Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report two cases of severe measles pneumonia. Patient 1, a 17-year-old boy who contracted measles in the acute phase of infectious mononucleosis caused by Epstein-Barr virus (EBV), transmitted the disease to patient 2, his father. Both patients presented severe pneumonia with bilateral diffuse micronodular shadows. Diagnoses were established in both patients by antibody titers for measles and reverse transcriptase-polymerase chain reaction (RT-PCR) of blood and throat swab. Multinucleated giant cells with intranuclear inclusion bodies were revealed in the transbronchial lung biopsy (TBLB) specimen of patient 2. Both patients recovered with pulse steroid therapy.
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PMID:Familial cases of severe measles pneumonia. 1093 45

Glucocorticoids remain the standard approach to initial systemic management of acute graft-versus-host disease (aGVHD). For patients refractory to steroids, antithymocyte globulin (ATG) is frequently used as salvage therapy. We decided to test whether the combination of corticosteroids and equine ATG would improve the outcome of initial management of aGVHD, especially in high-risk patients such as recipients of unrelated donor (URD) transplants. One hundred patients with grade II to IV aGVHD having undergone a related or URD marrow transplant were enrolled in the study. Of the patients, 46 were randomly assigned to therapy with prednisone (60 mg/m2 per day x 7 days) and 50 received ATG/prednisone (15 mg/kg ATG bid plus 20 mg/m2 prednisone bid x 5 days, each followed by an 8-week prednisone taper). An intent-to-treat analysis of the overall response at day 42 revealed equivalent complete plus partial response rates of 76% in both the prednisone and ATG/prednisone therapy groups (P > .80). In univariate analysis, patient age, donor type, site of involvement, or aGVHD stage did not influence overall response to therapy (all P > .2). When treatment arms were studied separately, no single clinical feature predicted outcome in either group. Complications were more frequent in the ATG/prednisone arm; patients experienced more infections with cytomegalovirus (44% versus 22%; P = .02) and more frequent pneumonitis, both infectious and noninfectious (50% versus 24%; P < .01). Epstein-Barr virus lymphoproliferative disease was uncommon (4 cases) and comparable in both arms (P = .35). There was no significant difference in survival at day 100, 6 months, and 2 years between the 2 treatment arms. The more intensive immunosuppressive combination of ATG/prednisone failed to improve control of aGVHD and may have affected survival by causing more infectious complications. Combination therapy with ATG should thus be reserved as second-line therapy in the management of aGVHD.
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PMID:A randomized trial comparing prednisone with antithymocyte globulin/prednisone as an initial systemic therapy for moderately severe acute graft-versus-host disease. 1097 13

The clinical picture of myocarditis/myopericarditis is of importance in differential diagnosis, especially in younger patients with suspected myocardial infarction. Myocarditis/myopericarditis commonly presents with chest pain, and the diagnosis is usually established on clinical grounds. However, endomyocardial biopsy is necessary to confirm the diagnosis. We evaluated the characteristics of acute myocarditis over the years 1980-1998 in 54 patients of the Department of Medicine of the University Hospital, Zurich. Two to 6 patients per year were hospitalised with this diagnosis. In most cases the diagnosis was established by a combination of criteria, such as a preceding infection of the upper respiratory tract, thoracic pain, ST segment elevations in different precordial leads followed by T wave inversions, arrhythmias, elevation of cardiac enzymes, reversible hypokinesia by echocardiography and normal coronary arteries. At least 3 of 5 criteria were requested. In a first step we analysed retrospectively all patients with acute myocarditis/myopericarditis in the years 1980-1993. Among 30 cases of acute myocarditis/myopericarditis the following causes could be identified: one influenza B, one Toxoplasma gondii infection, 2 Epstein-Barr infections and one bacterial myocarditis with gram-negative rods. The aetiology of the other 25 cases remained unknown. The majority of myocarditis/myopericarditis healed without complications. One patient with Epstein-Barr myocarditis and one with Toxoplasma gondii infection died. Two patients developed dilated cardiomyopathy. In a second phase we analysed prospectively all cases with acute myocarditis/myopericarditis over the period 1994-1998: 24 patients with acute myocarditis/myopericarditis were hospitalised. At that time coronary angiography and endomyocardial biopsies were performed more frequently. We found 2 patients with giant cell myocarditis and 2 with Toxoplasma gondii infection and HIV, all of whom died. In addition, there were 2 patients with eosinophilic myocarditis, one with Lyme carditis, one with Epstein-Barr myocarditis, one with myopericarditis after Campylobacter enteritis and one histologically proven myocarditis after pneumonia with Haemophilus influenzae. The aetiology of the remaining 13 cases with myocarditis/myopericarditis could not be established. Three patients with probable viral myocarditis developed cardiogenic shock requiring intraaortic balloon pump, and fully recovered. The patient with Lyme carditis manifested with total atrioventricular block and was treated with a temporary pacemaker. One patient with lymphocytic myocarditis required heart transplantation because of terminal heart failure and one female patient with histologically proven diffuse lympho-monocytic myocarditis died of cardiogenic shock. All the other cases healed without complications. Serologies are of little diagnostic value and should be restricted to serologies with therapeutic implications. We believe that the apparent increase in myocarditis/myopericarditis in recent years is a result of better diagnostic tools, such as more specific cardiac enzyme tests, coronary angiography and endomyocardial biopsies. In most cases the therapy remains symptomatic. In elected, severe cases steroids and other immunosuppressive drugs are sometimes used.
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PMID:[Diagnosis and course of myocarditis: a survey in the medical clinics of Zurich University Hospital 1980 to 1998]. 1102 70

