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)

Sera were investigated of patients possibly suffering from an EBV infection, without showing clinical features characteristic of infectious mononucleosis. The method of investigation was the detection of antibodies of the IgM-type by means of the immunofluorescent method using a three-layer technique. Diagnosis of EBV infection was established in 10 out of 90 patients with facial palsy, one with myelitis, one with sudden deafness and one with polyneuritis. In addition, 4 out of 19 cases of hepatitis (Hbs-negative) proved to be due to infection with EBV. The specific IgM test proved to be superior to the heterophil agglutination test.
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PMID:[IgM diagnosis of Epstein-Barr virus (EBV) infections by means of the immunofluorescent method]. 18 14

Lyme disease typically begins with a unique skin lesion, erythema chronicum migrans (ECM) (stage 1). Patients with this lesion may also have headache, meningeal irritation, mild encephalopathy, multiple annular secondary lesions, malar or urticarial rash, generalized lymphadenopathy and splenomegaly, migratory musculoskeletal pain, hepatitis, sore throat, non-productive cough, conjunctivitis, periorbital edema, or testicular swelling. After a few weeks to months (stage 2), about 15% of patients develop frank neurologic abnormalities, including meningitis, encephalitis, cranial neuritis (including bilateral facial palsy), motor or sensory radiculoneuritis, mononeuritis multiplex, or myelitis. At this time, about 8% of patients develop cardiac involvement--AV block, acute myopericarditis, cardiomegaly, or pancarditis. Throughout this stage, many patients continue to experience migratory musculoskeletal pain in joints, tendons, bursae, muscle, or bone. Months to years after disease onset (stage 3), about 60% of patients develop frank arthritis, which may be intermittent or chronic. Recently evidence suggests that Lyme disease may also be associated with chronic neurologic or skin involvement. Thus, Lyme disease occurs in stages with different clinical manifestations at each stage, but the course of the illness in each patient is highly variable.
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PMID:Clinical manifestations of Lyme disease. 355 39

Mice inoculated intraperitoneally with herpes simplex virus type 2 develop focal necrotizing hepatitis and eventually die from ascending myelitis and encephalitis. The genetics of resistance to the infection were analyzed in crosses between resistant C57BL/10 mice and susceptible BALB/c mice. It was shown that the resistance of C57BL/10 mice to hepatitis induction was influenced by an X-linked dominant gene as previously shown for the GR mouse strain. The course of infection in the liver pointed to early, natural defense mechanisms as being responsible for the difference between the mouse strains, whereas the clearance of virus from the liver, probably mediated by specific immunity, was exerted at the same time and with equal efficiency for all groups of mice. In mortality experiments, resistance was shown to be an autointerference phenomenon in that a considerable number of C57BL/10 mice survived an intraperitoneal injection of 10(6) PFU, whereas all mice were killed by 10(5) PFU. This resistance of C57BL/10 mice to high doses of HSV-2 was retrieved in all groups of F1 mice in crosses between C57BL/10 and BALB/c mice except the (BALB/c female X C57 male) male group, in which the mice receive the X chromosome from the susceptible BALB/c female. Thus, the autointerference phenomenon also seems to be influenced by loci on the X chromosome. A similar pattern of inheritance was observed when early interferon induction (4 to 5 h after infection) in response to HSV-2 was measured. The possible relevance of this early interferon response in conjunction with other potential natural defense mechanisms is discussed.
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PMID:X-linked resistance of mice to high doses of herpes simplex virus type 2 correlates with early interferon production. 619 93

An autopsy case with endotoxemia-induced diffuse myelitis and extensive, grossly patchy necrosis of the liver occurring in a 70-year-old female was examined histopathologically and electron microscopically. Leucopenia with prominent leukemoid reaction (myeloblasts 20%) preceded the terminal fulminant hepatitis by two weeks. Soon after the terminal event, bacteremia and endotoxemia were detected and negativity for HB antigen was proved. Diffuse myelitis was characterized by devastation of hyperplastic bone marrow structure mottled with destructed sinus architecture and scattered exudative necrosis, resulting in the loss of mature granulocytes and erythropoiesis. Regenerative clusters of myeloblasts and prominent increase of megakaryocytes were observed. Electron microscopically, the bone marrow contained fibrin and platelets within the exudate of the marrow stroma. Extensive, grossly patchy necrosis of the liver microscopically consisted of well demarcated coagulation necrosis of hepatic parenchyma with scattered fibrin thrombi in the sinusoids at the boundary. There were no definite thrombi but occasional fibrin accumulation in the small blood vessels of the liver. Both extensive diffuse myelitis and extensive, patchy necrosis of the liver seemed to be quite rare in incidence. The pathogenesis of these combined lesions was discussed in relation with endotoxemia.
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PMID:Endotoxemia-induced diffuse myelitis and extensive patchy necrosis of the liver. 673 Sep 64

