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)

Seventeen pediatric patients, ages 9.25--20.5 yr, were placed on a program of home parenteral nutrition (HPN) for severe, symptomatic Crohn's disease. Prior therapy with sulfasalazine in 14, adrenocorticosteroids in 12, inpatient total parenteral nutrition in 7, and/or surgical resections in 6 failed to suppress disease activity. Remission was attained in 12 of the 17 after one course of HPN alone. Four patients had surgical procedures and 1 required steroids in addition to HPN. Remissions have been maintained in 4 of those 12 for a mean duration of 315 days after discontinuation of HPN. Of the 8 who relapsed after a mean duration of 68 days, second courses of HPN were undertaken in 7 and third courses in 2. All 17 had a marked improvement in disease symptoms while receiving HPN in addition to gaining weight sufficient to place them at a higher percentile on standard growth charts. Ten patients demonstrated "catch-up" growth and 4 others increased their height appropriately. A chromium 51-labeled albumin stool collection of greater than 1% in 5 of 7 patients at the completion of a HPN course correlated with relapse within 4 mo. Serial radiographic contrast studies and erythrocyte sedimentation rates were not predictive of prolonged remissions. Home parenteral nutrition complications were minimal, with only one episode of sepsis per 5.8 catheter experience years. It is concluded that HPN is a safe and effective means of inducing remissions and providing optimal nutritional support in pediatric patients with severe Crohn's disease. Patients with less than adequate response to standard medical management should be considered candidates for this therapeutic modality.
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PMID:Home parenteral nutrition in children with Crohn's disease: an effective management alternative. 10 47

Under normal conditions the intestinal mucosa is impermeable to potentially harmful materials from the intestinal lumen. Mucosal disruption promotes bacterial translocation, which is postulated to be a fuel source for sepsis and multiorgan failure. We have previously demonstrated that mesenteric ischemia-reperfusion (I/R) injury increases intestinal permeability (IP); however, the mechanism remains unclear. This study was designed to examine the hypothesis that changes in IP, after I/R injury, are mediated by xanthine oxidase-generated, oxygen-derived free radicals. Thirty-three Sprague-Dawley rats (weighing 300 to 400 g) were included in this study. Group 1 (n = 10) received enteral allopurinol, a xanthine oxidase inhibitor, 10 mg/kg daily for 1 week prior to mesenteric ischemia. Group 2 consisted of 11 untreated, ischemic animals. Groups 1 and 2 were subjected to superior mesenteric artery occlusion with interruption of collateral flow for 20 minutes to produce ischemic injury to the intestine. An additional 12 rats (group 3), served as nonischemic controls (sham). A loop of distal ileum was isolated and cannulated proximally and distally to allow luminal perfusion with warmed Ringer's lactate at 1 mL/min. IP was determined in all groups by quantitatively measuring the plasma-to-luminal clearance of chromium (51Cr)-labeled ethylenediaminetetraacetate (EDTA) at baseline, during ischemia and 20, 40, and 60 minutes after reperfusion. Complete ischemia produced significant increases in IP over baseline values in the untreated rats (group 2, baseline: 0.49 +/- 0.006, ischemia: 0.149 +/- 0.039) compared with sham rats (baseline: 0.41 +/- 0.006; ischemia: 0.047 +/- 0.009) or allopurinol-treated rats (baseline: 0.098 +/- 0.020, ischemia: 0.073 +/- 0.012, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Allopurinol prevents intestinal permeability changes after ischemia-reperfusion injury. 140 60

