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)

Clinical studies in an acute medical unit were aimed at the analysis of the onset and clinical appearance of masked acute pneumonia. Such acute pneumonia masks as pulmonary edema, paroxysmal tachycardia, infective toxic shock, acute surgical conditions, hepatitis, pneumothorax considerably complicate the diagnosis of the underlying disease. However, some manifestations typical for acute pneumonia are recognizable. These, in combination with the above misleading symptoms, can be managed properly only provided close comprehensive examination of the patients is carried out.
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PMID:[Masks of acute pneumonia at an emergency care unit]. 262 13

We evaluated clinical presentations and complications retrospectively in 48 pediatric patients hospitalized for suspected measles during a measles epidemic in Chicago. Fifty-one percent were < 15 months of age and 75% were < 4 years of age. Measles, diagnosed in 44 patients, was culture-proved in 18. Presentations were not always classic. Respiratory complications, otitis media, hepatitis, preterm labor, keratitis and central nervous system involvement were reported. The presence of stomatitis and hypotension in some patients raised the differential diagnoses of Kawasaki disease and toxic shock syndrome. Six patients with stomatitis, admitted with a measles-like illness, fulfilled the Centers for Disease Control and Prevention criteria for Kawasaki disease. Three were diagnosed with Kawasaki disease and 3 with measles. In addition to serology and echocardiographic changes, the platelet count and the erythrocyte sedimentation rate may be useful in distinguishing between measles and Kawasaki disease. Two of 10 patients with hypotension met the Centers for Disease Control and Prevention criteria for toxic shock syndrome. The diagnosis of measles, solely on clinical grounds, may therefore not be as straightforward as is generally accepted.
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PMID:Clinical presentations and complications of suspected measles in hospitalized children. 828 20

Staphylococcal enterotoxin (SE) B causes serious gastrointestinal illness, and intoxication with this exotoxin can lead to lethal toxic shock syndrome. In order to overcome significant shortcomings of current rodent and nonhuman primate models, we developed a piglet model of lethal SEB intoxication. Fourteen-day-old Yorkshire piglets were given intravenous SEB, observed clinically, and sacrificed at 4, 6, 24, 48, 72, or 96 hrs posttreatment. Clinical signs were biphasic with pyrexia, vomiting, and diarrhea within 4 hrs, followed by terminal hypotension and shock by 96 hrs. Mild lymphoid lesions were identified as early as 24 hrs, with severe lymphadenopathy, splenomegaly, and prominent Peyer's patches found by 72 hrs. Widespread edema-most prominent in the mesentery, between loops of spiral colon, and in retroperitoneal connective tissue-was found in animals at 72 hrs. Additional histologic changes included perivascular aggregates of large lymphocytes variably present in the lung and brain, circulating lymphoblasts, and lymphocytic portal hepatitis. Preliminary molecular investigation using gene array has uncovered several gene profile changes that may have implications in the pathophysiology leading to irreversible shock. Five genes were selected for further study, and all showed increased mRNA levels subsequent to SEB exposure. The use of this piglet model will continue to elucidate the pathogenesis of SEB intoxication and facilitate the testing of new therapeutic regimens that may better correlate with human lesions.
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PMID:Functional piglet model for the clinical syndrome and postmortem findings induced by staphylococcal enterotoxin B. 1552 43

Exposure to bacterial superantigens such as staphylococcal enterotoxin B (SEB) leads to the induction of toxic shock syndrome which results in multiorgan failure, including liver damage. In the present study, we investigated the role of CD44 in SEB-induced liver injury. Injection of SEB into d-galactosamine-sensitized CD44 wild-type (WT) mice led to a significant increase in CD44 expression on liver T cells, NK cells, and NKT cells. Administration of SEB to CD44 knockout (KO) mice caused significantly enhanced liver damage which correlated with elevated numbers of T cells, NK cells, NKT cells, and macrophages in the liver and increased production of tumor necrosis factor alpha and gamma interferon compared to CD44 WT mice. Furthermore, liver mononuclear cells from CD44 KO mice were resistant to SEB-induced apoptosis, and cDNA microarray analysis revealed that SEB activation of such cells led to the induction of several antiapoptotic genes and repression of proapoptotic genes. Examination of CD44 isoforms revealed that SEB exposure altered CD44 variant 7 (v7) isoform expression. Interestingly, mice bearing a specific deletion of the CD44v7 exon exhibited increased susceptibility to SEB-induced hepatitis. Finally, treatment of CD44 WT mice with anti-CD44 monoclonal antibodies reduced expression of CD44 in liver mononuclear cells and caused increased susceptibility to SEB-induced liver injury. Together, these data demonstrate that the expression of CD44 and/or CD44v7 on SEB-activated liver mononuclear cells facilitates their rapid apoptosis, thereby preventing severe liver injury in wild-type mice, and suggest that CD44 plays an important role in the regulation and elimination of immune cells in the liver.
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PMID:Role of CD44 and its v7 isoform in staphylococcal enterotoxin B-induced toxic shock: CD44 deficiency on hepatic mononuclear cells leads to reduced activation-induced apoptosis that results in increased liver damage. 1561 40