Disseminated infection with Mycobacterium avium complex is described in 3 adult Siamese cats. All cats were the result of father-daughter matings. Clinical signs included anorexia, weight loss, and lethargy. Physical examination revealed pale mucous membranes, lymphadenopathy, splenomegaly, and pyrexia. Nonregenerative anemia was detected in all 3 cats, and macrocytosis was observed in 2. An antemortem diagnosis of mycobacterial infection was made on the basis of identification of acid-fast bacilli in tissue aspirates. The cats died or were euthanatized owing to clinical deterioration, despite antibiotic treatment. Necropsy findings included granulomatous lymphadenitis, enterocolitis, pneumonia, cellulitis, myelitis, and hepatitis. Organisms from the Mycobacterium avium complex were identified in bacteriologic cultures of tissue samples.
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PMID:Disseminated Mycobacterium avium complex infection in three Siamese cats. 812 27

Since recent treatment planning systems calculate volumetric dose distribution, an objective evaluation of potential toxicity in the main critical organs may be helpful in treatment optimization. Modeling the toxicity of radiotherapy must at least account for: (a) specific risks in every critical organ; (b) total dose and dose per fraction; (c) partial irradiation of critical organs; (d) heterogeneous dose distribution. The Radiation Damage Factor formula is aimed at estimating the delayed toxicity of a given treatment plan on every critical organ concerned. The formulation uses a double exponential function: RDF = 100 e-Ke-(a+bd)DVc, where: D is the total dose, and d the dose per fraction; a and b are coefficients representing the radiosensitivity of the critical organ, according to the linear-quadratic model, with a/b = alpha/beta. K represents the theoretical critical unit content of the organ, these critical units being groups of functionally related stem cells. The avoidance of a complication depends on the ability of surviving critical units to preserve organ function. V is the ratio:irradiated volume/total volume of the organ. Exponent c accounts for tissue organization: c is equal to or near 1 in "parallel organs" like the liver or the lung, where localized hot spots are tolerated; c is lower in "series organs" like the spinal cord where hot spots, even in a small portion, are dangerous. Heterogeneous irradiation, summarized by dose cumulative-volume histograms, is accounted for by calculating step by step the dose D' considered as having an equivalent effect when given in the largest irradiated volume ratio. Preliminary calibration of the RDF formula is attempted for radiation myelitis and radiation hepatitis.
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PMID:Radiotoxic model for three-dimensional treatment planning. Part 1: Theoretical basis. 847 43

An indirect fluorescent antibody test for Bartonella henselae, B quintana, and B elizabethae was performed in all 18 children who presented to our paediatric outpatient clinic with cat scratch disease over a six year period. Serum samples were taken on admission, after 15 days, and after six months. Diagnosis was confirmed in 15 patients (83%) and was based on seroconversion or a fourfold change of the antibody titre to B henselae in 12 patients and on a single high titre (> 128) in three patients. Lymphadenopathy was present in all patients, erythema nodosum in one, osteomyelitis in one, hepatitis in one, transverse myelitis in one, and liver or spleen granulomata, or both, in three patients. Cat scratch disease developed in autumn or winter in 12 patients. All had a history of physical contact with a cat. Our study shows that our clinical suspicion was accurate in the diagnosis of cat scratch disease in a high percentage of patients presenting to a hospital and that indirect fluorescent antibody testing for B henselae is a useful diagnostic tool.
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PMID:Cat scratch disease in Greece. 953 80

Clinical features, laboratory findings, and complications of typhoid fever were correlated with sex through a retrospective case note review of 102 hospitalized culture-positive patients in Durban, South Africa. Intestinal perforation (P = 0.04), occult blood losses in stools (P = 0.04), and a mild reticulocytosis in the absence of hemolysis (P = 0.02) occurred more frequently in males than in females. A single pretreatment Widal O antibody titer > or = 1:640 was also a statistically significant occurrence in males (P = 0. 006). Female patients were significantly more severely ill (P = 0.0004) on admission and had chest signs consistent with bronchopneumonia (P = 0.04), transverse myelitis (P = 0.04), abnormal liver function test results (P = 0.0003), and abnormal findings in urinalyses (P = 0.02). Typhoid hepatitis (P = 0.04) and glomerulonephritis (P = 0.02) were present significantly more frequently in females. Whether these differences were due to differences in host's immune response to acute infection need to be determined in a prospective study.
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PMID:Influence of sex on clinical features, laboratory findings, and complications of typhoid fever. 1043 53