Granulocyte transfusions are increasingly being used as therapy for newborns with sepsis and neutropenia. We injected either group B Streptococcus or phosphate-buffered saline solution intraperitoneally into adult and newborn rats. Human granulocytes, labeled with chromium 51, were transfused seven hours later. When the newborn rats were killed 13 to 19 hours after injection, they had 10(2) to 10(6) cfu/gm Streptococcus organisms in both lung and brain. Only one third of the adult rats had 10(2) to 10(4) cfu/gm Streptococcus organisms in either lung or brain. A greater proportion of the transfused granulocytes was present in lung and brain tissue of newborn rats, compared with adult rats (p less than 0.05), irrespective of infection. Granulocyte transfusion did not change the peripheral blood leukocyte count in adult rats but increased the count in newborn rats (p less than 0.05). The immature myeloid pool in the bone marrow of adult rats increased significantly with either infection or transfusion (p less than 0.01). The immature pool in newborn rats increased significantly only with infection (p greater than 0.001), although the combination of infection and transfusion also had a significant effect on the pool (p less than 0.01). Infection and both infection and transfusion, but not transfusion alone, significantly affected the mature myeloid bone marrow pool in adult and newborn rats (p less than 0.001). The depletion of the mature myeloid elements of the bone marrow in response to infection was dramatic in neonatal rats, compared with that in adult rats. Both transfused granulocytes and hematogenously spread streptococci lodge in the brains and lungs of neonatal rats more effectively than in those of adult rats.
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PMID:Granulocyte transfusions in septic adult and newborn rats: distribution of granulocytes and effect on peripheral blood and bone marrow. 231 59

Thrombocytopenia without other hemostatic changes is the most common coagulopathy associated with sepsis. We studied pneumococcus (PNC)-induced hemostatic changes, including thrombocytopenia, in rabbits. Nonviable PNC or saline solution was injected into rabbits preinfused with chromium 51-labeled platelets or iodine 125-fibrinogen. Blood was serially obtained for determination of platelet counts, 51Cr activity or 125I activity, and fibrinogen and fibrin degradation products. Lung, liver, and spleen tissues were counted for 51Cr or 125I activities per gram of wet tissue. PNC-challenged animals displayed profound thrombocytopenia from 0.5 to 48 hours with the mean nadir (-80% relative to the baseline) at 3 hours and a significantly (P less than 0.025) shortened 51Cr-platelet survival of 1.45 +/- 0.71 days vs. 2.72 +/- 1.09 days for saline-injected controls. Circulating fibrinogen level increased, whereas 125I-fibrinogen survival was unchanged (2.6 +/- 0.5 days in PNC-challenged vs. 2.8 +/- 1.0 days in saline-injected). No increased tissue deposition of either 51Cr-labeled platelets or 125I-fibrinogen was found. Rabbits infused with either serum, plasma, or saline solution after each was incubated with PNC all developed significant thrombocytopenia of less than 1 hour duration with maximal mean decreases relative to the baseline of -76% (P less than 0.001), -65% (P less than 0.0005), and -84% (P less than 0.0005), respectively. Inactivation of serum or plasma complement before PNC incubation or heat treatment after PNC incubation in serum or saline solution did not alter the thrombocytopenia. The thrombocytopenia-promoting activity was also trypsin resistant, did not require the presence of serum, plasma, or PNC capsular polysaccharide for its in vitro generation, and had a mol wt of 100,000 to 300,000. Therefore, PNC-induced thrombocytopenia, in the absence of other hemostatic changes, may be explained on the basis of the direct action of a PNC-derived substance(s) on circulating platelets.
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PMID:Pneumococcus-induced thrombocytopenia in rabbits. 403 31

In vitro cellular immune responses to metallic and polymeric implant materials in particulate form were measured preoperatively in 185 patients. The patients were candidates for either primary total joint replacement (n = 65) or revision arthroplasty (n = 120). Proliferative cellular responses to polymethylmethacrylate particles in patients with osteoarthritis at revision surgery for aseptic loosening were significantly higher than the responses of patients with osteoarthritis at either primary surgery or surgical revision for mechanical failure of the prosthesis or sepsis. The responses to particles of cobalt-chromium alloy at revision surgery were also higher than the responses at primary surgery. The responses were reevaluated in 32 patients after a minimum of 10 months following surgery to correlate individual changes in the biological responses with clinical progress. Reevaluation at early follow-up of patients who had undergone primary surgery revealed significantly elevated proliferative responses and in vitro cytokine production in response to polymethylmethacrylate and cobalt-chromium alloy particles compared with their preoperative responses. In contrast, the response at follow-up to polymethylmethacrylate was significantly reduced in patients who had undergone revision surgery, and this reduction corresponded with a marked improvement in pain, joint motion, and function following revision surgery. These data suggest that specific cellular responses to polymethylmethacrylate or cobalt-chromium alloy particles, or both, may be associated with loose or painful prostheses.
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PMID:Cellular immune responses to orthopaedic implant materials following cemented total joint replacement. 949 13

