Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive hemophagocytic syndrome (RHS) is a disease of overwhelming macrophage activity triggered by infection, malignancy or autoimmune disorders. Currently used laboratory markers for the quantitative assessment of monocyte/macrophage activation lack lineage-restricted expression patterns and thus specificity. Serum levels of the macrophage specific scavenger receptor CD163 were determined by enzyme-linked immunosorbent assay (ELISA) and were found to be highly increased in patients with RHS (median 39.0 mg/L). Significantly lower levels were determined in patients with sepsis (median 9.1 mg/L), acute mononucleosis (median 8.2 mg/L), Leishmania infection (median 6.7 mg/L) and healthy controls (median 1.8 mg/L). Follow-up of patients with a relapsing course of the disease revealed close correlations of sCD163 with clinical disease activity, serum ferritin and other markers of macrophage activity. Large sinusoidal accumulations of CD163 expressing macrophages actively engaged in phagocytosis of blood cells were detected in spleen sections of RHS patients. Our data suggests sCD163 to be a macrophage-specific marker in patients with disorders of inappropriate macrophage activation.
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PMID:Soluble hemoglobin-haptoglobin scavenger receptor CD163 as a lineage-specific marker in the reactive hemophagocytic syndrome. 1561

Posttransplant lymphoproliferative disorder (PTLD) is a well-known complication of both solid organ and bone marrow transplantation. It includes a wide spectrum of proliferative changes ranging from reactive hyperplasia, borderline lesions to malignant lymphomas. PTLD develops in 1% to 10% of transplant recipients. We present 10 cases of PTLD. Five developed after renal, four after liver, and one after heart transplantation. Among the early lesions, we diagnosed two reactive plasmacytic hyperplasias; one infectious mononucleosis-like PTLD; one polymorphic lesion; and one "mixed" case of plasmacytic hyperplasia in one tonsil with a polymorphic PTLD in the second one. Among the lymphomas, we observed three diffuse large B-cell lymphoma (DLBCL); one mantle lymphoma; and one Hodgkin lymphoma-like PTLD. The morphological pictures of six PTLD cases were typical and posed no diagnostic problems. In the one case of plasmacytic hyperplasia, the lymph node morphology was atypical with atrophy of lymphoid components accompanying plasma cell proliferation. Contrary to a good prognosis of early, reactive PTLD, this patient experienced a rapid course and succumbed to sepsis. The most difficult case was a rare Hodgkin lymphoma-like PTLD, which was diagnosed only by a bone marrow biopsy. Because of its noncharacteristic immunophenotype, it was primarily diagnosed as an anaplastic lymphoma of the T-cell type. After additional immunohistochemical studies (BOB and OCT2), we established the final diagnosis of Hodgkin lymphoma-like PTLD. Due to the increasing number of organ transplantations, doctors of various specialties may encounter PTLD.
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PMID:Posttransplant lymphoproliferative disorder: morphological picture and diagnostic difficulties. 1650 94

We report herein a case of a 20-year-old previously healthy man who presented, 25 days after the onset of clinically and serologically confirmed Epstein-Barr virus (EBV) infectious mononucleosis, Fusobacterium necrophorum septicemia. The diagnosis of postanginal septicemia was confirmed by repeated demonstration of fusiform, obligate anaerobic, Gram-negative bacilli in anaerobic blood cultures, identified as F. necrophorum 15 days after admission. This case report aims at underlining the need of taking into consideration the possibility of severe Fusobacterium septicemia in previously healthy patients following EBV infectious mononucleosis in order to prevent increased mortality and morbidity.
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PMID:Fusobacterium necrophorum septicemia following Epstein-Barr virus infectious mononucleosis. 1688 13

Spontaneous rupture of the spleen is a rare complication of infectious mononucleosis with no clear consensus on appropriate management. Although management of traumatic splenic rupture has largely moved to nonoperative treatment, splenectomy is still frequently used in dealing with rupture of the diseased spleen. Here we report the case of a 16-year-old boy with splenic rupture secondary to laboratory-confirmed infectious mononucleosis in the absence of trauma. Nonoperative management including ICU admission, serial computed tomography scans, and activity limitation was used successfully. Our experience, along with a review of the literature, leads us to conclude that splenic preservation can be a safe alternative to splenectomy in hemodynamically stable patients with spontaneous splenic rupture. This is of particular importance in the pediatric population, which is at higher risk for postsplenectomy sepsis.
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PMID:Nonoperative management of spontaneous splenic rupture in infectious mononucleosis: a case report and review of the literature. 1767 Oct 47

