Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A child with acute encephalopathy and liver dysfunction subsequently developed acute chylous ascites. Titers for cytomegalovirus increased from less than 1:2 to 1:32 during the illness, and cytomegalovirus was isolated from the urine. The case is the first one possibly linking cytomegalovirus and acute encephalopathy and liver dysfunction in a child. In our patient, enlargement of the abdominal lymph nodes, as seen on a lymphangiogram, resulted in a severe obstruction of abdominal lymphatic flow, producing a transudation of lymph into the peritoneal cavity. The acute chylous ascites associated with mesenteric lymphadenitis was likely caused by the cytomegalovirus infection.
Infection 1977
PMID:Acute encephalopathy with liver dysfunction, chylous ascites and cytomegalovirus infection. 20 66

To assess the role of complement and complement receptors in HIV-1 infection of monocytes and macrophages, we studied the infectivity of HIV-1, isolated from the peripheral blood of a patient with subacute AIDS-related encephalopathy, on the human monoblastoid cell line U937. HIV-1 and HIV-1-infected cells were capable of activating the complement system via the classical and the alternative pathways, respectively. Low concentrations of HIV-1 were able to infect U937 cells more easily in the presence than in the absence of complement. At higher virus concentrations, infectivity was no longer facilitated by the presence of complement. Infection of U937 cells was reduced in the presence of any of the monoclonal antibodies (MAbs), OKT4a (anti-CD4), OKM1 (anti-CR3), or M522 (anti-CR3). A combination of all three of these MAbs reduced the infection by an even greater amount. These data indicate that complement receptors may be a port of entry for complement-coated HIV-1.
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PMID:Complement-mediated enhancement of HIV-1 infection of the monoblastoid cell line U937. 226 Nov 26

Recent improvements in the results of orthotopic liver transplantation (OLT) have made this a well-accepted treatment for patients with severe hepatic failure. Current problems encountered following OLT are discussed. Immediate complications comprise surgical bleeding, primary graft non-function, and graft failure due to hepatic artery occlusion. Secondary complications are frequent. Surgical ones include biliary and vascular (hepatic artery thrombosis most often) problems, as well as intra-abdominal abscesses associated with gastrointestinal perforation, biliary leak, graft ischaemia or an infected haematoma. 40% of patients having undergone OLT will be reoperated on, 2/3 of them within 3 months. Non-surgical complications are mostly pulmonary. The risk of pneumonitis is increased by prolonged mechanical ventilation; it is always potentially disastrous in the immunosuppressed, transplanted patient. Hypertension is also often seen in the early postoperative period; it requires prompt treatment. Early renal impairment after OLT is common, and of better prognosis than late onset renal failure, which is generally associated with shock, graft failure, sepsis or use of nephrotoxic agents. Seizures, usually only one, occur in about 10% of patients; recovery is complete. Encephalopathy with intracranial oedema related to fulminant hepatitis has a worse prognosis, but survival figures are quite encouraging. Three type of rejection are described after OLT: 1) severe accelerated rejection (very rare), 2) acute rejection encountered in about 70% of patients over the first 3 months, and 3) late rejection, which can lead to the vanishing bile duct syndrome (VBDS). Diagnosis of rejection is made by liver biopsy. Prophylactic immunosuppression includes cyclosporin, methylprednisolone and azathioprine. Cyclosporin toxicity and drug interactions are reviewed. Treatment of acute rejection episodes comprises an initial bolus of high doses of corticoid drugs; if there is no response, antilymphocyte globulin or monoclonal antibodies may have to be used. Infection is the main cause of death following OLT. Early infections, mostly intra-abdominal and pulmonary, are bacterial or fungal. Vital (especially CMV) and other opportunistic infections occur generally after the second week. Retransplantation, carried out in 10 to 25% of patients, may be urgent in case of primary graft failure, or hepatic artery thrombosis associated with graft failure, or hepatic artery thrombosis associated with graft failure. Other indications are early graft rejection with severe hepatic dysfunction, chronic rejection with severe VBDS, and recurrence of the initial disease.
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PMID:[Liver transplantation in adults: postoperative management and development during the first months]. 262 46