Two adults with primary liver cancer underwent liver transplantation from 5/6 and 4/6 major HLA-antigen mismatched unrelated donors. They were then conditioned with 4 x 2 Gy of total lymphoid irradiation, 120 mg/kg cyclophosphamide, 7.5 Gy total body irradiation and anti-T cell antibodies. Thereafter, the patients received T cell-depleted autologous: unrelated mismatched bone marrow in a proportion of 0.5:3.0 and 0.35:1.1 x 10(6) CD34+ cells/kg, respectively. After allogeneic stem cell transplantation (ASCT), both became mixed chimeras, as determined with polymerase chain reaction amplification of variable number tandem repeats from DNA obtained from CD3+, CD19+ and CD45+ magnetic bead-separated cells. Due to a reduction in donor T cells, the first patient was given 10(5) donor T cells/kg and became a complete donor chimera within 3 months. The second patient rejected all donor cells within 1 month after ASCT. Leucocytes normalized in both patients within 1 month. CD8+ cells normalized after 4 and 2 months in the two patients, respectively. However, CD4+, CD56+ and CD19+ cells remained low, except for a transient increase in patient 2. Lymphocyte responses to mitogens were negative in patient 1 from 1 to 5 months after ASCT. This patient also showed an oligoclonal pattern of the B cell repertoire, performed by CDR3 spectratyping. Epstein-Barr virus DNA in lymphocytes increased by 4-5 log in both patients. Prior to ASCT, recipients and donors were mutually reactive in mixed lymphocyte cultures (MLC). In the first patient, who became a complete donor chimera, the chimera cells showed no response to recipient or donor, but a positive response to third party. In the other patient, recipient cells reacted vigorously against donor lymphocytes at the time of rejection. Both patients suffered from overwhelming bacterial, fungal and viral infections, and died of pneumonia 5 and 3 months after ASCT, respectively. To conclude, with a major HLA-mismatch barrier, stable mixed chimerism seems difficult to achieve. The first patient became a full donor chimera and the second one rejected the graft. Both suffered from immune incompetence.
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PMID:Poor immune reconstitution after four or five major HLA antigens mismatched T cell-depleted allogeneic and autologous stem cell transplantation. 1116 14

