Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242429 (sore throat)
 2,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The IgA anti-EBV (Epstein-Barr virus) response during the course of IM (infectious mononucleosis) was investigated. The IgA anti-VCA (viral capsid antigen) response was found not to be restricted to the early acute phase of the EBV infection as is the IgM anti-VCA response. Some patients with normal total serum IgA levels did not respond with measurable EBV specific IgA. These patients and those with low titers of IgA anti-VCA had shorter duration of sore throat than responders with high titers indicative of a strong correlation between the IgA anti-VCA titers and the duration of sore throat. In this way the EBV specific IgA response is unique since recent observations show that local oropharyngeal symptoms during IM appear poorly synchronized with the IgM and the IgG antibody responses. As EB virus is excreted into the oropharynx during IM, antigens are available for local EBV immunization. The results of the present study imply a possible local immunization process as a positive correlation was found between serum IgA anti-VCA and total salivary IgA.
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PMID:IgA antibodies to Epstein-Barr virus in infectious mononucleosis. 301 Apr 47

The efficacy of tinidazole was studied in 24 patients with infectious mononucleosis (IM), 13 of whom were randomized for 5 days of tinidazole treatment and 11 for control without placebo. In judging the comparability of the 2 groups not only was the distribution of confounding factors such as age, sex or duration of symptoms before admission considered, but also the distribution of the Epstein-Barr virus (EBV) serological stage at entry. In these respects the groups were well matched. The duration of sore throat and pharyngotonsillitis after admission was significantly shorter for the patients treated with tinidazole than for the controls. Orosomucoid and lactodehydrogenase concentrations normalized more readily in IM patients with a short duration of sore throat after admission and in patients treated with tinidazole compared to those with a long duration of sore throat and to the tinidazole controls. Clinical and laboratory findings were thus parallel and showed a clinical effect of tinidazole, believed to be mediated via the well-known activity of this drug against anaerobic bacteria. The EBV serological stage of each patient at entry could not predict the duration of symptoms. The results showed that the course of the angina was not primarily dependent on the virus host interaction but probably on other factors, still unknown. One such factor could be the balance between the mucosal defence and the normal oropharyngeal microflora.
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PMID:Evidence of tinidazole interference in the oropharyngeal inflammatory process during infectious mononucleosis. 302 84

A cluster of 134 patients who had undergone Epstein-Barr virus (EBV) serological testing because of suspected chronic EBV syndrome was investigated in Nevada. Fifteen case-patients were identified who had severe, persistent fatigue of undetermined etiology for more than two months. When compared with the remaining 119 patients who had less severe illnesses and with 30 age-, sex-, and race-matched control-persons, these 15 patients had significantly higher antibody titers against various components of EBV and against cytomegalovirus and herpes simplex and measles viruses. Epstein-Barr virus serology could not reliably differentiate individual case-patients from the others, and the reproducibility of the tests within and among laboratories was poor. As a group, the case-patients appear to have had a syndrome that is characterized by chronic fatigue, fever, sore throat, and lymphadenopathy. The relationship of this fatigue syndrome to EBV is unclear; further studies are needed to determine its etiology.
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PMID:A cluster of patients with a chronic mononucleosis-like syndrome. Is Epstein-Barr virus the cause? 303 37

Twenty-one percent of 500 unselected patients, aged 17 to 50 years, seeking primary care for any reason were found to be suffering from a chronic fatigue syndrome consistent with "chronic active Epstein-Barr virus (EBV) infection," They had been experiencing "severe" fatigue, usually cyclic, for a median of 16 months (range, six to 458 months), associated with sore throat, myalgias, or headaches; 45% of the patients were periodically bedridden; and 25% to 73% reported recurrent cervical adenopathy, paresthesias, arthralgias, and difficulty in concentrating or sleeping. The patients had no recognized chronic "physical" illness and were not receiving psychiatric care. While antibody titers to several EBV-specific antigens were higher in patients than in age- and sex-matched controls subjects, the differences generally were not statistically significant. A chronic fatigue syndrome consistent with the chronic active EBV infection syndrome was prevalent in our primary care practice. However, our data offer no evidence that EBV is causally related to the syndrome. Indeed, we feel that among unselected patients seen in a general medical practice currently available EBV serologic test results must be interpreted with great caution.
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PMID:Frequency of 'chronic active Epstein-Barr virus infection' in a general medical practice. 303 38

