Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to present neurological complications of influenza infections. Infections caused by influenza viruses can be very serious and may lead even to death resulted from the post-infectious complications. The most often occurring complications are pneumonia, bronchitis, bronchiolitis, myocarditis and otitis media. The other group is neurological post-influenza complications, including dementia, epileptic disorders, cerebrovascular disease, febrile convulsions, toxic encephalopathy, encephalitis, meningitis, subarachnoid hemorrhages, lethargic encephalitis, psychosis or increase in the number of cases of Parkinson's disease. The first way of prevention of influenza is vaccination that results in healthy, social and economic benefits.
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PMID:[Neurological complication of influenza infections]. 1219 26

In 1916, von Economo first described encephalitis lethargica (EL), a CNS disorder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkinsonism) and neuropsychiatric sequelae. Since the 1916-1927 epidemic, only sporadic cases have been described. Pathological studies revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell) infiltration. The EL epidemic occurred during the same time period as the 1918 influenza pandemic, and the two outbreaks have been linked in the medical literature. However, von Economo and other contemporary scientists thought that the 1918 influenza virus was not the cause of EL. Recent examination of archived EL brain material has failed to demonstrate influenza RNA, adding to the evidence that EL was not an invasive influenza encephalitis. By contrast, the findings of intrathecal oligoclonal bands (OCB) and beneficial effects of steroid treatments have provoked the hypothesis that EL may be immune-mediated. We have recently seen 20 patients with a similar EL phenotype, 55% of whom had a preceding pharyngitis. The patients had remarkable similarity to the historical descriptions of EL: sleep disorder (somnolence, sleep inversion or insomnia), lethargy, parkinsonism, dyskinesias and neuropsychiatric symptoms. CSF examination commonly showed elevated protein and OCB (75 and 69% respectively). Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism. MRI of the brain was normal in 60% but showed inflammatory changes localized to the deep grey matter in 40% of patients. We investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea. Anti-streptolysin-O titres were elevated in 65% of patients. Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens. These antibodies were also present in the CSF in four patients tested. By contrast, antibodies reactive against the basal ganglia were found in only 2-4% of child and adult controls (n = 173, P < 0.0001). Rather than showing polyspecific binding, these antibodies bound to common neural autoantigens of molecular weight 40, 45, 60 and 98 kDa. Regional tissue comparisons showed that the majority of these autoantigens were specific to or enriched in CNS tissue. Immunohistochemistry with secondary staining localized antibody binding to neurons rather than glial populations. Further investigation is required to determine whether these antibodies affect neuronal function (i.e. whether they are pathogenic anti-neuronal antibodies). Histopathology in one case demonstrated striatal encephalitis with perivenous B- and T-lymphocytic infiltration. We believe an EL-like syndrome is still prevalent, and propose that this syndrome may be secondary to autoimmunity against deep grey matter neurons.
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PMID:Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity. 1467 31

Interferon-alpha (IFN) is widely used for the treatment of viral illnesses and other chronic diseases, though its usefulness is hampered by a problematic side-effect profile. In particular, IFN-alpha induces neuropsychiatric and neurotoxic side effects, including depression, anxiety, insomnia, lethargy, confusion, and psychosis. Of particular interest, a number of patients develop full psychiatric syndromes, particularly depressive disorders. Recent evidence suggests that conventional antidepressants (especially selective serotonin reuptake inhibitors) are effective in preventing or reducing IFN-induced side-effects, but even these compounds are not 100% effective in preventing these symptoms. As such, alternative treatments must be considered. Non-steroidal anti-inflammatory drugs (NSAIDs) are known to counteract a number of IFN-induced side effects, including cytokine activation, stress hormone release, and neurochemical alterations (reduced 5-HT [serotonin]). NSAIDs are widely recommended for various aspects of flu-like symptoms or sickness behaviors in humans, including those induced specifically by IFN. In addition, NSAIDs appear to be effective in treating premenstrual dysphoric disorder. These data indirectly specify a role for NSAIDs in syndromes with a prominent depression component. Drawing from an extensive pre-clinical and clinical research base, we hypothesize that pretreatment with NSAIDs will not only reduce the incidence of flu-like symptoms, but also prove effective for the prevention or reduction of IFN-induced depression.
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PMID:IFN-induced depression: a role for NSAIDs. 1460 39