Efalizumab is a recombinant humanised IgG1 kappa isotype monoclonal antibody against the CD11a molecule. Efalizumab is approved for the treatment of moderate-to-severe psoriasis and is currently administered as a weekly subcutaneous injection. Throughout October 2005, 19,000 patients were treated with efalizumab. According to the package insert that is based on 2762 subjects, the most common adverse reactions associated with efalizumab are a first dose reaction complex that includes headache, chills, fever, nausea and myalgia within two days following the first two injections. These reactions are dose-level-related in incidence and severity and were largely mild-to-moderate in severity when a conditioning dose of 0.7 mg/kg was used as the first dose. Adverse events occurring at a rate between 1 and 2% greater in the efalizumab group compared with placebo were arthralgia, asthenia, peripheral oedema and psoriasis. Efalizumab is associated with a rebound flare reaction in approximately 5% of patients when therapy is ceased. Antiefalizumab antibodies develop in approximately 5% of the subjects who were treated with efalizumab, but the clinical significance of these antibodies is unclear. Efalizumab has rare but serious haematological side effects. Immune-mediated thrombocytopenia platelet counts at or below 52,000 cells/microl have been observed in 0.3% of cases and monitoring of platelet counts monthly for the first 3 months of use and each 3 months thereafter. Reports of four cases of haemolytic anaemia diagnosed four to six months after patients started on the monoclonal antibody exist. Infrequent new onset or recurrent severe arthritis events, including psoriatic arthritis events, have been reported in clinical trials and postmarketing surveillance. Symptoms associated with a hypersensitivity reaction (e.g., dyspnoea, asthma, urticaria, angioedema, maculopapular rash) were rarely noted in the first 12 weeks of the controlled clinical studies. The overall incidence of malignancies of any kind was 1.8 per 100 patient-years for efalizumab-treated patients compared with 1.6 per 100 patient-years for placebo-treated patients. One case each of the following serious adverse reactions was observed: transverse myelitis, bronchiolitis obliterans, aseptic meningitis, idiopathic hepatitis, sialedenitis and sensorineural hearing loss. In the complete safety data from both controlled and uncontrolled studies, the overall incidence of hospitalis ation for infections was 1.6 per 100 patient-years for efalizumab-treated patients compared with 1.2 per 100 patient-years for placebo-treated patients. The rate of infection was 26% in the control group and 29% in treated cases. The most common findings on laboratory assessments in patients using efalizumab were reversible increases in lymphocyte count and total white blood cell. Efalizumab is a safe, effective, but expensive treatment for psoriasis.
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PMID:Efalizumab: a review of events reported during clinical trials and side effects. 1650 42

Disseminated encephalitozoonosis was diagnosed in 2 sibling, juvenile, cotton-top tamarins (Saguinus oedipus) and 3 sibling, neonatal, emperor tamarins (S. imperator) by use of histologic examination, histochemical analysis, electron microscopy, and polymerase chain reaction (PCR) analysis with nucleotide sequencing. All tamarins were captive born at zoos in North America and died with no premonitory signs of disease. The main pathologic findings were myocarditis (4/5), hepatitis (3/5), interstitial pneumonia (3/5), skeletal myositis (3/5), meningoencephalitis (2/5), adrenalitis (2/5), tubulointerstitial nephritis (1/5), myelitis (1/5), sympathetic ganglioneuritis (1/5), and retinitis (1/5). Central nervous system lesions were the most prominent findings in cotton-top tamarins. The inflammation was predominantly lymphocytic and suppurative in cotton-top tamarins, whereas emperor tamarins had granulomatous or lymphoplasmacytic lesions. Intralesional periodic acid-Schiff-, gram-, or acid-fast (or all 3)-positive, oval-to-elliptical shaped organisms were found in 1 cotton-top and the 3 emperor tamarins. By electron microscopy, these organisms were consistent with microsporidia of the genus Encephalitozoon. E. cuniculi genotype III was detected by PCR analysis and sequencing in paraffin-embedded brain, lung, and bone marrow specimens from the cotton-top tamarins. Although PCR results were negative for one of the emperor tamarins, their dam was seropositive for E. cuniculi by ELISA and Western blot immunodetection. These findings and recent reports of encephalitozoonosis in tamarins in Europe suggest that E. cuniculi infection may be an emerging disease in callitrichids, causing high neonatal and juvenile mortality in some colonies. The death of 2 less than 1-day-old emperor tamarins from a seropositive dam supports the likelihood of vertical transmission in some of the cases reported here.
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PMID:Disseminated encephalitozoonosis in captive, juvenile, cotton-top (Saguinus oedipus) and neonatal emperor (Saguinus imperator) tamarins in North America. 1684 85


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