polyneuropathy after receiving 150 mg of intramuscular aurothioglucose (gold). Positive lymphocyte transformation test to gold indicated a cell mediated hypersensitivity to the drug, while multiple investigations ruled out other underlying causes for his illness. After cessation of gold therapy a complete recovery occurred.
- - - - - - - - - -
ranking = 0.83333333333333
keywords = hepatitis
(Clic here for more details about this article)

3/50. A combination of autoimmune hepatitis, sensory-dominant peripheral neuropathy, and primary sjogren's syndrome in the same patient: a rare association.

    Although autoimmune hepatitis and sensory-dominant neuropathy have been known to independently accompany primary sjogren's syndrome, the combination of all these conditions in the same patient has not been described. We report the case of a woman who initially suffered from autoimmune hepatitis and later was diagnosed with primary sjogren's syndrome upon the development of sensory-dominant neuropathy. In this patient, autoimmune hepatitis preceded neuropathy by one year. All of the diagnoses were confirmed by histological examinations of the liver, sural nerve, and minor salivary gland. Her autoimmune hepatitis was relieved with conservative treatment, and her sensory-dominant neuropathy was alleviated by prednisolone therapy. Our case indicated that the multiple organ involvement, especially that in the liver and peripheral nerves, should be taken into account in the course of primary sjogren's syndrome.
- - - - - - - - - -
ranking = 1.3333333333333
keywords = hepatitis
(Clic here for more details about this article)

4/50. Sensory neuropathy in the prodromal phase of hepatitis a and review of the literature.

    We report an unrecognized clinical presentation of hepatitis a with unilateral peripheral acute sensory loss in the prodromal phase of the illness. Although rare, focal neurological signs are known to occur in hepatitis a before, during and after the icteric phase; a pure peripheral sensory neuropathy is distinctly uncommon. Possible lesions could include radiculopathy of the lower thoraco-lumbo-sacral dorsal nerve roots or a partial transverse myelitis of Brown-Sequad like distribution. The signs and symptoms lasted only a few days and the patient had an uneventful recovery.
- - - - - - - - - -
ranking = 1
keywords = hepatitis
(Clic here for more details about this article)

5/50. Toxic metronidazole-induced MRI changes.

    OBJECTIVE: To report a case of changes documented by magnetic resonance imaging (MRI) of the head probably due to accumulation of metronidazole in a patient with liver dysfunction. CASE SUMMARY: A 34-year-old Hispanic man with cirrhosis and hepatitis c being treated with metronidazole for bacteroides fragilis meningitis and bacteremia developed ataxia, disorientation, and peripheral neuropathy. An MRI at the time meningitis was diagnosed was negative. After the patient received > 60 g of metronidazole, an MRI revealed increased signal intensity below, behind, and lateral to the fourth ventricle. Concomitant metronidazole serum concentration was toxic at 35.1 micrograms/mL. DISCUSSION: This is the second reported case of metronidazole-induced MRI changes. metronidazole is known to accumulate in patients with liver dysfunction and can cause peripheral neuropathy and central nervous system (CNS) dysfunction; these effects may take up to two years to completely resolve. CONCLUSIONS: metronidazole dosages should be reduced in patients with liver dysfunction to prevent the accumulation of metronidazole, which can lead to CNS dysfunction and peripheral neuropathy.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = hepatitis
(Clic here for more details about this article)

6/50. hepatitis c virus infection with peripheral neuropathy is not always associated with cryoglobulinaemia.

    OBJECTIVES: To describe cases of peripheral neuropathy associated with chronic hepatitis c virus infection without mixed cryoglobulinaemia. methods: Four cases of peripheral neuropathy associated with chronic hepatitis c virus infection with persistent negativity of mixed cryoglobulinaemia were found. RESULTS: All patients had small increases of transaminase levels and a positive viraemia. Liver biopsy showed chronic active hepatitis in all but one case (Knodell 4-9, Metavir A0F0-A3F3). Neuromuscular biopsy showed axonal neuropathy associated with lymphoid infiltrates around small vessels in two cases. rheumatoid factor was always negative and C4 complement level was always normal. In three patients, neuropathy improved with interferon alpha, interferon alpha ursodesoxycholic acid, or steroids plasma exchange. CONCLUSION: Peripheral neuropathy may be associated with hepatitis c virus infection without mixed cryoglobulinaemia.
- - - - - - - - - -
ranking = 0.66666666666667
keywords = hepatitis
(Clic here for more details about this article)

7/50. "Hepatitic flare", asthenia, peripheral polyneuropathy and diffuse liver steatosis in a hepatitis c virus asymptomatic chronic carrier.