FK 506 (Tacrolimus) was used with steroids to treat 61 pediatric patients who received living related partial liver transplantation. Fifty-two recipients survived and 9 died between 6 months and 3 years after transplantation. In the surviving patients, oral doses of Tacrolimus were tapered from 0.298 +/- 0.277 mg/kg daily at 1 month after transplantation to 0.078 +/- 0.054 at 24 months after transplantation. The 12 h trough levels of Tacrolimus were 12.6 +/- 7.1 ng/ml and 4.1 +/- 2.4 at 1 and 24 months after transplantation, respectively. The percentage of recipients free from steroids was 77%, 97%, and 94% at 6, 12, and 24 months after transplantation, respectively. Liver allograft rejection was encountered in seven recipients, five of whom were treated by steroid pulse therapy and a dose increase of Tacrolimus; the remaining two required OKT3. However, there was no episode of rejection that required retransplantation. Infectious complications encountered in 34 patients included 12 bacterial, 3 fungal, and 19 viral infections. Two recipients died one of fungal pneumonia and one of Epstein-Barr virus-associated lymphoproliferative disorder. Regarding adverse reactions of Tacrolimus, hypertension was observed in 28 patients, diabetes mellitus in 3, pancreatitis in 3, convulsion in 1, tremor in 12, itching in 5, and pigmentation in the oral mucosa in 2. Slightly increased values of creatinine were observed in most of the patients; however, an abnormal increase of serum of serum creatinine (> 1.0 mg/dl) was confined to the complicated cases. Improvement of somatic growth was observed in 21 patients (62%) and 13 (75%) at 12 and 24 months after transplantation, respectively. The long-term use of Tacrolimus is highly effective in terms of its immunosuppressive potential and reduced adverse reaction. Steady growth development can be expected in pediatric recipients free from steroids.
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PMID:Long-term use of FK 506 in living related liver transplantation. 1127 41

In contrast to solid organ transplantation (Tx), the incidence of post-transplant lymphoproliferative disease (PTLD) after hematopoietic stem cell Tx (HSCT) is generally low. This risk, however, is significantly elevated in patients receiving human leukocyte antigen (HLA) mis-matched or T-cell-depleted grafts, or after treatment for severe graft-versus-host disease (GvHD). An 18-yr-old patient with positive Epstein-Barr virus (EBV) serology received a fully matched, unmanipulated bone marrow graft from an unrelated EBV-positive donor for treatment of acute myeloid leukemia (AML) in second complete remission. GvHD prophylaxis was performed with cyclosporin A (CsA) and a short course of methotrexate. Four months after Tx, the patient developed ulcerative tonsillitis that was unresponsive to antibiotic treatment. Diarrhea appearing simultaneously was interpreted as gastrointestinal GvHD and steroids were added to CsA. A few days later the patient was admitted to hospital because of generalized seizure and pneumonia. Despite reduction of immunosuppression, intensification of anti-viral treatment, and subsequent mechanical ventilation, the patient died of acute respiratory distress 6 days later. Autopsy demonstrated disseminated EBV-induced, multi-nodular lymphoma infiltration of the entire colon but no signs of GvHD. Moreover, both lungs, paratracheal lymph nodes, kidneys, thyroid gland, and liver were infiltrated with large B-cell non-Hodgkin's lymphomas. This case underlines the rapid and aggressive course of EBV-induced disseminated PTLD after HSCT, initially mimicking intestinal GvHD because of massive colonic lymphoma infiltration. Tissue biopsies should be performed early for establishing correct diagnosis, thus enabling specific therapy, e.g. infusion of donor leukocytes with cytotoxic T-lymphocytes.
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PMID:Epstein-Barr virus-associated post-transplant lymphoproliferative disease after bone marrow transplantation mimicking graft-versus-host disease. 1127 9

