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)

Two fatal cases of haemophagocytic syndrome diagnosed on the basis of autopsy findings at the Queen Elizabeth Hospital, Barbados, are presented. They were both young patients, a male 20 years of age and a female 28 years of age, with common clinical features of severe constitutional symptoms, pharyngeal haemorrhages, pancytopenia, and fever. The female patient had elevated titres to herpes simplex virus indicative of recent infection as well as postmortem evidence of overwhelming mixed bacteria sepsis. In both cases, histopathological studies showed lymphoid depletion and histiocytes displaying haemophagocytosis.
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PMID:Haemophagocytic syndrome. 178

We reported 3 fatal cases of primary Epstein-Barr virus (EBV) infection resembling histiocytic medullary reticulosis (HMR) in young children in Taiwan, where an HMR-like illness has been previously found to be prevalent. The disease ran a fulminant course, manifesting as fever, anemia, jaundice, skin rash, pulmonary infiltration, and/or hepatosplenomegaly lasting for only 1-3 weeks. Laboratory tests revealed no hemolytic anemia and Coombs test was negative. Sepsis or HMR was the main clinical differential. At autopsy, the spleen, liver, lymph node, lung, and bone marrow showed infiltration of atypical "histiocytes" or blasts, lymphocytes, and mature histiocytes with hemophagocytosis. Immunophenotype and gene rearrangement studies of the lymphoid tissues revealed that these atypical "histiocytes" were actually polyclonal B immunoblasts in one case and transformed T lymphocytes in the remaining 2 cases, representing two different types of virus-host interaction. Southern blot and in situ hybridization studies on frozen lymphoid tissues demonstrated the presence of EBV DNA in all 3 patients; the study for cytomegalovirus was negative. The young age of these patients, closely correlated with the prevalent age of primary EBV infection in the general populations in Taiwan, strongly suggest that these childhood cases of previously diagnosed HMR-like disease may actually represent a lethal form of primary EBV infection or fatal infectious mononucleosis.
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PMID:Fatal primary Epstein-Barr virus infection masquerading as histiocytic medullary reticulosis in young children in Taiwan. 196 24

We describe a case of intestinal T-cell lymphoma which was histologically diagnosed of malignant histiocytosis of the intestine. A 47-year-old man was admitted to our hospital because of fever and generalized lymphadenopathy. Mild anemia, leukocytosis, positive CRP and a high level of LDH were noted. Pathological finding of the lymph node was compatible with dermatopathic lymphadenopathy with a slight increase in atypical lymphoid cells. At the 14th day after admission, he suffered from abdominal pain and was diagnosed as having perforative peritonitis. In laparotomy, the infiltration of histiocyte-like atypical cells were found around a site of small perforation of the terminal ileum. The findings were compatible with that of malignant histiocytosis of the intestine (MHI). He had recurrent perforations of the small intestine and died of peritonitis and sepsis at the 42nd day. Southern blot analysis of the biopsied lymph node showed TCR-beta gene rearrangement. Some patients diagnosed clinically and pathologically as having MHI may have a T-cell lymphoma like our case.
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PMID:[Intestinal T-cell lymphoma (so-called malignant histiocytosis of the intestine) complicated by multiple perforations]. 202 Jan 15

The activity of phosphate-dependent glutaminase and glutamine metabolism by tissues known markedly to utilize or synthesize glutamine (or both) were studied in rats made septic by cecal ligation and puncture technique and compared with the same measures in rats that underwent sham operation (laparotomy). Blood glucose level was not markedly different in septic rats, but lactate, pyruvate, alanine, and glutamine levels were markedly increased. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon levels were markedly elevated in response to sepsis. The maximal activity of phosphate-dependent glutaminase was decreased in the small intestine, increased in the kidney and mesenteric lymph nodes, and unchanged in the liver of septic rats. Arteriovenous concentration difference measurements across the gut showed a decrease in the net glutamine removed from the circulation in septic rats. Arteriovenous concentration difference measurements for glutamine showed that both renal uptake and skeletal muscle release of the amino acid were increased in response to sepsis, whereas measurements across the hepatic bed showed a net uptake of glutamine in septic rats. Enterocytes isolated from septic rats exhibited a decreased rate of utilization of glutamine and production of glutamate, alanine, and ammonia, whereas lymphocytes isolated from septic rats showed an enhanced rate of utilization of glutamine and production of glutamate, aspartate, and ammonia. It is concluded that, during sepsis, glutamine uptake and metabolism are enhanced in renal and lymphoid tissue but decreased in that of the small intestine, with increased rates of release by skeletal muscle; however, the liver appears to utilize glutamine in septic rats.
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PMID:Maximal activity of phosphate-dependent glutaminase and glutamine metabolism in septic rats. 206 39