    In July 2000, a 62-year-old female, with a ten-year history of chronic hepatitis C virus infection and persistently normal aspartate amino-transferase and alanine aminotransferase levels, presented with asthenia, weight loss, peripheral polyneuropathy and increased levels of aspartate aminotransferase (8 times upper normal limit), alanine aminotransferase (10 times upper normal limit) and gamma glutamyl-transferase (6 times upper normal limit). The ultrasound findings were consistent with massive liver steatosis. The patient had been previously diagnosed elsewhere as having hepatitis c virus-related "hepatitic flare" with neurological involvement related to concomitant mixed type-III cryoglobulinaemia. However intense exposure to trichloroethylene since April 2000 was revealed and liver histology was fully consistent with non-alcoholic steatohepatitis. The pathogenetic role of the solvent was definitely supported by the complete clinical and biochemical remission within six months of trichloroethylene withdrawal.
- - - - - - - - - -
ranking = 1.1666666666667
keywords = hepatitis
(Clic here for more details about this article)

8/50. Rapid improvement of autonomic and peripheral neuropathy after liver transplantation: a single case report.

    Peripheral and autonomic neuropathies are known but often unrecognized associations of cirrhosis from any cause. The pathogenesis of these effects are ill understood. liver transplantation has been shown to reverse autonomic manifestations, but little evidence exists for an effect on peripheral neuropathy. This case report documents improvement in peripheral and autonomic neuropathy in a 40-year-old man with hepatitis b virus--related cirrhosis. A return to normal neurophysiological function was seen within 9 months of successful liver transplantation, suggesting a metabolic, rather than a structural, cause of such changes in the peripheral nervous system.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = hepatitis
(Clic here for more details about this article)

9/50. cryoglobulinemia is a frequent cause of peripheral neuropathy in undiagnosed referral patients.

    cryoglobulinemia represents an emerging cause of peripheral neuropathy, especially in Southern europe, in view of its relationship with hepatitis c virus infection. In a series of 100 consecutive referral patients with uncharacterized peripheral neuropathies, we systematically investigated cryoglobulinemia to assess its diagnostic yield. The most frequent diagnosis was hereditary neuropathy (33%), 29% were acquired neuropathies of different types, and no cause could be identified in 27%. Cryoglobulinemic neuropathy was diagnosed in 11 patients (7 women and 4 men), aged 54-77 (mean = 63.5 years), most presenting with sensory polyneuropathy, often asymmetrical. Cryoglobulin was also detected in 2 additional patients in whom a final diagnosis of non-Hodgkin lymphoma was made. purpura was absent in 4 patients (and in 2 with lymphoma), or restricted to discrete manifestations in the remaining patients, which did not provide a clue to the diagnosis. Thus, search for cryoglobulin proves useful in a substantial number of undiagnosed peripheral neuropathies (11% to 13% in our series), even in the absence of typical skin lesions, and it is recommended as a first-line investigation in patients with unexplained neuropathy presenting in middle to older age.
- - - - - - - - - -
ranking = 0.16666666666667
keywords = hepatitis
(Clic here for more details about this article)

10/50. Severe exacerbation of hepatitis c-associated vasculitic neuropathy following treatment with interferon alpha: a case report and literature review.

    Vasculitic neuropathy may occur in association with chronic hepatitis c infection. Interferon alpha (IFN(alpha)), an effective treatment for chronic hepatitis c, can precipitate or worsen autoimmune diseases. We report a patient with chronic hepatitis c and mild indolent vasculitic sensorimotor peripheral polyneuropathy, who developed severe mononeuropathy multiplex soon after IFN(alpha) was initiated, and review the literature on worsening vasculitic neuropathy after IFN(alpha) treatment for chronic hepatitis c. Care should be taken after starting patient with chronic hepatitis c-associated vasculitic neuropathy on IFN(alpha), as there is evidence that IFN(alpha) may exacerbate the neuropathy.
- - - - - - - - - -
ranking = 1.5
keywords = hepatitis
(Clic here for more details about this article)
| Next ->


Leave a message about 'Peripheral Nervous System Diseases'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.