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)

A 3-month old female infant was transferred from another hospital where she had been hospitalized from the age of 1 month for protracted secretory diarrhea. The diarrhea had begun at birth and was unresponsive to various therapeutic formulas and to total parenteral nutrition (TPN). The parents were consanguineous. There were 6 normal siblings, while 3 siblings had died in infancy, including a sister who had succumbed to protracted diarrhea at the age of 6 months. In our patient duodenal biopsy showed flattening of villi and proliferation of mononuclear cells in the lamina propria. Specific circulating IgG antibodies against gut epithelium were found, as well as thyroglobulin antibodies. Repeated trials of oral feeding were unsuccessful and TPN was required for 8 months. Complications included septicemia, osteomyelitis and acute renal failure. Therapeutic trials with intravenous hydrocortisone, zinc sulphate and metronidazole were unsuccessful and the infant died at the age of 11 months. Intestinal tissue taken postmortem showed nearly absolute flattening of intestinal villi. This is the first report in Israel of intractable infantile diarrhea due to autoantibodies to intestinal epithelium.
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PMID:[Autoimmune enteropathy causing protracted diarrhea]. 235 45

An increasingly large number of dietary components have been found to alter immune system function and, therefore, may be considered to have a pharmacologic effect (pharmacologic nutrition). Those dietary factors which have already been shown to influence outcome by producing a pharmacologic effect rather than correcting or preventing a simple deficiency include proteins (both type and amount), arginine, glutamine, omega-6 and omega-3 fatty acids, short-chain fatty acids, the metals iron and zinc, and the vitamins E, C, and A. Therapeutic outcome has already been influenced by dietary therapy (pharmacologic nutrition) in patients after burn injury or who have vascular diseases, and in experimental animals for the prevention of gut origin sepsis, the prevention and treatment of infection, prevention and development of secondary lesions in autoimmune diseases, augmentation of immunosuppression in transplantation, and in the treatment of cancer. Nutritional therapy using disease-specific formulations or supplements is an old idea now undergoing rapid evolution to increasing importance for successful therapeutic outcome.
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PMID:Future prospects for adjunctive therapy: pharmacologic and nutritional approaches to immune system modulation. 240 69

Sepsis with subsequent multiple organ failure is the commonest complication seen in the surgical intensive care unit today. A gut mucosal barrier dysfunction is assuming an increasingly important role as one possible explanation for the initiation of the septic process. It is known that the gut bacteria and endotoxins can, in the presence of a seemingly intact epithelium, translocate to extraintestinal sites, but the exact mechanism behind this process is not understood. In the present study we have approached this problem by testing the gut permeability to two macromolecules, bovine serum albumin (BSA) and fluorescein isothiocyanate (FITC)-dextran, after 7 days of enteral or parenteral nutrition in the rat. The plasma values of FITC-dextran after 4 h of marker feeding showed a significant increase in gut permeability after parenteral but not after enteral nutrition as compared with the controls. The plasma values of BSA, however, did not show any significant change in any of the groups. Thus, parenteral nutrition, with the changes occurring in the gut mucosa, may be one of the etiologic co-factors behind a gut mucosal barrier dysfunction, eventually leading to absorption of noxious agents into the systemic circulation with subsequent multiple organ failure.
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PMID:Increased gut permeability to fluorescein isothiocyanate-dextran after total parenteral nutrition in the rat. 247 82

Clinical and bacteriological data of 145 inpatients with septicemia, treated at the hospital of Chiba University School of Medicine from 1972 to 1987, were reviewed by dividing them into three stages. (stages I: 1972-76, stage II: 1978-82, stage III: 1983-87) Patients with underlying diseases have been increasing: 91.8% of the total patients in stage III. Among the patients with underlying diseases, malignant and hematological diseases occupied about 60%, and in the other diseases, congenital heart diseases have been increasing in number. As to the organisms isolated, gram positive bacteria have increased, while gram negative bacteria have decreased. In stage III, the rate of gram positive organisms and gram negative ones accounted for 43.1% and 41.2% of all the isolates from the septic patients with malignant & hematological diseases, respectively. In patients with malignant & hematological diseases, alpha-streptococcus, coagulase-negative staphylococcus, and Fusobacterium sp. have been increasing, whereas, Escherichia coli, Enterobacter sp., Klebsiella sp., and Pseudomonas aeruginosa decreasing. In patients with other underlying diseases, S. aureus, CNS, and non Fermenters have been increasing. Among the patients without underlying diseases, gram positive bacteria accounted for the major part. The decrease of gram negative organisms in patients with malignant and hematological diseases may partially depend on the introduction of polymixin B as the drug of gut decontamination. The outcome of septicemia in the patients with malignant & hematological diseases has been markedly improving through all the three stages. During stage III, episode mortality and case mortality rate proved to be 23% and 31%, respectively. The introduction of the third generation cephems has decreased the mortality rate for gram negative organisms and contributed to the improvement of the total prognosis. The prognosis was worst in the case of P. aeruginosa, showing a mortality rate of 50% during stage III. Coincidence rate of blood and other cultures have been largest in the case of P. aeruginosa, so, the drug sensitivity of the strain cultured from other sites is sometimes useful in the choice of antibiotics.
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PMID:[Studies on 145 cases of septicemia in infancy and childhood--especially on septicemic patients with malignant and hematological diseases]. 250 84