Pneumonia is still a major problem in human immunodeficiency virus (HIV)-infected patients, and despite extensive investigation the aetiology remains unknown in many cases. The prevalence of the eight human herpesviruses was determined by polymerase chain reaction in 91 samples of bronchoalveolar lavage (BAL) fluid from 72 HIV-infected patients with 91 episodes of suspected pneumonia. The presence of herpesviruses was related to clinical and immunological findings and the prevalence of herpesviruses in HIV-infected patients was compared with the prevalence in BAL fluid from 50 healthy, immunocompetent individuals. Epstein-Barr virus, cytomegalovirus and human herpesvirus-8 (HHV8) were found in 5.5%, 36% and 5.5% of BAL fluid samples from HIV-infected patients. No herpesviruses were detectable in BAL fluid from healthy, immunocompetent individuals. The herpesviruses occurred mainly in patients with CD4+ counts <200 x 10(6) L(-1). All patients with herpesviruses recovered without specific antiviral treatment. Two patients with HHV8 had the diagnosis of Kaposi's sarcoma. It is concluded that cytomegalovirus, Epstein-Barr virus, and human herpesvirus-8 are frequently present in bronchoalveolar lavage fluid from severely immunocompromised human immunodeficiency virus-infected patients with pulmonary symptoms. In bronchoalveolar lavage fluid from healthy, immunocompetent individuals, herpesviruses are absent. Apart from human herpesvirus-8, the present results indicate that the herpesviruses do not play a serious pathogenic role in the development of pulmonary symptoms in human immunodeficiency virus-infected patients.
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PMID:Herpesvirus type 1-8 in BAL fluid from HIV-1-infected patients with suspected pneumonia and from healthy individuals. 1151 Jul 85

This is a case report of a child with severe respiratory syncytial virus (RSV) pneumonia and concurrent infection with Epstein-Barr virus. We hypothesize that immunosuppression due to EBV may have contributed to the severity of his RSV infection. The diagnosis of RSV infection was facilitated by bronchoalveolar lavage.
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PMID:Severe respiratory syncytial virus pneumonia associated with primary Epstein-Barr virus infection. 1194 86

The identification of specific antimicrobial activity of intravenous immunoglobulin (IVIG) preparations against particular microbial pathogens can assist in determining their therapeutic potential for specific infectious diseases. We analysed five different commercial IVIG preparations for the presence of antibodies directed against a large panel of viral, bacterial, fungal and parasitic pathogens. All IVIG batches contained high activity against herpesviruses types 1, 2, 6 and 7, as well as against varicella zoster virus, Epstein-Barr virus (EBV), measles, mumps, rubella and parvovirus B19. Some IVIG batches also had a significant activity against adenovirus and Saint Louis encephalitis virus. The IVIGs held high activity against several bacterial pathogens, including Mycoplasma pneumonia, Chlamydia pneumonia, Helicobacter pylori and tetanus. No activity was found against various parasitic and fungal pathogens. Our findings may provide further support for the use of IVIG for the prevention and treatment of infections caused by specific viral and bacterial pathogens.
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PMID:In vitro antiviral and antibacterial activity of commercial intravenous immunoglobulin preparations--a potential role for adjuvant intravenous immunoglobulin therapy in infectious diseases. 1198 67

Human herpesvirus type 8 (HHV-8; Kaposi's sarcoma-associated herpesvirus) is frequently identified in tumor tissue obtained from human immunodeficiency virus (HIV)-infected patients with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), or multicentric Castleman's disease. The association between HHV-8 and acquired immunodeficiency syndrome (AIDS)-associated solid lymphomas is less clear. Herein, I describe the case of a man with a CD4+ count of 30 cells/microL, and HIV viral load of 90,000 copies/mL, multi-drug resistant HIV infection, and limited stage KS. Biopsy of a progressive dorsal foot rash revealed a dense, deep, lymphoid infiltrate that extended into papillary dermis but without epidermotrophism. Microscopy showed a homogeneous population of anaplastic large B cells that stained positive for CD20 (L26), CD30, and lambda light chain. In situ hybridization of tumor tissue identified Epstein-Barr virus (EBV)-encoded RNA, and polymerase chain reaction amplification yielded HHV-8-specific gene products. Staging studies did not reveal lymphoma elsewhere, and the patient began chemotherapy, but died from septic complications. Autopsy was notable only for the presence of a consolidative pneumonia. Although extranodal presentations are common in the setting of immunodeficiency, reports of AIDS-associated lymphoma presenting as a nonepidermotrophic foot lesion are rare. Such a presentation serves to broaden the differential of skin and foot lesions in the setting of HIV infection. More importantly, this case provides further support that HHV-8 can be associated with solid lymphomas that have an anaplastic large cell morphology.
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PMID:HHV-8- and EBV-associated nonepidermotrophic large B-cell lymphoma presenting as a foot rash in a man with AIDS. 1201 67


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