Tumor necrosis factor (TNF, TNFalpha) is implicated in various pathophysiological processes and can be either protective, as in host defense, or deleterious, as in autoimmunity or toxic shock. To uncover the in vivo functions of TNF produced by different cell types, we generated mice with TNF ablation targeted to various leukocyte subsets. Systemic TNF in response to lipopolysaccharide was produced mainly by macrophages and neutrophils. This source of TNF was indispensable for resistance to an intracellular pathogen, Listeria, whereas T-cell-derived TNF was important for protection against high bacterial load. Additionally, both T-cell-derived TNF and macrophage-derived TNF had critical and nonredundant functions in the promotion of autoimmune hepatitis. Our data suggest that T-cell-specific TNF ablation may provide a therapeutic advantage over systemic blockade.
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PMID:Distinct and nonredundant in vivo functions of TNF produced by t cells and macrophages/neutrophils: protective and deleterious effects. 1566 62

In the last years has been observed an increased incidence of invasive group A beta-hemolytic streptococcal infections, including the toxic shock syndrome. The most common portal of entry is the skin and mucous membranes. The toxic shock syndrome can occurred as a rare complication of pharyngitis. The association between varicella and the use of nonsteroidal antiinflammatory drugs with necrotizing fasciitis by Streptococcus pyogenes has been discussed without reach at consensus, but some authors disapproved the use of nonsteroidal antiinflammatory drugs in this viral infection. The authors reported the clinical case of a 12 year old adolescent, that 15 days after the diagnosis of mononucleosis infectious confirmed by serology and treated with ibuprofen, was internment by streptococcal toxic shock syndrome with rhabdomyolysis, hepatitis, cellulitis of the leg, arthritis of the knee and pleural effusion. Therapeutics was made with penicillin G and clindamycin. We present this case for the severity of the clinical situation and for the questions that rise.
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PMID:[Group A beta-hemolytic streptococcal toxic shock]. 1619 48

Human and animal infections by Anaplasmataceae are increasingly recognized as important and potentially fatal arthropod-transmitted diseases. Since the first recognition and implementation of diagnostic methods for human infection by Ehrlichia chaffeensis and Anaplasma phagocytophilum, the incidence of infections has linearly increased. Moreover, diagnostic and epidemiological testing indicates that "ehrlichia" infections are globally distributed and suggests that additional agents of human and veterinary "ehrlichiosis" will be identified. With increasing disease identification has come recognition that the infections can be severe, with approximately one-half of patients requiring hospitalization for complications including respiratory distress, myocarditis, neurological complications, hepatitis, a septic or toxic shock-like disease, opportunistic infections, and death in 0.5 to 3.0%. An understanding of the diseases, pathophysiology, pathogenesis, control, and management will best be developed through fundamental investigations. Advances in comprehension as to the separate contributions of bacteria and host are crucial since most data now suggest that alterations in host neutrophil function and protection from innate and adaptive immunity also contribute to disease manifestations. It is reasonable to operate from the hypothesis that these host cell functional changes ultimately benefit bacterial survival while inadvertently eliciting clinical disease in poorly adapted hosts. A firmer basis for the scientific understanding of Anaplasmataceae biology will allow logical and rational approaches toward infection control, prevention, and treatment.
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PMID:Anaplasma and Ehrlichia infection. 1648 44

Any process that substantially diminishes arterial blood flow or arterial oxygen content to the liver can result in hypoxic (ischaemic) hepatitis. 90% of hypoxic hepatitis occurs in unstable patients in intensive care units with haemodynamic failure secondary to heart failure, respiratory failure and toxic shock. The rate of in-hospital mortality in hypoxic hepatitis is very high with studies recording mortalities of 61.5%. It tends to be very uncommon in healthy, young patients with no underlying medical problems. We report here the case of a young healthy athlete who developed heat stroke associated with rhabdomyolysis and hypoxic hepatitis while he was running the final stages of a marathon. The patient required intensive care admission and inotropic support for a few hours after he was admitted with heat stroke. He underwent a rapid recovery after he was resuscitated with fluids. N-acetyl cysteine was also given during the acute stage of the hepatitis. This case highlights an uncommon case of hypoxic hepatitis in a young, healthy patient secondary to hypotension and heat stroke. Inotropic support might have precipitated the hypoxic hepatitis in this young patient.
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PMID:Acute Liver Impairment in a Young, Healthy Athlete: Hypoxic Hepatitis and Rhabdomyolysis following Heat Stroke. 2301 16

Ulinastatin (UTI) is a trypsin inhibitor observed in urine. UTI can treat some diseases by inhibiting the broad-spectrum hydrolysis activity of various enzymes and other pharmacological effects. UTI can widely treat pancreatitis, systemic multiple organ dysfunction syndrome, circulatory failure, and toxic shock clinically. The liver is a major metabolic organ of the human body. Various biological metabolic reactions require the liver's participation. When various physical and chemical factors drive the body, it will damage the liver to varying degrees. As a clinically effective drug, UTI is also known to treat some liver diseases. This article mainly describes UTI's research progress in treating septic liver injury, hepatitis, liver fibrosis, autoimmune liver disease with liver failure, and liver ischemia-reperfusion injury.
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PMID:Research progress of ulinastatin in the treatment of liver diseases. 3328 67