The use of interleukin-2 (IL-2), either alone or in combination with lymphokine-activated killer cells, tumor infiltrating lymphocytes, or other immunotherapeutic agents has added a new list of alternatives to conventional antineoplastic regimens. Little information is available about the pathologic changes occurring in patients treated with these agents. In this study, we reviewed the necropsy materials from 19 patients, 12 men and 7 women, with a variety of malignancies including melanoma, renal cell carcinoma, gastrointestinal and pulmonary adenocarcinoma, and metastatic gastrinoma, who died after receiving IL-2-based immunotherapy. Death occurred at intervals ranging from less than 1 hour to 143 days following the last dose of therapy. All patients dying at or less than 43 days following cessation of therapy had lymphoid infiltrates of varying intensity in residual tumor. At necropsy, the major cause of death unrelated to the presence of metastatic tumor was bacterial sepsis. In addition, we found evidence of significant cardiac and pulmonary toxicity: two patients with acute myocardial infarction, one with and one without significant coronary artery disease, two cases of unexplained lymphocytic myocarditis, and one case of fatal pulmonary capillary plugging following an infusion of lymphokine-activated killer cells. Thus, not unlike other forms of therapy for cancer, IL-2-based immunotherapy does not appear to be without significant toxicity.
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PMID:Pathologic findings associated with interleukin-2-based immunotherapy for cancer: a postmortem study of 19 patients. 233 30

Seventeen patients with advanced stage Hodgkin's disease who relapsed or failed to respond to multiple regimens of combination chemotherapy (mostly Mechlorethamine, Vincristine, Procarbarzine, Prednisone and Adriamycin, Bleomycin, Vinblastine, Dacarbazine) were treated with accelerated hyperfractionated total lymphoid irradiation (TLI) and high-dose chemotherapy followed by autologous bone marrow transplantation (AuBMT). Candidates for the protocol did not have prior radiation therapy and had no evidence of bone marrow involvement. Their bone marrow was initially harvested and cryopreserved. The treatment protocol consisted of reinduction with conventional doses of combination chemotherapy followed by boost local field irradiation to areas of residual disease (1500 cGy within 5 days) and total lymphoid irradiation (2004 cGy given in 12 fractions of 167 cGy each t.i.d. delivered within 4 days). The patients were treated with Etoposide (250 mg/m2/day I.V. X 3 days) and high-dose Cyclophosphamide (60 mg/kg/day I.V. X 2 days). Cryopreserved (unpurged) autologous bone marrow was infused 48 hr after completion of chemotherapy. Of the 17 patients treated, four were in relapse and 13 refractory to multiple regimens of combination chemotherapy. Four patients died during the immediate peritransplant period (2--septicemia, 2--pulmonary complications). Of the 13 surviving patients, 12 entered a complete remission and one had a partial remission and died of disease 6 months later. One patient relapsed 5 months after treatment and is currently alive with disease. Eleven patients (65%) are alive with no evidence of disease 4-35 months (median 20 months) following completion of therapy. Treatment with this protocol results in a high rate of complete remission and a potential for long-term disease-free survival in previously unirradiated patients with advanced stage refractory or relapsed Hodgkin's disease who have exhausted conventional modes of chemotherapy.
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PMID:Total lymphoid irradiation, high-dose chemotherapy and autologous bone marrow transplantation for chemotherapy-resistant Hodgkin's disease. 247 11

We used preparative regimens consisting of cyclophosphamide and total lymphoid irradiation in 4 children with severe aplastic anemia undergoing allogeneic bone marrow transplantation. All 4 children engrafted successfully in spite of the number of donors exposed in the previous blood components transfusion. Three of 4 transplanted children have survived for 390 days, 540 days, and 1,235 days respectively. One child died of graft-versus-host disease related sepsis. The actual survival rate was 75% at one year. Further efforts must be aimed at the elimination of graft-versus-host disease and the control of fatal infections.
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PMID:Bone marrow transplantation for severe aplastic anemia in children: conditioning with cyclophosphamide and total lymphoid irradiation. 263 81

Seventeen patients, who presented with unhealing ulcers or destructive lesions of the upper aero-digestive tract at Ramathibodi hospital from 1977 to 1985 were reported. Lesions caused by infection, Wegener's granulomatosis or non-hematopoietic malignancy were excluded. A spectrum of histopathologic findings were evident in our patients, ranging from acute and chronic inflammatory changes with or without necrosis, polymorphic reticulosis or lymphamatoid granulomatosis, and malignant lymphoma of the non-Hodgkin's type (NHL). Although some initial histopathologic findings were non-specific, evidence of lymphoproliferative disorders finally emerged. These malignant lymphoid cells had a predilection for the GI tract and skin. Lymphoma staging should thus be done. Bleeding from the lesion, treatment-induced leucopenia, and sepsis were common in these patients. Early aggressive treatment including adequate antibiotic coverage for superimposed infection, improved nutritional status, and early radiation to the primary lesion are suggested for those diseases.
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PMID:Lethal midline granuloma and lymphoproliferative disorders. 276 18

An immunologically normal 70-year-old male developed fever and disturbance of consciousness after aortocoronary bypass; this was followed by diarrhea, systemic erythroderma and granulocytopenia. He died as a result of sepsis and acute renal failure. The skin biopsy showed basel vacuolar degeneration, epidermal eosinophilic necrosis and invasion of T-lymphocytes. The autopsy showed necrotic small interlobular bile ducts, severely hypoplastic bone marrow and widespread necrosis of lymphoid tissue. Based on these clinicopathological findings, we made a diagnosis of graft-versus host reaction after transfusion.
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PMID:[A case report of graft-versus-host reaction after aortocoronary bypass--a clinicopathological study]. 280 2

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41


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