The human immunodeficiency virus (HIV) penetrates the central nervous system, particularly the cerebrospinal fluid, early in the course of HIV infection, and may cause a progressive encephalopathy in patients prior to the development of the acquired immunodeficiency syndrome. Neither the specific mechanism for penetration of the virus into the central nervous system nor the pathophysiological basis for these abnormalities is well understood. We cultured cells from the choroid plexus of 3 individuals who died of causes unrelated to the acquired immunodeficiency syndrome and demonstrated that these cells can be infected with type 1 HIV. Infection of cells of the choroid plexus may provide an initial route of entry of HIV into the cerebrospinal fluid and, together with the macrophage, a route of entry into the brain.
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PMID:Human choroid plexus cells can be latently infected with human immunodeficiency virus. 265 76

Bacterial infection is a serious and often fatal complication of patients with liver disease and can prove fatal either directly or by precipitation of gastrointestinal bleeding, renal failure, or hepatic encephalopathy. At greatest risk are patients with alcoholic cirrhosis or decompensated chronic liver disease, or cases of acute liver disease who progress to fulminant hepatic failure or subacute hepatic necrosis. Infection appears to be unusual in patients with primary biliary cirrhosis. The site and type of infection is unrelated to the aetiology of the liver disease. Bacteraemia, pneumonia, urinary tract infection and spontaneous bacterial peritonitis are most common but infective endocarditis and meningitis, especially with pneumococci, are easily overlooked. Clinical suspicion of infection must be high as the only indication may be a general deterioration in the patients' clinical state, increasing encephalopathy or renal impairment. In the case of patients with fulminant hepatic failure, infection may precipitate the initial or recurrent encephalopathy and contributes to death in 10% of fatal cases. Spontaneous bacterial peritonitis is now recognized to occur in the absence of clinical features of peritonitis. The PMN content of the ascitic fluid may provide the only indication of infection and is the most readily available screening test. The most common types of organism responsible for all types of infection are Gram-negative enteric and streptococci, especially pneumococci, while infection with anaerobes is rare. Risk factors for infection include decompensated alcoholic liver disease, fulminant hepatic failure, gastrointestinal bleeding, invasive practical procedures and impaired host defence mechanisms against infection. Of the host defence mechanisms, impaired function of the reticuloendothelial system, complement, and PMNs represent the most common and serious defects. Defects of humoral immunity are present in ascitic fluid from patients with cirrhosis and are probably a major reason for development of spontaneous bacterial peritonitis. Diuresis improves these functions and reduces the risk of peritonitis. Treatment of infections even with the appropriate antibiotic is still associated with a high mortality but the use of adjuvant gut sterilization is promising, particularly in cases infected with Gram-negative enteric organisms. Infusions of fresh frozen plasma, blood and cryoprecipitate improve some systemic host defences and may be beneficial in the treatment and reduction of risk of infection.
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PMID:Bacterial infections complicating liver disease. 265 49

Infection with the AIDS virus itself (HIV, HTLV-III, LAV, ARV) is associated with a full spectrum of neurological disorders. The application of diagnostic studies for HTLV-III infection has demonstrated that these neurologic disorders can be the first manifestation of AIDS or occur in the absence of AIDS. The most common conditions associated with HTLV-III infection alone are a subacute encephalopathy (AIDS dementia) and peripheral neuropathy; however, vacuolar myelopathy and both acute and chronic aseptic meningitis are also common. Congenital (or neonatal) transmission of the virus can result in a mental retardation syndrome of delayed onset. The AIDS virus is neurotropic as well as targeting T-helper lymphocytes. The virus has been readily identified in neural tissues and cerebrospinal fluid, including instances in which other central nervous system infections, such as toxoplasmosis, coexist. Hence, recognition of an appropriate syndrome, neurodiagnostic studies, and exclusion (or treatment) of other infections, as well as evidence for HTLV-III infection are required for diagnosis. The development of successful therapy will require agents which cross the blood-brain barrier.
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PMID:Neurology of AIDS virus infection: a clinical classification. 282 50

