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Query: UMLS:C0019158 (
hepatitis
)
30,205
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Biological agents are increasingly used for a rapidly-expanding number of rheumatic and systemic autoimmune diseases, with a growing number of reports of the paradoxical induction of autoimmune processes, overwhelmingly associated with anti-TNF agents. In this review, we analyze the clinical characteristics and outcomes of autoimmune diseases developing after biological therapies through a baseline Medline search as one of the objectives of the BIOGEAS project, created by the Spanish Society of Internal Medicine. The latest update of our registry (15 July 2009) included more than 800 cases of autoimmune diseases secondary to biological therapies, including a wide variety of both systemic (lupus, vasculitis, sarcoidosis and antiphospholipid syndrome) and organ-specific (interstitial lung disease, uveitis,
optic neuritis
, peripheral neuropathies, multiple sclerosis and autoimmune
hepatitis
) autoimmune processes. The majority of cases appeared between one month and one year after initiation of the biological agent and complete resolution was observed in nearly 75% of cases after cessation of therapy. The induced autoimmune diseases with the poorest outcomes were interstitial lung disease, inflammatory ocular disease and central nervous system demyelinating diseases.
...
PMID:Autoimmune diseases induced by biological agents: a double-edged sword? 1985 1
After intracranial inoculation, neurovirulent mouse
hepatitis
virus (MHV) strains induce acute inflammation, demyelination, and axonal loss in the central nervous system. Prior studies using recombinant MHV strains that differ only in the spike gene, which encodes a glycoprotein involved in virus-host cell attachment, demonstrated that spike mediates anterograde axonal transport of virus to the spinal cord. A demyelinating MHV strain induces
optic neuritis
, but whether this is due to the retrograde axonal transport of viral particles to the retina or due to traumatic disruption of retinal ganglion cell axons during intracranial inoculation is not known. Using recombinant isogenic MHV strains, we examined the ability of recombinant MHV to induce
optic neuritis
by retrograde spread from the brain through the optic nerve into the eye after intracranial inoculation. Recombinant demyelinating MHV induced macrophage infiltration of optic nerves, demyelination, and axonal loss, whereas
optic neuritis
and axonal injury were minimal in mice infected with the nondemyelinating MHV strain that differs in the spike gene. Thus,
optic neuritis
was dependent on a spike glycoprotein-mediated mechanism of viral antigen transport along retinal ganglion cell axons. These data indicate that MHV spreads by retrograde axonal transport to the eye and that targeting spike protein interactions with axonal transport machinery is a potential therapeutic strategy for central nervous system viral infections and associated diseases.
...
PMID:Macrophage-mediated optic neuritis induced by retrograde axonal transport of spike gene recombinant mouse hepatitis virus. 2157 36
The areas of Europe in which West Nile virus (WNV)-transmission to humans is observed have expanded over the last few years, with endemic circulation amongst animals of southern Europe. This situation calls for heightened vigilance to the clinical presentation of WNV infection in humans. The average incubation period lasts 2-6 days. Of those infected, 20% will experience a mild, non-specific disease presentation such as high fever, headache, myalgia, possibly with rash and lymphadenopathy; <1% will develop severe neurological symptoms. Rare complications include: myelitis,
optic neuritis
, rhombencephalitis, polyradiculitis, myocarditis, pancreatitis and fulminant
hepatitis
. Clinicians should take WNV infection into consideration when making a differential diagnosis for such symptoms in patients who have returned from areas with potential virus circulation. Given the increase in the spread of WNV within Europe, this now holds true for continental travellers as well as those destined for the Americas, Africa and Asia. It is important to include the patient's travel history, clinical symptoms and any occurrences of vaccination against viruses causing Japanese encephalitis, tick-borne encephalitis and yellow fever into the diagnostic workup, as the antibodies against these diseases show cross-reactivity.
...
PMID:[West Nile virus expanding in Europe]. 2196 90
Neuromyelitis optica spectrum disorder (NMOSD) is characterized by
optic neuritis
or transverse myelitis with anti-aquaporin 4 (AQP4) antibodies (1). We herein present the case of a patient with NMOSD who also was affected with peripheral neuropathy. A 58-year-old woman developed gait disturbance and sensory impairment in the lower limbs. She exhibited longitudinally extensive transverse myelitis with anti-AQP4 antibodies. Nerve conduction studies showed demyelinating changes. Laboratory findings showed
hepatitis
-C virus (HCV) infection. Her peripheral neuropathy improved after immunotherapy. There have been no previous reports of NMO or NMOSD associated with neuropathy. The HCV infection or undetermined humoral factors other than the anti-AQP4 antibodies may have caused her peripheral neuropathy.