The authors present data from four patients with acute heterophil-negative mononucleosis-like illnesses who were initially thought to have primary Epstein-Barr virus (EBV) infections but eventually were shown to be seroconverting to the human immunodeficiency virus (HIV). Widespread lymphadenopathy and blood smears indistinguishable from those typically encountered in the acute phase of infectious mononucleosis were present in all cases. There were also varying combinations of fever, sore throat, and malaise, as well as mild abnormalities of hepatic function and elevated cold agglutinins (anti-I). Anti-HIV was detected by both enzyme-linked immunosorbent assay and Western blot techniques in all cases, with increasing titers noted in two of three serially studied cases. In one patient, a dual infection with the hepatitis B virus was also documented. Diagnostic possibilities in patients with acute mononucleosis-like illnesses dominated by prominent lymphadenopathy should include primary seroconversions to HIV.
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PMID:Heterophil-negative mononucleosis-like illnesses with atypical lymphocytosis in patients undergoing seroconversions to the human immunodeficiency virus. 339 57

A detailed clinicopathologic analysis of 30 patients with sporadic fatal infectious mononucleosis and 31 males with fatal infectious mononucleosis and the X-linked lymphoproliferative syndrome was performed to determine the extent of hepatic dysfunction in these cases. At death, the median age of patients with sporadic infectious mononucleosis was 10.7 yr vs. 2.4 yr for X-linked lymphoproliferative syndrome. The median survival time was 8 wk for sporadic infectious mononucleosis and only 4 wk for X-linked lymphoproliferative syndrome. The male to female ratio was 3:2 in sporadic infectious mononucleosis; all patients with X-linked lymphoproliferative syndrome were males. Fever, sore throat, lymphadenopathy, hepatomegaly, and splenomegaly were prominent findings. Hepatic dysfunction was uniformly present and caused death in 13 of 30 sporadic infectious mononucleosis cases and 18 of 31 X-linked lymphoproliferative syndrome cases. Diagnosis of infectious mononucleosis was confirmed by heterophile antibody titers or Monospot, Epstein-Barr virus antibody studies, viral culture, molecular hybridization studies, clinical and histologic findings, and pedigree analysis.
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PMID:Hepatitis in fatal infectious mononucleosis. 367 38

In a prospective study 43 consecutive children in hospital, aged between 6 months and 7 years and displaying at least one of the clinical signs of infectious mononucleosis (IM), were investigated for Epstein-Barr (EB) virus-specific IgM antibodies by an indirect immunofluorescence test. On this basis EB virus infection was considered confirmed in 8 patients, each of whom had IgM antibodies in the initial serum sample. In one additional patient, IgM antibodies were only detected in a second sample. The IgM antibodies disappeared with 3-11 weeks. Assessment of IgG antibodies had no diagnostic value in the acute phase of IM. Clinically the 3 youngest children, about 1 year of age, were diagnosed as having pneumonia or hepatitis, the 5 other consecutive patients as having IM. Hepatosplenomegaly was fairly frequently associated with IM, while sore throat, lymphadenopathy, and rash were often signs of other diseases. Only the oldest child had heterophil antibodies. Atypical lymphocytes (greater than 10%) were present in 4 of the 9 IM cases and were seen in children with other diseases as well. Our data stress the importance of measuring EB virus-specific IgM antibodies in order to diagnose IM in early childhood.
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PMID:Primary Epstein-Barr virus infection in early childhood. 625 87

Twelve renal transplant patients with lymphoproliferative disorders (LPDs) were studied. Two clinical patterns were identified: (1) Young patients present with an infectious mononucleosis-like illness with fever, sore throat, and lymphadenopathy soon after transplantation or antirejection therapy. Many organs are ultimately involved, and the clinical course is one of a rapidly fatal LPD. (2) Older patients present a longer time after transplantation with symptoms of solid tumors involving the central nervous system, oropharynx, liver, or small bowel. The clinical course is slower, but it is progressive and fatal. Morphologically these LPDs can all be classified as polymorphic diffuse B-cell hyperplasia (PDBH) or polymorphic diffuse B-cell lymphoma (PBL). Cell marker studies in four patients demonstrated a polyclonal B-cell proliferation. Transition from a polyclonal B-cell proliferation to a monoclonal tumor may occur. Epstein-Barr virus (EBV) specific antibody titers, anticomplement immunofluorescence staining of tumors for the presence of the Epstein-Barr nuclear antigen (EBNA), and EBV complementary ribonucleic acid (cRNA)/deoxyribonucleic acid (DNA) hybridization and vDNA/DNA reassociation analysis implicate EBV as the probable etiologic agent in these disorders. Successful management of these lethal LPDs may depend on discontinuation of immunosuppression and removal of the allograft. Antiviral therapy, however, may prove to be useful.
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PMID:The Epstein-Barr virus in the pathogenesis of posttransplant lymphoproliferative disorders. Clinical, pathologic, and virologic correlation. 626 59