In this report, the authors present a detailed immunological and virological assessment of an immunocompetent 17-year-old Caucasian male with a fatal Epstein-Barr virus (EBV) infectious mononucleosis presenting with meningoencephalitis and hemophagocytic syndrome. The patient with serologically confirmed EBV infectious mononucleosis was admitted to the hospital because of 3 weeks' fever. Fine-needle aspiration of lymph nodes showed reactive hyperplasia with prominent hemophagocytosis. Percentages of intracellular interferon-gamma (IFN-gamma) in CD4(+) and CD8(+) T cells in the peripheral blood progressively increased during the course of disease (10.2% and 8.5% on day 35; 30.1% and 53.2% on day 44; 42.2% and 75.2% on day 50; 36.1% and 50.6% on day 59, respectively). On day 50, the patient developed meningoencephalitis. Brain computed tomography (CT) was normal. Brain magnetic resonance imaging (MRI) showed multifocal inflammatory lesions in frontal and temporal cortex of the right hemisphere as well as severe perivascular inflammatory reaction. The patient was treated with steroids, cyclosporin A, and methotrexate intratecally. Following treatment, EBV viremia in the blood and cerebrospinal fluid (CSF) decreased from pretreatment values (54,490 copies of EBV DNA/ml and 39,500 copies/ml, respectively) to 8715 copies/ml in the blood and 14,690 in the CSF. Despite treatment, the patient remained unconscious and died of sepsis and pneumonia 3 months after initial symptoms. Immunohistochemical staining showed the presence of EBV in both perivascular infiltrates and grey matter. Enhanced Th1 response as shown by high levels of IFN-gamma in peripheral blood lymphocytes may be a predictor of severe complications during acute EBV infection. Early implementation of immunosuppressive therapy in these patients should be considered.
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PMID:Virological and immunological characteristics of fatal Epstein-Barr virus mononucleosis in a 17-year-old Caucasian male presenting with meningoencephalitis and hemophagocytic syndrome. 1784 23

Human infection with Fusobacterium necrophorum usually involves F. necrophorum subsp. funduliforme rather than F. necrophorum subsp. necrophorum, which is a common pathogen in animals. Lemierre's syndrome, or postanginal sepsis, is the most common life-threatening manifestation. Tonsillitis is followed by septic thrombophlebitis of the internal jugular vein and then a septicemia with septic emboli in lungs and other sites. Recent evidence suggests that F. necrophorum can be limited to the throat and cause persistent or recurrent tonsillitis. F. necrophorum is unique among non-spore-forming anaerobes, first for its virulence and association with Lemierre's syndrome as a monomicrobial infection and second because it seems probable that it is an exogenously acquired infection. The source of infection is unclear; suggestions include acquisition from animals or human-to-human transmission. Approximately 10% of published cases are associated with infectious mononucleosis, which may facilitate invasion. Recent work suggests that underlying thrombophilia may predispose to internal jugular vein thrombophlebitis. Lemierre's syndrome was relatively common in the preantibiotic era but seemed to virtually disappear with widespread use of antibiotics for upper respiratory tract infection. In the last 15 years there has been a rise in incidence, possibly related to restriction in antibiotic use for sore throat.
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PMID:Human infection with Fusobacterium necrophorum (Necrobacillosis), with a focus on Lemierre's syndrome. 1793 77

We report the case of an 18-year-old woman who was admitted to the medical intensive care unit in Innsbruck with severe septic shock and respiratory insufficiency following a prolonged infection of the upper airways (pharyngitis, sinusitis). Abscessing pneumonia and bilateral pleural empyema were diagnosed as focus. Cultures of pleural fluids were positive for Fusobacterium necrophorum. In addition to multiple organ dysfunction syndrome (acute lung injury, acute renal failure, disseminated intravascular coagulation), she developed tenderness in the right neck followed by septic arthritis of the right sternoclavicular joint a few days later. Further history revealed a previous period of infectious mononucleosis (EBV infection). The previously healthy patient eventually made a complete recovery after prolonged treatment in the ICU including antibiotic therapy and multiple surgical interventions and drainage. Lemierre's syndrome is characterized by severe infection, with pharyngitis, sepsis and thrombosis of the internal jugular vein, and is most frequently associated with upper airway infection with Fusobacterium necrophorum, often preceded by infection with Epstein-Barr virus which enables bacteria growing in the oral cavity to invade.
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PMID:Lemierre's syndrome following infectious mononucleosis. 1836 59