...
PMID:Acute combined central and peripheral demyelination showing anti-aquaporin 4 antibody positivity. 2297 65
Fulminant hepatitis due to acute hepatitis C virus (HCV) infection is rarely observed. We present a case study of a 21-year-old male patient who developed HCV-associated fulminant
hepatitis
after receiving steroid pulse therapy for
optic neuritis
. Despite daily plasmapheresis, the disease progressed to irreversible liver failure with grade 3 hepatic encephalopathy by the 6th day after symptom onset. The patient received a liver transplant on the 8th day. Serum anti-HCV antibody was negative at that time, but became positive on the 12th day. Positive HCV RNA in the serum at admission was reported after transplantation. Positive changes in anti-HCV antibodies and acute hepatitis with massive necrosis in the histology of the explanted liver indicated fulminant
hepatitis
due to acute HCV infection. Because of severe
hepatitis
recurrence, he started 12 months of interferon therapy on the 48th day, and obtained sustained virological response. His anti-HCV antibodies became negative again by 1.5 years after cessation of therapy. HCV genomes recovered from the patient's serum on the 7th and 48th days revealed 2 different clones out of 20 clones with 30 % amino acid difference in hypervariable region 1 of HCV second envelope glycoprotein. One of the 2 clones expanded further after liver transplantation. We conclude that early diagnosis of HCV-associated fulminant
hepatitis
requires the detection of HCV RNA in the serum. Severe
hepatitis
recurrence after liver transplantation might occur in patients with fulminant
hepatitis
due to HCV because of its monoclonal expansion.
...
PMID:A case of fulminant liver failure associated with hepatitis C virus. 2618 36
The classical presentation of secondary syphilis comprises skin rashes, mucosal ulceration and lymphadenopathy. However, this disseminated stage can also present with symptoms and signs of ocular, neurological, pulmonary, renal, musculoskeletal and digestive tract disease. We report the case of a gay man who presented with icteric
hepatitis
. Although he underwent an exhaustive series of investigations (some of which were invasive), syphilis was not initially considered in the differential diagnosis. His jaundice resolved spontaneously, but he subsequently developed an acute
optic neuritis
. Early syphilis is relatively common in men who have sex with men (MSM). Prompt diagnosis and treatment in this case would have prevented ocular involvement. Syphilis testing should be considered in all MSM presenting with unexplained symptoms and signs.
...
PMID:Syphilitic jaundice: a rare manifestation of the secondary stage presenting a missed opportunity to prevent ocular syphilis. 2930 12
Neurotropic strains of mouse
hepatitis
virus (MHV) induce acute inflammation and chronic demyelination in the spinal cord and optic nerves mediated by axonal spread following intracranial inoculation in mice, with pathologic features similar to the human demyelinating disease multiple sclerosis. Spinal cord demyelination is also induced following intranasal inoculation with neurotropic MHV strains, however much higher viral doses are required as compared to intracranial inoculation. Recently, it was shown that intranasal administration of low concentrations of proteins leads to significant, rapid accumulation of protein in the optic nerve and in the eye, with only low levels reaching spinal cord and other brain regions. Thus, we examined whether intranasal inoculation with MHV at doses equivalent to those given intracranially could induce
optic neuritis
-inflammation, demyelination and loss of retinal ganglion cells (RGCs) in the optic nerve with or without inducing spinal cord demyelination. Four week old male C57BL/6J mice were inoculated intracranially with the recombinant demyelinating strain RSA59, or intranasally with RSA59 or the non-demyelinating strain RSMHV2 as control. One month post-inoculation, mice inoculated intracranially with RSA59 had significant myelin loss in both spinal cord and optic nerves, with significant loss of RGCs as well, consistent with prior studies. As expected, intranasal inoculation with RSA59 failed to induce demyelination in spinal cord; however, it also did not induce optic nerve demyelination. No acute inflammation was found, and no viral antigen was detected, in the optic nerve or retina 1 day after inoculation. Results confirm the neurotropic effects of RSA59 following intracranial inoculation, and suggest that direct infection with axonal transport of virus from brain to spinal cord and optic nerve is required to induce demyelinating disease. These studies suggest that MHV does not selectively concentrate in optic nerve and retina to sufficient levels to induce demyelination following intranasal inoculation. Intracranial inoculation should continue to be considered a preferred method for studies of MHV-induced
optic neuritis
and central nervous system (CNS) demyelinating disease.
...
PMID:Intracranial Inoculation Is More Potent Than Intranasal Inoculation for Inducing Optic Neuritis in the Mouse Hepatitis Virus-Induced Model of Multiple Sclerosis. 3023 31
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