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 adults, toxic megacolon is a relatively uncommon but potentially lethal complication of inflammatory bowel disease (IBD), infectious colitis, or ischemic colitis caused by cancer chemotherapeutic agents. Patients have distension of the colon and signs of toxicity such as elevated temperature, hypotension, decreased level of consciousness and electrolyte imbalances. Factors thought to increase the risk include premature discontinuation of IBD medications; procedures that increase colon trauma, such as barium enema and colonoscopy; medications that decrease gastrointestinal motility; and electrolyte imbalances, especially hypokalemia. Differential diagnosis is made based on the patient's history and results of stool cultures and assay for Clostridium difficile toxin. Medical management in the intensive care unit includes careful monitoring, fluid volume and electrolyte replacement, bowel rest and decompression, antibiotic therapy, and cessation of medications that slow gastric motility. Surgical management may be necessary if there are signs of deterioration, perforation, hemorrhage, or sepsis.
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PMID:Toxic megacolon: diagnosis and treatment challenges. 1086 33

Regulated on activation, normal T cell expressed and secreted (RANTES) serum concentrations were explored in a prospective observational study of haematological-malignancy patients undergoing chemotherapy. During systemic inflammatory response syndrome/sepsis or severe sepsis/septic shock mean concentrations were 3394 or 2939 pg/ml, respectively, significantly lower than those prior to fever (6031 pg/ml) (P < 0.01) or at bone-marrow recovery (6433 pg/ml, P < 0.001). Levels during febrile-bacteraemia were lower compared with febrile-non-bacteraemia (3022 pg/ml vs. 5111 pg/ml, respectively, P < 0.01). Sixty-three of 67 infection episodes resolved despite low RANTES concentrations, suggesting RANTES is not a prerequisite for recovering from most infection events. However, in four patients dying from septic shock associated with aspergillosis, candidosis, pneumonia or infectious colitis, RANTES concentrations were persistently and extremely low (1629 pg/ml), compared with four matched patients who recovered (6780 pg/ml). RANTES concentrations were highly correlated to platelet counts [median correlation coefficient 0.82 (inter-quartile range, 0.72-0.89)]. RANTES concentrations rose 4.5 d before platelet counts (P < 0.001), suggesting an additional extra-platelet source for RANTES. A nested mixed model regression analysis demonstrated that platelet level was the only independent variable associated with RANTES concentration (P < 0.001) among steroids, haematopoietic-colony-stimulating-factor, recombinant-human-interleukin-11, sepsis status, and neutropenia. A significant 'hypo-RANTES' serum environment occurs following chemotherapy, is driven by thrombocytopenia, but does not affect the ability of most patients to recover from infection.
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PMID:Significance of the CC chemokine RANTES in patients with haematological malignancy: results from a prospective observational study. 1568 55

Enteropathogenic Escherichia coli and enterohemorrhagic E. coli cause an inflammatory colitis in human patients characterized by neutrophil infiltration, proinflammatory cytokine expression, and crypt hyperplasia. Citrobacter rodentium causes a similar colitis in mice and serves as a model for enteropathogenic E. coli infection in humans. C. rodentium induces systemic T-cell-dependent antibody production that facilitates clearance of the bacteria and protects the host from reinfection. The role of innate immune cells in infectious colitis, however, is less well understood. In this study, we have determined the role of mast cells in the inflammatory response and disease induced by C. rodentium. Mice deficient in mast cells exhibit more severe colonic histopathology and have a higher mortality rate following infection with C. rodentium than do wild-type animals. Despite unimpaired neutrophil recruitment and lymphocyte activation, mast cell-deficient mice have a disseminated infection evident in crucial organ systems that contributes to sepsis. Importantly, mast cells also have the capacity to directly kill C. rodentium. Together, these results suggest that mast cells protect the host from systemic infection by reducing the bacterial load and preventing dissemination of the bacterium from the colon.
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PMID:Mast cells limit systemic bacterial dissemination but not colitis in response to Citrobacter rodentium. 1578 38

We experienced two autopsy cases of fulminant sepsis due to anaerobes. Case 1: A 67-year-old female with uncontrolled diabetes mellitus (DM) was admitted to a hospital because of sudden onset of mid-abdominal pain. She was diagnosed with infectious colitis and given a laxative and an enema. However, 9h later, her blood pressure suddenly dropped with metabolic acidosis, and she died 20 h after admission. Autopsy revealed massive pneumohemia and a dark-brown colored mucosal surface from the terminal ileum to the sigmoid colon. Histopathological findings were compatible with marginal ischemic colitis. Anaerobes were positive in blood culture. Case 2: A 53-year-old male with alcoholic liver cirrhosis (LC) was found dead in his room. He had been alive 24 h before the discovery, but postmortem changes appeared to accelerate more rapidly than usual cases. Autopsy revealed severe LC with muddy ascites and many Gram-negative rods in several organs. These cases suggest the possibility of sepsis as causes of death, especially in immuno-compromised hosts when unexplained putrefactive changes are seen on forensic autopsy.
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PMID:Fulminant sepsis due to anaerobic bacterial infection in immuno-compromised state. 1964 68

Twin infants born at 34 week gestation had frank blood in stools on day three of life on mixed feeds of formula and maternal breast milk. Sepsis work up was negative in these relatively well appearing infants with pneumatosis in the colon on abdominal x-ray. Blood in stools recurred on reintroduction of breast milk in Twin A. Both infants recovered from episodes of bloody stools on amino-acid based formula and were thriving at discharge. Early necrotizing enterocolitis in both twins is rare and has not been reported. Cow's milk protein sensitivity, possibly from in-utero sensitization, could explain non-infectious colitis in these twins, precipitated by formula or breast milk after birth.
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PMID:Early onset necrotizing enterocolitis (NEC) in premature twins. 2830 17