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)

In a hamster model of non-Hodgkin's lymphoma which closely parallels the disease in man, and which is induced by an unusual agent(s), a diarrheal bowel disease was a major cause of mortality. This study was initiated to characterize this bowel disease and its relation to lymphoma induction and to natural diseases seen in the hamster. The studies showed that the bowel disease was an ulcerative process and was distinct from natural diseases. The incidence of the bowel disease correlated directly with that of the lymphoma in repeated epizootics, in titration studies, and in agent inactivation tests. The ulcerative bowel lesions were seen at the same stage of the disease as acute and chronic inflammatory infiltrates with necrosis in the thymus and mesenteric lymph nodes. Since necrosis in the gut-associated lymphoid tissue can lead to perforation and sepsis, these bowel lesions were lethal, whereas similar necrosis in other lymphoid tissues (thymus and lymph nodes) could be clinically undetectable. Similar lesions have been reported in man. The ulcerative bowel disease was a reliable early clinical marker for exposure of hamsters to this lymphomagenic agent(s).
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PMID:Lymphoma-associated ulcerative bowel disease in the hamster (Mesocricetus auratus) induced by an unusual agent. 637 5

The DiGeorge syndrome is a rare congenital abnormality of absent of hypoplastic thymus and parathyroid glands. Thirty neonates who had cardiac lesions and the DiGeorge syndrome are reviewed. The early mortality for 10 neonates undergoing palliative procedures was 80%. Seventy-five percent of the deaths were secondary to sepsis. Twenty neonates did not undergo palliative procedures. In this group, early mortality was 60% and late mortality was 65%. Sixty percent of the deaths in this group were associated with sepsis, with cardiac failure responsible for the remaining deaths. Survival in both groups has improved with appropriate treatment of the immunological and metabolic consequences of the DiGeorge syndrome.
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PMID:Congenital cardiac anomalies associated with the DiGeorge syndrome: a neonatal experience. 646 92

The immune system was studied in 30 cases of local infection (pneumonia) and 56 cases of generalized infection (sepsis). Predominantly children with immunologic deficiency of the humoral type (77% of the cases) characterized by unscheduled fatty transformation of the thymus, underdevelopment of B-zones of lymphoid organs, low level of IgM production and the lack of IgG and IgA production were found to die with pneumonia, whereas children with physiological immaturity of the immune system and in smaller numbers (41% of the cases) with deficiency of immunity of the cellular and phagocytic type as confirmed by immaturity of the thymic tissue or its dysplasia with hypoplasia of lymphoid organs died with sepsis. Immunological deficiency of the humoral type is accompanied by suppurative destructive lesions of the respiratory organs, immunodeficiency of the cellular and phagocytic type by necrotic changes in the septic focus and mucous membranes of the organs contacting the environment.
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PMID:[The immune system and its relation with infection process in children]. 660 38

Morphological changes of the thymus, tonsils, lymph nodes, spleen, and other organs in two observations of severe combined insufficiency (SCIN) in infants of the first year of life are described. In both cases there was hypoplasia of the thymus with the lack or occasional thymic bodies and poor content of thymocytes in the lobules. In one infant, hypoplasia of the thymus was combined with intestinal angiomatosis which suggested the syndrome of ataxia-teleangiectasia. In the other infant, SCIN was associated with severe granulocytopenia of the Kostman type. In this case epithelial cells of the lobules formed adenomatous structures. Both infants died with sepsis developing against the background of SCIN.
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PMID:[Hypoplasia of the thymus gland in children]. 686 Jan 70

Lymphoid system was studied morphologically in 61 infants aged under 1 year dying of sepsis, nonseptic inflammatory diseases and non-inflammatory processes. It was established that in sepsis generalization of the immune response and decompensation of the lymphoid system occurred in the development of which previous disorders of immune responsiveness (thymus pathology, immaturity of the lymphoid system of premature babies, respiratory viral infections) are of great importance. Unlike sepsis, local inflammatory processes are characterized predominantly by limited immune reaction and decompensation of lymphoid system has a local character. In babies of the first month of age reactions of the T-lymphocyte system predominate, in older babies those of the B-lymphocyte system.
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PMID:[Immunomorphologic aspects of sepsis in children under 1-year-old]. 708 93

In this report, we present a 5 months old male baby, who suffered from watery diarrhea since 4 days old. From then on, he had been admitted 3 times in 3 different hospitals but the symptoms still bothered him off and on. During the days of hospitalization, sepsis with positive blood culture of Klebsiella was noted. The patient expired at 5 months of age. The T cell count was 20% active T was 0. Delayed hypersensitivity skin tests including Candida (10 X), PHA (10 micrograms), PHA (1 microgram), SK/SD (50 units) were negative. The granulocyte function study showed normal. Immunoglobulin analysis revealed IgG: 1320 mg%, IgA: 120 mg%, IgM: 100 mg%. Agenesis of thymus, failure of lymphoid differentiation and abnormal lymphoid architecture with absence of germinal centers were noted at autopsy. Combined immunodeficiency with normal immunoglobulins (Nezelof syndrome) is a disease of primary immunodeficiency characterized by recurrent infections, failure to thrive, lymphopenia, diminished lymphoid tissue, abnormal structure or agenesis of the thymus, and presence of normal or increased levels of one or more of the major immunoglobulin classes, but with impaired antibody synthesis. Since its original description by Nezelof and associates in 1964, it has been reported on the subsequent occasion. In this report, we present our one experience and review the clinical and laboratory data in 33 reported cases.
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PMID:Report of a case of Nezelof syndrome. 744 23