Recombinant human colony-stimulating factor-1-treated human peripheral blood-derived monocytes-macrophages are efficient host cells for recovery of the human immunodeficiency virus (HIV) from blood leukocytes of patients with acquired immunodeficiency syndrome. These cells can be maintained as viable monolayers for intervals exceeding 3 months. Infection with HIV resulted in virus-induced cytopathic effects, accompanied by relatively high levels of released progeny virus, followed by a prolonged low-level release of virus from morphologically normal cells. In both acutely and chronically infected monocytes, viral particles were seen budding into and accumulating within cytoplasmic vacuoles. The number of intravacuolar virions far exceeded those associated with the plasma membrane, especially in the chronic phase, and were concentrated in the perinuclear Golgi zone. In many instances, the vacuoles were identified as Golgi elements. Fusion of virus-laden vacuoles with primary lysosomes were rare. The pattern of cytoplasmic assembly of virus was observed with both HIV types 1 and 2 and in brain macrophages of an individual with acquired immunodeficiency syndrome encephalopathy. Immunoglobulin-coated gold beads added to acutely infected cultures were segregated from the vacuoles containing virus; relatively few beads and viral particles colocalized. The assembly of HIV virions within vacuoles of macrophages is in contrast to the exclusive surface assembly of HIV by T lymphocytes. Intracytoplasmic virus hidden from immune surveillance in monocytes-macrophages may explain, in part, the persistence of HIV in the infected human host.
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PMID:Cytoplasmic assembly and accumulation of human immunodeficiency virus types 1 and 2 in recombinant human colony-stimulating factor-1-treated human monocytes: an ultrastructural study. 326 Jun 31

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

In a five-year retrospective study, there were 57 episodes of bacteremia among 1623 admissions (3.5%) of patients suffering from cirrhosis. Gram-positive bacteria were found in 70% of the episodes, gram-negative bacteria in 30%. All of the gram-positive bacteria found were fully sensitive to methicillin and to gentamicin. The gram-negative bacteria found were all sensitive to gentamicin, but only 50% were sensitive to ampicillin. The distribution between gram-positive and gram-negative bacteria was the same, irrespective of whether the patients acquired the infection inside or outside the hospital. More than 50% of the patients suffered from one or more of the following complications of cirrhosis: ascites, encephalopathy and haematemesis. Twenty-one patients died within seven days after the bacteremia was diagnosed. Bacteremia is a serious complication of advanced cirrhosis, and it is recommended that adequate antibiotic treatment is started when septicemia is suspected.
Infection
PMID:Bacteremia in patients suffering from cirrhosis. 371 May 95

Infection by JE virus still constitutes major cause of encephalitis in Chiang Mai Area, although some cases of possible dengue encephalopathy were observed. In spite of many apparent encephalitis cases, infection of vector mosquitoes by JE virus was not demonstrated. Virus isolation from hospitalized patients showed that the principal type of dengue virus circulating in Chiang Mai in 1982 was type 1 virus. Seroepidemiological survey on healthy humans indicated that the northern part of Chiang Mai Province in the region of the Maekong Valley has not yet been invaded so much by dengue viruses, compared with the Chiang Mai Valley, where dengue infection apparently became more prevalent than 12 years ago. The survey also indicated that the spread of JE virus in the study area was not uniform. Survey on vertebrates showed that anti-JE antibodies were highly prevalent among swine, horses, mules, sheep, and dogs. On the other hand, antibody prevalence was low in monkeys, ducks, and sparrows, and was negative among chickens and lizards. IgM-ELISA appeared to help differential diagnosis on JE from dengue even when the HI test did not give positive results.
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PMID:Flavivirus infections in Chiang Mai area, Thailand, in 1982. 632 86


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