Posttransplant lymphoproliferative disease was first reported in 1968. Posttransplant lymphoproliferative disease encompasses a range of abnormalities from benign infectious mononucleosis-like illnesses to non-Hodgkin's lymphomas with nodal and extranodal site involvement. We evaluated five children who had posttransplant lymphoproliferative disease after liver transplantation. Since 2001, we have performed 118 liver transplantations in 115 children. Five children (4.6%), including three girls and two boys of overall mean age, 3.9 year, developed posttransplant lymphoproliferative diseases. The indications for liver transplant were hepatoblastoma in one recipient and cholestatic liver disease in the remaining four subjects. Posttransplant lymphoproliferative disease was diagnosed at 6, 11, 17, 22, and 27 months after the liver transplantation. Imaging modalities identified generalized lymphadenopathy in one, multiple liver masses in one, a large portal mass in one, multiple stomach ulcers in one, and a large mediastinal mass in one recipient. At diagnosis, the recipient with the large mediastinal mass displayed cough; the remaining four recipients were asymptomatic. Histological findings showed B-cell lymphomas in three recipients and T-cell lymphomas in two. The results of in situ hybridization for Epstein-Barr virus were negative in one recipient and positive in four. Four recipients were treated with chemotherapy; the remaining recipient was treated with anti-CD20 monoclonal antibodies. The one recipient who had a large mediastinal mass died at 2 months after receiving the diagnosis of chemotherapy-related sepsis; the remaining four children are alive at 9, 11, 18, and 34 months after treatment. Our rate of posttransplant lymphoproliferative disease was similar to that in the literature. From a few months to several years after liver transplantation, radiologists must be alert to the possibility of posttransplant lymphoproliferative disease. Thorough imaging is required to detect the wide variety of potential presentations.
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PMID:Posttransplant lymphoproliferative disease in pediatric liver transplant recipients. 1976 63

IL-27 is a heterodimeric cytokine composed of p28 and Epstein Barr virus induced gene 3 (Ebi3) protein subunits. In the present study, we questioned whether murine gammaherpesvirus 68 (HV-68) could induce expression of Ebi3, p28, and IL-27 in this mouse model of an EBV-like infection. Cultured macrophages and dendritic cells exposed to HV-68 upregulated p28 mRNA expression and increased secretion of the p28 and IL-27 (p28+Ebi3) proteins. B220(+) and CD11b(+) cells also upregulated p28 mRNA expression following in vivo infection with this virus. Surprisingly, no significant increases in p28 or IL-27 protein production were observed in vivo during the acute or mononucleosis phases of the disease. The possibility that HV-68-induced upregulation of p28 mRNA expression primed cells for IL-27 secretion was suggested by the ability of a TLR4 agonist to augment cytokine production. When cultured macrophages and dendritic cells were exposed to virus plus a suboptimal dose of LPS, increased levels of p28 protein expression were observed. More importantly, when latently infected mice were challenged with a sublethal dose of LPS, augmented p28 and IL-27 protein production occurred. Using a model of sepsis, mice latently infected with HV-68 had exaggerated p28 protein production when compared to mice that were singularly infected or subjected to cecal ligation and puncture. Taken together, these studies define expression of HV-68 induced IL-27, and suggest that mice latently infected with this gammaherpesvirus will have exaggerated responses when confronted with other stimuli capable of inducing this member of the IL-12 family of cytokines.
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PMID:Interleukin-27 expression following infection with the murine gammaherpesvirus 68. 2049 22

Seriously ill patients presenting with purpura fulminans, sepsis and multi-organ failure often require extensive diagnostic workup for proper diagnosis and management. Host of common infections prevalent in the tropics, e.g. malaria, dengue; other septicemic infections e.g. meningococcemia, typhoid, leptospirosis, toxic shock syndrome, scarlet fever, viral exanthems like measles, infectious mononucleosis, collagen vascular diseases (Kawasaki disease, other vasculitis) diseases, and adverse drug reactions are often kept in mind, and the index of suspicion for rickettsial illness is quite low. We present a case of Indian tick typhus presenting with purpura fulminans (retiform purpura all over the body), sepsis and multiorgan failure without lymphadenopathy and eschar, successfully treated with doxycycline and discharged home. Hence, a high index clinical suspicion and prompt administration of a simple therapy has led to successful recovery of the patient.
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PMID:Indian tick typhus presenting as Purpura fulminans. 2509 65


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