The use of elevated dosages of vitamin E in humans has led to the discovery of vitamin E deficiency syndromes in neurological areas. This evidence comes from careful clinical studies in which elevated vitamin E dosages were applied. In long-term studies it has now been established that retinal and neurological abnormalities are due to vitamin E deficiency and can be ameliorated by therapy with a large amount of the vitamin enterally or parenterally, which can possibly completely prevent the development of clinical manifestations if adequate treatment is given from an early age. It has also become clear that similar neurological and ocular lesions occur in other chronic fat malabsorptive states such as cholestatic liver diseases, cystic fibrosis, and extensive resection of the gut, with respect to an elevated dosage of vitamin E therapy. More recently, several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption have been reported on in whom the progression of the diseases is cessated by the vitamin E therapy. Whether or not the use of elevated dosages of vitamin E should be recommended for certain diseases in premature infants is controversial. Previously, it has been thought that newborn infants, especially premature infants, suffer from vitamin E deficiency, because of their low plasma vitamin E concentrations and high susceptibility of erythrocytes to hydrogen peroxide hemolysis test. Furthermore, tocopherol deficiency has been implicated in four neonatal conditions: anemia of prematurity, retrolental fibroplasia (RLF), bronchopulmonary dysplasia (BPD), and intraventricular hemorrhage (IVH). A hemolytic anemia, associated with thrombocytosis and edema, which is responsive to vitamin E therapy, is not well recognized and occurs in a minority of preterm infants, who were given high amounts of polyunsaturated fatty acids in their formula. However, prophylactic use of an elevated dosage of vitamin E to prevent anemia in the majority of premature infants is controversial. There is no evidence for beneficial effects in BPD. In addition, the prophylactic use of pharmacological dosages of vitamin E for prevention of RLF and IVH has also had conflicting results. In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use and safety of elevated dosages of vitamin E in infants and children. 250 8

Two antibiotic regimens commonly used in neonatal intensive care were compared for the rate at which Clostridium difficile appeared in the faeces. Over a nine month period neonates with suspected sepsis admitted to a Special Care Baby Unit (SCBU) were randomly allocated to receive either cefotaxime or penicillin and netilmicin. A contemporaneous group also admitted to SCBU but without sepsis served as non-treated controls. Four hundred and sixteen stool specimens from 158 neonates without diarrhoea were analysed every five to seven days until discharge. The results showed that these antibiotics did not encourage gut colonization by C. difficile, that they might even be protective in this respect and that monotherapy with cefotaxime was no more likely to generate C. difficile overgrowth than the penicillin-aminoglycoside regimen.
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PMID:Antibiotic exposure delays intestinal colonization by Clostridium difficile in the newborn. 260 1

The present case report describes a patient with an adrenal phaeochromocytoma who presented with infarction of the small intestine. The clinical features, diagnosis and treatment of this case are described. Despite excision of the tumour and necrotic intestine, this patient died in the postoperative period from overwhelming sepsis and multi-organ failure. Special reference is made to the delayed effects of established intestinal ischaemia on immune function and it is suggested that this was major contributory factor to the fatal outcome in the present case. The onset of gastro-intestinal symptoms in patients with phaeochromocytoma should suggest the possibility of imminent gut ischaemia and indicate the necessity for prompt excision of the tumour.
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PMID:Intestinal ischaemia associated with phaeochromocytoma. 234 95

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome represents the transition from a hypermetabolic response to injury to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, persistent hypermetabolism, and preexisting fibrotic liver disease. Once initiated, most treatment modalities for the organ failure syndrome become progressively ineffective including: ventilation, antibiotics, nutrition, and surgery. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred. The metabolic response to injury involves alterations in physiology and in the metabolism of carbohydrate, fat and amino acids. These changes seem to reflect the modulation of the end-organs by the mediator systems activated in response to the stress stimuli. The transition from hypermetabolism to organ failure appears to reflect the clinical appearance of liver failure. It is hypothesized that this liver failure may represent a state of regulatory dysfunction induced in large part by the activated hepatic macrophage, the Kupffer cell. The activation of these macrophages is hypothesized to represent the final stage of a series of stimulating events, eg. hypoxia, endotoxin, bacteria, and gut translocated toxins. The precise monokine(s) responsible are not yet completely characterized, although Interleukin-1 (IL-1) and tumor necrosis factor (TNF) appear to be involved as do prostaglandins (Pg) such as PgE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of monokines in altering hepatic metabolism in sepsis. 264 13

Two children with the short-gut syndrome and secondary liver failure were treated with evisceration and transplantation en bloc of the stomach, small intestine, colon, pancreas, and liver. The first patient died perioperatively, but the second lived for more than 6 months before dying of an Epstein-Barr virus-associated lymphoproliferative disorder that caused biliary obstruction and lethal sepsis. There was never evidence of graft rejection or of graft-vs-host disease in the long-surviving child. The constituent organs of the homograft functioned and maintained their morphological integrity throughout the 193 days of survival.
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PMID:Transplantation of multiple abdominal viscera. 291 40

Between 1983 and 1986, four newborns who had primary closure of gastroschisis had postoperative ischemic bowel. Suspicion was raised almost immediately after closure that something was wrong inside the abdomen when there was persistent acidosis, sepsis, abdominal wall redness, and a generalized worsening condition. All four neonates were re-explored. Necrotic bowel was found, and three required silon pouch closure. The two survivors were left with a temporary short gut. Whether the cause of the bowel ischemia in the four babies was due to excessive intraabdominal pressure, volvulus, or the intestines being too vigorously manipulated, is speculative. Therefore, excessive manipulation and compression of gastroschisis contents seem unwise; if such a newborn has persistence of the above signs and symptoms, immediate reoperation and decompression are warranted.
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PMID:Ischemic bowel after primary closure for gastroschisis. 297 92


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