Six renal transplant recipients with abnormal lymphoproliferative disorders were studied in an attempt to define their clinical features and the role of Epstein-Barr virus (EBV) in their pathogenesis. Patients were either teenage (three) or in the sixth decade (three). The younger patients presented an average of 3 months after transplantation with fever, sore throat, and lymphadenopathy; had been markedly immunosuppressed; frequently had preceding or concomitant cytomegalovirus infections; and two of three had a rapidly fatal course. The older patients presented an average of 5 years after transplantation while on maintenance immunosuppressive drugs; in two of three cases with an oropharyngeal tumor; and had a more indolent, but frequently fatal, clinical course. The most frequent sites of biopsy-proven involvement in these patients were lymph nodes (three), the oropharynx (three), liver (three), bone marrow (three), transplanted kidney (three), colon (two), and central nervous system (two). EBV-specific antibody titers including anti-viral capsid antigen IgG, anti-viral capsid antigen IgM, anti-early antigen, and anti-Epstein-Barr nuclear antigen were serially measured in all patients. Four patients demonstrated serological evidence of a primary (one) or reactivation (three) EBV infection. No patient had significant changes in anti-early antigen or anti-Epstein-Barr nuclear antigen titers. All three patients tested for oropharyngeal shedding of EBV were positive. A touch imprint of one tumor was stained for the presence of Epstein-Barr nuclear antigen, and a majority of cells were positive. EBV complementary RNA/DNA filter hybridization and/or viral DNA/DNA reassociation analysis performed on tumor biopsy specimens in five patients demonstrated multiple EBV genome equivalents per cell in all eight specimens tested. Clinical, pathological, serological, and molecular hybridization studies provide substantial evidence that EBV was the cause of these lymphoproliferative disorders occurring after renal transplantation. Impaired host defenses allow the EBV-transformed B-lymphocytes to escape normal control mechanisms. This impairment is invariable and influenced by many factors resulting in the observed spectrum of disease. Cytogenetic changes, however, may also be important.
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PMID:Clinical spectrum of lymphoproliferative disorders in renal transplant recipients and evidence for the role of Epstein-Barr virus. 627 71

A 20-year-old man, a college student, was admitted to Kochi Municipal Central Hospital with a month's history of slurring of speech and unsteadiness of gait. He had developed fever, sore throat and cervical lymphadenopathy. On admission, the throat was mildly injected, and enlarged lymph nodes were palpable in the lateral cervical regions. His speech was slightly slurred. Bilateral dysmetria, dyssynergia and intention tremor were noted in both extremities. The gait was grossly ataxic. Plantar responses were extensor. Examination of his peripheral blood revealed atypical lymphocytes, and the titer of Paul-Bunnell was 1:16. The CSF protein was 25 mg/dl with normal cell count. Epstein-Barr virus (EBV) antibody titers by indirect immunofluorescence in the serum of the second hospital day were as follows: VCA-IgG was 1:640, VCA-IgM less than 1:10, EBV-EA 1:160, and EBNA less than 1:10, while the CSF-EBV antibody titer was negative. Treatment with prednisolone was started and within 7 days he began to recover. Six weeks after admission he was completely free of neurological symptoms and signs. We also reviewed 18 cases of acute cerebellar ataxia with infectious mononucleosis in the literature. It was postulated that the neurological symptoms complicating infectious mononucleosis were possibly caused by infectious and immuno-allergic mechanisms.
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PMID:[Acute cerebellar ataxia associated with infectious mononucleosis--a case report and review of the literature]. 630 27


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