The pathology of lymphoid organs in 38 low birth weight (LBW) human infants has been evaluated by morphological and morphometric features. The gestational ages of infants ranged from 22 to 32 wks and their age at death varied from 1 hr to 153 days post partum. Infants were divided into 3 groups: 1) without antigenic effects, 2) with mild (bronchopneumonia), and 3) with severe antigenic effects, mainly sepsis. In mildly affected LBW infants, the fetal type of the immune reaction was found. It continued during the period studied (till 5 mths) and was manifested in the reaction of macrophages and the transformation of lymphocytes to lymphoblasts. Reactive centres of follicles and mature plasmocytes were not found. During the first months of postnatal development, an increase in the amount of lymphocytes in the lymphoid organs and in the rate of proliferation of reticular epithelium and a decrease in the area of the cortex in the thymus were found in all infants. In severely affected infants, the number and the size of follicles in the spleen decreased significantly and the total number of cells decreased more than 3 times. Similar changes were found in lymph nodes. These changes as well as the weak reaction of the thymus are the main features of the insufficiency and fast devastation of the lymphoid system. A compensatory increase in the number of neutrophils and eosinophils in the red pulp of the spleen and lymph nodes was found after the second week.
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PMID:Pathology of lymphoid organs in low birth weight infants subjected to antigen-related diseases: a morphological and morphometric study. 756 36

Thymic programmed cell death (PCD) or apoptosis (Ao) is elevated during inflammation by a variety of stressors in vitro (i.e., glucocorticoids, tumor necrosis factor (TNF), prostanoids, etc.), however, little or no information is available concerning its presence in polymicrobial sepsis. To establish whether or not PCD is accelerated in the thymus following the onset of sepsis, thymocytes were harvested from C3H/HeN mice at 1, 2, 12, and 24 h following cecal ligation and puncture (CLP; to induce sepsis) or Sham-CLP (Sham), and assessed for changes in thymocyte viable cell yield, increased Ao + cells based on FACS analysis (propidium iodide staining) or by evidence of fragmentation of the genomic DNA. The results indicate that at 1 h post-CLP there were no marked changes in any of these parameters. However, by 4 h post-CLP the percentage of Ao + thymocytes increased and the septic mouse genomic DNA exhibited trace amounts of fragmentation. These changes increased in the septic animals cells through both 12 and 24 h. Alternatively, thymic viable cell yield did not significantly decrease until 12 h. Marked changes in systemic mediators, corticosterone and TNF, were also detected in septic mouse blood at all time points. In an effort to determine the contribution of these two agents to the induction of the accelerated PCD seen here, mice were randomized to receive either RU-38486 (11 beta-[p-(dimethylamino)phenyl]-17 beta-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one (Mifepristone); a steroid receptor blocker), polyethylene glycol (PEG)-(rsTNF-R1)2 (a TNF inhibitor) immediately following CLP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The induction of accelerated thymic programmed cell death during polymicrobial sepsis: control by corticosteroids but not tumor necrosis factor. 760 Jan 93

Antibody levels to the protein antigen tetanus toxoid (TTx) and the carbohydrate antigens pneumococcal capsular polysaccharides (PCP) were studied by enzyme immunoassay in 14 patients with acute lymphocytic leukemia (ALL) and 32 patients with acute non lymphocytic leukemia (ANLL) before and three weeks after initiation of chemotherapy. The antibody levels to TTx were significantly lower in ALL patients than in controls. This was associated with elevated levels of sCD8 (soluble CD8) in the serum of 12 out of the 14 ALL patients. Patients with ANLL had normal antibody levels before chemotherapy. After chemotherapy ANLL patients with septic complications had a reduced increase of antibody titers to TTx than patients without sepsis. The average antibody titers to PCP decreased in patients with sepsis, while they increased slightly in patients without sepsis. We conclude that in contrast to ANLL patients ALL patients have preexisting decreased antibody levels to thymus dependent protein antigens, while antibody levels to thymus independent carbohydrate antigens are normal in both types of leukemias.
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PMID:Impaired antibody levels to tetanus toxoid and pneumococcal polysaccharides in acute leukemias. 769 35

Ectodermal dysplasia is a heterogeneous disorder that includes a constellation of congenital malformations occasionally associated with mild to moderate immune dysfunction. In this report, we describe a female infant with ectodermal dysplasia who was found to have thymic hypoplasia but no other phenotypic features of the DiGeorge anomalad. She experienced Candida parapsilosis sepsis at 1 week of age and a skin infection with Mycobacterium chelonii at 6 months. The numbers of blood B cells were normal and serum immunoglobulins normal to slightly reduced, but serum antibody responses of all immunoglobulin isotypes to protein immunogens were absent. Blood T cells were profoundly reduced and proliferative responses of T cells to mitogens were blunted. In contrast, there was an increased number of natural killer (NK) cells and increased NK activity in the blood. Over the first year of life, some of the immunodeficiencies resolved. Although the numbers of blood T cells (17% of total lymphocytes) remained low, proliferative responses to mitogens normalized and specific antibody responses improved. It seems likely that the thymic hypoplasia in this case was due to a paucity of ectodermal elements in the developing thymus, and that the immune defects were largely secondary to that event. In that respect, this human model of ectodermal dysplasia and thymic hypoplasia resembled the ectodermal/thymic defects found in the nude mouse.
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PMID:Thymic hypoplasia and T-cell deficiency in ectodermal dysplasia: case report and review of the literature. 813 58


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