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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pathomorphological investigation of 115 lethal cases of various forms of meningococcal infection was carried out. Meningococcemia, its instantaneous forms in particular, are characterized by acute decompensation of the lymphoid system and generalized microangiopathy with the thrombohaemorrhagic syndrome. Haemorrhagic necrosis of the adrenals and damage of the hypophysis represented manifestations of the acute decompensation of the hormonal regulation. Inflammatory changes in meningococcemia were observed not in all the cases (they were absent in 1/4 of the deceased). In meningitis (meningoencephalitis) without sepsis no generalized angiopathy was noted, immunomorphological changes were of a proliferative character. Previous sensibilization of the macroorganism was an important prerequisite for the development of meningococcal infection.
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PMID:[Vascular and immunological processes in the pathogenesis of meningococcal infection]. 12 76

Sepsis is a frequent cause of morbidity following extensive bowel resection. It has been suggested that the lymphoid tissues of the gut may be essential to normal humoral immunity. This study evaluates: (1) the effect of endotoxin on mortality following selective massive bowel resection and jejunoileal bypass; (2) cellular immunity by skin allograft rejection and bypass, and (3) T and B cell lymphocyte subpopulations is mesenteric lymph nodes, intestine and appendix. Endotoxin increased mortality in rats with more distal bowel resection but not following bypass. Skin allograft rejection was similar in each group. Peyer's patches, mesenteric lymph nodes and appendices were evaluated for T & B cell subpopulations. These tissues had a greater percentage of B cells (53% lymph nodes, 63% appendix) with IgM the predominant immunoglobulin. Cellular immunity was not a factor. Lymphoid tissues of the distal bowel and mesentery contain abundant B cells and IgM that may contribute to humoral immunity. Massive bowel resection may increase the risk of morbidity from gram negative sepsis and/or endotoxin presumably due to decreased humoral immunity.
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PMID:Adverse effects of endotoxin following massive distal bowel resection. 31 29

Splenomegaly is usually the result of systemic disease. The differential diagnosis can logically be subdivided into infectious, hematologic, metabolic, vascular, and neoplastic diseases which result in abnormalities of the lymphoid, reticuloendothelial, or vascular components of the spleen. Splenic enlargement increases the risk of traumatic rupture of the spleen. Splenectomy, although indicated in some conditions, does not always relieve the hypersplenic state, and its benefit must be weighed against the hazard of life-threatening episodes of sepsis.
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PMID:Splenomegaly in children. Identifying the cause. 42 50

In ten experiments, 53 castrated male 4- to 8-week-old weanling pigs were given adriamycin (ADR) IV at mean dosages of 0.64, 1.0, 1.6, 3.2, or 6.4 mg/kg/week at various frequencies for up to 20 weeks. Mortalities in pigs given these dosages were 0% after 112 days, 100% after 134 days (survival time was 48 to 134 days), 91% after 75 days (survival time was 5 to 75 days), 100% after 28 days (survival time was 23 to 28 days), and 100% after 14 days (survival time was 10 to 14 days), respectively. Survival time was prolonged in younger pigs and in pigs given smaller but more frequent dosages of ADR. Characteristic gross and histopathologic alterations of ADR toxicosis were observed in pigs given 1.0, 1.6, 3.2, or 6.4 mg/kg/week mean dosages. The most frequent lesions were in the alimentary tract, myeloid and lymphoid tissues, skin, and perivascular tissues at injection sites. Alimentary tract lesions were mucosal epithelial atrophy, with secondary fibrinonecrotic inflammation in the oral cavity and large intestine. Marked hypoplasia was seen in bone marrow and lymphoid tissues, with frequent terminal hemorrhagic diathesis and septicemia. Several days before death, the pigs developed severe dermatitis over the ventral portion of the abdomen and inner surfaces of the limbs. Perivascular necrosis and cellulitis produced by extravasation of ADR was a frequent complication of treatment. Terminal severe acute pneumonia occurred in most pigs. Pericarditis or cardiomyopathy (or both) developed in 14 pigs, given 0.64, 1.0, or 1.6 mg/kg each week (mean cumulative dosage 520.5 mg/m2 of body surface). Characteristic histopathologic and ultrastructural alterations in affected cardiac muscle cells were vacuolar degeneration, myocytolysis, and hyaline necrosis. Nephrotoxicosis also was in pigs with chronic ADR toxicosis. Systemic antibiotic treatment did not prolong survival of ADR-treated pigs in two experiments, but did in one other experiment.
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PMID:Pathologic features of adriamycin toxicosis in young pigs: nonskeletal lesions. 52 72