The 2004 outbreaks of H5N1 influenza viruses in Vietnam and Thailand were highly lethal to humans and to poultry; therefore, newly emerging avian influenza A viruses pose a continued threat, not only to avian species but also to humans. We studied the pathogenicity of four human and nine avian H5N1/04 influenza viruses in ferrets (an excellent model for influenza studies). All four human isolates were fatal to intranasally inoculated ferrets. The human isolate A/Vietnam/1203/04 (H5N1) was the most pathogenic isolate; the severity of disease was associated with a broad tissue tropism and high virus titers in multiple organs, including the brain. High fever, weight loss, anorexia, extreme lethargy, and diarrhea were observed. Two avian H5N1/04 isolates were as pathogenic as the human viruses, causing lethal systemic infections in ferrets. Seven of nine H5N1/04 viruses isolated from avian species caused mild infections, with virus replication restricted to the upper respiratory tract. All chicken isolates were nonlethal to ferrets. A sequence analysis revealed polybasic amino acids in the hemagglutinin connecting peptides of all H5N1/04 viruses, indicating that multiple molecular differences in other genes are important for a high level of virulence. Interestingly, the human A/Vietnam/1203/04 isolate had a lysine substitution at position 627 of PB2 and had one to eight amino acid changes in all gene products except that of the M1 gene, unlike the A/chicken/Vietnam/C58/04 and A/quail/Vietnam/36/04 viruses. Our results indicate that viruses that are lethal to mammals are circulating among birds in Asia and suggest that pathogenicity in ferrets, and perhaps humans, reflects a complex combination of different residues rather than a single amino acid difference.
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PMID:Lethality to ferrets of H5N1 influenza viruses isolated from humans and poultry in 2004. 1568 21

Highly pathogenic H5N1 influenza viruses have infected an increasing number of humans in Asia, with high mortality rates and the emergence of multiple distinguishable clades. It is not known whether antiviral drugs that are effective against contemporary human influenza viruses will be effective against systemically replicating viruses, such as these pathogens. Therefore, we evaluated the use of the neuraminidase (NA) inhibitor oseltamivir for early postexposure prophylaxis and for treatment in ferrets exposed to representatives of two clades of H5N1 virus with markedly different pathogenicities in ferrets. Ferrets were protected from lethal infection with the A/Vietnam/1203/04 (H5N1) virus by oseltamivir (5 mg/kg of body weight/day) given 4 h after virus inoculation, but higher daily doses (25 mg/kg) were required for treatment when it was initiated 24 h after virus inoculation. For the treatment of ferrets inoculated with the less pathogenic A/Turkey/15/06 (H5N1) virus, 10 mg/kg/day of oseltamivir was sufficient to reduce the lethargy of the animals, significantly inhibit inflammation in the upper respiratory tract, and block virus spread to the internal organs. Importantly, all ferrets that survived the initial infection were rechallenged with homologous virus after 21 days and were completely protected from infection. Direct sequencing of the NA or HA1 gene segments in viruses isolated from ferret after treatment showed no amino acid substitutions known to cause drug resistance in conserved residues. Thus, early oseltamivir treatment is crucial for protection against highly pathogenic H5N1 viruses and the higher dose may be needed for the treatment of more virulent viruses.
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PMID:Efficacy of oseltamivir therapy in ferrets inoculated with different clades of H5N1 influenza virus. 1729 44

Interferon-alpha-2a, a single interferon-alpha subtype manufactured by use of recombinant DNA technology, has immmunomodulatory, antiviral and antiproliferative properties. It is a beneficial treatment for about 30% of patients with well-compensated chronic hepatitis C. Biochemical responses [defined as normalisation of serum alanine aminotransferase (ALT) levels] are achieved in 37 to 76% of patients at the end of treatment with interferon-alpha-2a at dosages of 3 to 6MU 3 times weekly (given intramuscularly or subcutaneously) for 6 to 12 months. In contrast, evidence of disease remission is seldom observed in untreated patients. Improvements in liver histology in patients receiving interferon-alpha-2a are associated with complete biochemical responses to the drug. Virological responses (defined as an absence of hepatitis C-RNA in the serum) occur in up to 86% of patients after treatment with interferon-alpha-2a 3 to 6MU 3 times weekly for 12 months. After cessation of interferon-alpha-2a therapy, a considerable proportion of treatment responders experience disease reactivation. Rates of sustained biochemical response are generally higher after 12 months' therapy (27 to 57%) than after 6-month courses of treatment (27 to 30%). The long term efficacy of interferon-alpha-2a in patients with chronic hepatitis C is improved by the concomitant administration of ribavirin. Interferon-alpha-2a shows efficacy similar to that of interferon-alpha-2b or interferon-alpha-n1 in patients with chronic hepatitis C. During the first few days of therapy with interferon-alpha-2a (or other forms of interferon-alpha), most patients experience a transient 'influenza-like' reaction, characterised by fatigue, fever, chills and headache. These symptoms are usually alleviated by paracetamol (acetaminophen). Lethargy, mild myelosuppression, alopecia and neuropsychiatric symptoms are dose-limiting adverse effects that may occur during longer term therapy. Severe adverse effects, experienced by <2% of interferon-alpha-2a recipients, include severe depression, seizures and generalised bacterial infections. Autoimmune thyroid dysfunction develops in 3 to 12% of patients during treatment with interferon-alpha-2a. Conclusion. Interferon-alpha-2a produces sustained responses in about 30% of adults with chronic hepatitis C. Its efficacy appears to be similar to that of other interferon-alpha products. Thus, the drug remains a useful first-line treatment option for adults with well-compensated chronic hepatitis C. Further research into the optimal dosage of interferon-alpha-2a and its role in combination with other agents is likely to contribute towards future advances in the management of chronic hepatitis C.
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PMID:Interferon-alpha-2a: a review of its use in chronic hepatitis C. 1802 May 86