The state of immunological reactivity was studied on 250 albino mice treated with gentamycin and pentoxyl used alone or in combination because of sepsis caused by Ps. aeruginosa. Morphological changes in the spleen and lymph nodes, as well as the dynamics of the agglutinins accumulation in the blood serum were investigated. Gentamycin had no significant effect on the plasmocytal reaction in the lymph nodes and at the same time lowered the number of the immunocompetent cells in the spleen and the titer of agglutinins in the blood serum. The use of gentamycin in combination with pentoxyl had a stimulating effect on transformation of the plasmic cells in the lymphoid organs and resulted in increased titers of agglutinins in the blood serum of the animals treated.
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PMID:[Effect of gentamicin and pentoxyl on the immunological reactivity of the body in the treatment of sepsis caused by Ps. aeruginosa]. 81 53

Causes of death of 260 tumorous patients autopsied in 1974 were analyzed. Most common causes were inflammation and tumorous and non-tumorous organ insufficiencies; the others, in order of decreasing incidence, massive tumorous dissemination, infarct and haemorrhage. Pneumonia was predominating over the inflammatory causes although peritonitis and sepsis were also not rarely encountered. Death due to inflammation occurred most frequently in cases of myeloid-lymphoid, urogenital and gastro-intestinal tumours and in postoperative states. The incidence of insufficiencies due to tumorous or non-tumorous origin differed but slightly. Of the various organ insufficiencies, massive hepatic metastases, occlusion of the biliary duct and cardiac failure were the most common. In cases of tumors of the small pelvis, compression of the ureters led most often to death. Massive dissemination was observed most of all in breast and ovarian carcinomas. Myeloid-lymphoid tumors led to death through extensive organ infiltration in about one thirds of the cases. After hearth infarction, venous thrombosis was often followed by pulmonary embolism, however, coronary occlusion was also not rare. Death due to haemorrhage originated from acute or chronic ulcers of the gastrointestinal tract or from vascular invasion of tumors in the head and neck regions or from thrombocytopaenia induced by cytostatics.
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PMID:[Causes of death in cancer patients]. 92 45

The distribution of joint lesions in rats with Salmonella-associated arthritis (SSA), as determined in a detailed survey, resembles to a great extent the pattern of small joint involvement in human rheumatoid arthritis. Such lesions, though regularly induced in the rat by the intravenous injection of live S.enteritidis, could not be evoked by the heat-killed organisms injected by various routes with and without extrinsic adjuvants. Efforts to transfer SAA from sensitized donors to either normal or primed recipients, employing lymphoid ce-ls from several sources, also failed repeatedly. Two observations, however, virtually exclude the possibility that joint damage in SAA can be the direct result of sustained intra-articular sepsis. First, the inoculation of as many as 10-3 viable inflammation. Second, the incidence of SAA was significantly lower in weanling rats in the adult controls although the growth and distribution of intravenously injected S. enteritidis was virtually identical in the two groups. Together these observations indicate that the joint damage occurring in SAA is determined by the host and not by the infecting organism. From this, it seems fair to conclude that the destructive arthritis characteristic of this syndrome is immunologically mediated.
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PMID:Pathogenesis of Salmonella-associated arithritis in the rat. 108 97

Cardiac pathologic findings were analyzed in 22 necropsy cases from a series of 29 patients with leukemia, aplastic anemia, or metastatic cancer who had been treated with ablative therapy followed by bone marrow transplantation. Some cardiac alterations were similar to those that occur in patients with hematologic and neoplastic diseases not treated with bone marrow transplantation, and consisted of cardiomegaly, cardiac atrophy, hemorrhage, foci of necrosis due to shock associated with sepsis or hepatic failure, myocardial abscesses secondary to systemic candidiasis or staphylococcal infection, fibrinous pericarditis, and hemosiderosis. Other cardiac alterations were more specifically related to factors associated with transplantation procedure. Six patients exhibited a distinctive interstitial reactive change characterized by the presence of (1) moderate to large numbers of Anitschkow cells, occurring alone or in small cellular aggregates and histiocytes, histiocytic cells with nuclei of the Anitschkow type, lymphoid cells, and plasma cells, and (2) nuclei of the Anitschkow type in cardiac vascular and endocardial smooth muscle, endothelial and Schwann cells, and occasional cardiac muscle cells. This alteration may have been induced by abnormal immune mechanisms, as suggested by the observation that five of the six patients with interstitial change had clinical evidence of graft-versus-host disease. Two patients developed fatal congestive cardiac failure in the early post-transplant period and exhibited myocardial damage with histologic and post-transplant period features indicative of severe acute injury. Findings in these two patients consisted of necrotic muscle cells, which exhibited multiple contraction bands, diastase-resistant PAS staining, and intracellular fibrin deposits; microthrombi, which were composed of fibrin and occasionally of fibrin and platelets; and extravasated erythrocytes and fibrin strands in the interstitium. One of the two patients also exhibited unusual nuclear alterations, which were characterized by replacement of normal chromatin by palely stained fibrous and filamentous material. Clinicopathologic analysis strongly suggested that the fatal cardiotoxicity in both patients resulted primarily from effects of high doses of cyclophosphamide, which were administered as part of a four drug regimen that provided tumor ablation and immunosuppression for bone marrow transplantation. Our findings emphasize the need for less toxic antineoplastic and immunosuppressive therapy for use in bone marrow transplantation procedures.
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PMID:Cardiac pathologic findings in patients treated with bone marrow transplantation. 110 69

We phenotyped blood and bone marrow cells from a patient with acute Ph1+ acute leukemia longitudinally during the four months he received intensive chemotherapy. At presentation this case of biphenotypic acute leukemia had two immunologically different types of blast cells, one expressed CD10 (CALLA), CD13 (MY7) and CD33 (MY9) but lacked CD20 (B1), the other type expressed no CD10 or CD33. The phenotype, during AML induction therapy, changed to a more CD10+, CD20+ ALL one. ALL therapy based on these findings induced improvement in bone marrow function but the patient died of septicemia at day 134. The use of concomitant immunophenotyping (IP) and cell cycle analysis had shown proliferation advantage of the more lymphoid malignant cells. These results suggest that it is possible to induce lineage-associated changes in the phenotype of hybrid malignant cells and that these leukemias might be treated best according to longitudinal immunophenotyping of the blast cells.
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PMID:Hybrid acute leukemia: therapeutical implications of immunological phenotyping. 155 Jul 96

A 33-year-old man was hospitalized because of thrombocytopenia and severe splenomegaly. On admission 78% of peripheral lymphoid cells were abnormally large, with pale cytoplasm. Flow cytometry of the abnormal lymphocytes showed that they expressed CD 2, CD 3, CD 11, CD 16, and CD 56, but not CD 4 nor CD 8, so they were T-cell large granular lymphocytes (T-LGL). Abnormal lymphocytes obtained from a lymph node expressed CD 2, CD 16, CD 38, and CD 56, but not CD 3, CD 4, and CD 8, so they were natural killer(NK) cells. Splenectomy was performed and the operative specimen showed diffuse infiltration of pleomorphic lymphocytes, probably chronic lymphocytic leukemia cells. After splenectomy, the platelet count returned to normal but the lymphocytosis continued. Two years after discharge, chemotherapy was done because of thrombocytopenia and hepatomegaly. The patient died of disseminated intravascular coagulation arising from sepsis. The differences and similarities between peripheral and lymph-node lymphocytes suggest that LGL and NK cells may be differentiated from the same kind of cell, somewhat differentiated from stem cells.
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PMID:[Chronic lymphocytic leukemia with peripheral T lymphocytes expressing CD 2+, CD 3+, CD 4-, CD 8-, CD 16+, and CD 56+ and lymph-node lymphocytes expressing CD 2+, CD 3-, CD 4-, CD 8-, CD 16+, CD 38+, and CD 56+]. 171 68


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