We report a case of HIV-1 infection transmission caused by a fist fight between brothers. A 30-year-old Caucasian UK resident man developed 'flu-like illness with symptoms of lethargy and weakness. Persistent lymphadenopathy six months later lead to HIV antibody testing, which was positive. Of note, his 37-year-old brother, who was HIV antibody-positive since August 2000, was taking HAART (combivir and nevaripine) with CD4 350 x 106/L (16%) with viral load 4800 copies/mL (log 2.58). A bloody fight had occurred between them four weeks prior to onset of symptoms. Phylogenetic analysis was undertaken. Analysis of the pol gene region indicated that samples from both brothers belonged to the subtype C clade of HIV-1, and that the sequences were closely related to one another. Exposure risk data are extremely useful in helping counsel patients prior to HIV-testing but, as this case illustrates, does not cover all situations.
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PMID:Transmission of HIV-1 infection due to a fist fight. 1833 72

Swine origin influenza was first recognized in the border area of Mexico and United States in April 2009 and during a short span of two months became the first pandemic. The currently circulating strain of swine origin influenza virus of the H1N1 strain has undergone triple reassortment and contains genes from the avian, swine and human viruses. It is transmitted by droplets or fomites. Incubation period is 2 to 7 days. Common clinical symptoms are indistinguishable by any viral respiratory illness, and include fever, cough, sore throat and myalgia. A feature seen more frequently with swine origin influenza is GI upset. Less than 10% of patients require hospitalization. Patients at risk of developing severe disease are - younger than five years, elderly, pregnant women, with chronic systemic illnesses, adolescents on aspirin. Of the severe manifestations of swine origin influenza, pneumonia and respiratory failure are the most common. Unusual symptoms reported are conjunctivitis, parotitis, hemophagocytic syndrome. Infants may present with fever and lethargy with no respiratory symptoms. Diagnosis is based on RT PCR, Viral culture or increasing neutralizing antibodies. Principle of treatment consist of isolation, universal precautions, good infection control practices, supportive care and use of antiviral drugs. Antiviral drugs effective against H1N1 virus include: oseltamivir and zamanavir. With good supportive care case fatality is less than 1%. Preventive measures include: social distancing, practicing respiratory etiquette, hand hygiene and use of chemoprohylaxis with antiviral drugs. Vaccine against H1N1 is not available at present, but will be available in near future.
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PMID:Swine origin influenza (swine flu). 1980 52

This flu season, health care providers must be prepared to treat patients who have the seasonal flu and also those who have contracted a novel strain of the H1N1 influenza virus. Although H1N1 flu is sometimes incorrectly called "swine flu," the virus is transmitted from person to person; it cannot be contracted from pigs or from eating pork products. Symptoms of the H1N1 flu include fever, chills, nausea, vomiting, body aches, lethargy, and fatigue, which usually appear in rapid succession. People at high risk include children, pregnant women, and those with certain medical conditions. The most common cause of death from the virus is respiratory failure, but other causes of mortality include sepsis, dehydration, and electrolyte imbalance. The first line of defense against H1N1 flu is vaccination. Treatment includes use of antiemetics, antipyretics, and respiratory support.
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PMID:The enigma of the H1N1 flu: are you ready? 1996 71

Seasonal flu is caused by influenza viruses A and B. These enveloped viruses have a genome made up of seven or eight RNA fragments. The different subtypes are determined by the nature of the two surface glycoproteins HA and NA. Seasonal flu is an epidemic wintertime illness occurring in temperate climate zones. Its epidemiology is linked to the great variability of the virus in time, necessitating an alert system that detects dominating circulating variants each year and that determines the vaccination composition. Clinical flu symptoms are not sufficiently specific to allow for diagnosis with virological tests. This is especially true during non-epidemic periods as well as in subjects older than 65 and younger than five. Children are especially vulnerable to influenza virus infections. Hospitalization occurs more frequently, the younger the child. In children younger than two years, the infection can be pauci-symptomatic and is sometimes detected from non-respiratory symptoms such as lethargy, convulsions, and dizziness. In all cases of respiratory syndrome compatible with influenza virus infection in hospitalized subjects, virological flu diagnosis is of utmost interest. Several tools are available to allow for direct viral detection in respiratory specimens: cell culture isolation, antigenic detection, RNA molecular detection. Choice of method is based on the characteristics of the test: sensibility, specificity, speed and ease of realization, and cost.
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PMID:[Seasonal flu]. 2030 76


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