Rhabdomyolysis results from skeletal muscle injury and release of muscle cell contents into plasma. A number of etiologic factors have been reported for the condition, including strenuous exercise, weight lifting, trauma, seizure, sepsis, and alcohol and drug abuse. Hundreds of drugs also reportedly cause rhabdomyolysis. A 24-year-old body builder developed the disease after ingesting 1200 microg of chromium picolinate (6-24 times the daily recommended allowance of 50-200 microg) over 48 hours. We believe this to be the first reported case of chromium-induced rhabdomyolysis.
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PMID:Suspected chromium picolinate-induced rhabdomyolysis. 969 62

Heme oxygenases (HOs), essential enzymes for heme metabolism, play an important role in the defense against oxidative stress. In this study, we evaluated the expression and functional significance of HO-1 and HO-2 in the ventilatory muscles of normal rats and rats injected with bacterial lipopolysaccharide (LPS). Both HO-1 and HO-2 proteins were detected inside ventilatory and limb muscle fibers of normal rats. Diaphragmatic HO-1 and HO-2 expressions rose significantly within 1 and 12 h of LPS injection, respectively. Inhibition of the activity of inducible nitric oxide synthase (iNOS) in rats and absence of this isoform in iNOS(-/-) mice did alter sepsis-induced regulation of muscle HOs. Systemic inhibition of HO activity with chromium mesoporphyrin IX enhanced muscle protein oxidation and hydroxynonenal formation in both normal and septic rats. Moreover, in vitro diaphragmatic force generation declined substantially in response to HO inhibition both in normal and septic rats. We conclude that both HO-1 and HO-2 proteins play an important role in the regulation of muscle contractility and in the defense against sepsis-induced oxidative stress.
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PMID:Role of heme oxygenases in sepsis-induced diaphragmatic contractile dysfunction and oxidative stress. 1211 11

There is evidence suggesting that early fluid resuscitation is beneficial in the treatment of septic shock. The question as to which solution should be used remains controversial. Using a porcine septic shock model, we tested the effects of a new synthetic colloid hydroxyethyl starch (HES 130 kD) and a crystalloid regimen with Ringer's solution (RS) on plasma volume (PV) maintenance as well as on systemic and regional hemodynamics. Fourteen anaesthetized mechanically ventilated pigs received 0.75 g kg body weight of feces into the abdominal cavity to induce sepsis. They were randomly allocated to receive 6% HES 130 kD (n = 5) or RS (n = 5) and were compared with nonseptic controls receiving 6% HES 130 kD (n = 4). The infusion rate was titrated to maintain a central venous pressure of 12 mmHg. PV was determined by chromium-51-tagged erythrocytes and hematocrit. Albumin escape rate (AER) was calculated using iodine-125-labeled albumin. Arterio-intramucosal pCO2 gap, systemic hemodynamics, and oxygenation were obtained before and 6 h after induction of sepsis. AER increased in the HES (+38%) and RS groups (+38%) compared with control. PV was reduced in the RS group (-39%), but was maintained in the HES group (-1%). After 6 h of sepsis, HES 130 kD-treated animals had a significantly higher cardiac output (166 +/- 28 mL min kg vs. 90 +/- 18 mL min kg, P < 0.05), and a significantly higher mixed-venous oxygen saturation (65% +/- 8% vs. 40% +/- 14%, P < 0.05) than RS animals. In this porcine septic shock model with concomitant capillary leakage syndrome, resuscitation with HES 130 kD but not RS could maintain PV and preserve systemic hemodynamics and oxygenation.
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PMID:Resuscitation from septic shock with capillary leakage: hydroxyethyl starch (130 kd), but not Ringer's solution maintains plasma volume and systemic oxygenation. 1517 34

Intercellular adhesion molecule-1 (ICAM-1) is involved in neutrophil transmigration across endothelium during sepsis-induced acute lung injury and anti-ICAM-1 interventions may represent new strategy of pulmonary protection. Haem oxygenase-1 (HO-1) has been demonstrated to exert anti-inflammatory actions via decrease of expression of adhesion molecules. We investigated the role of HO-1 in the action of curcumin, a naturally occurring yellow pigment isolated from plant Curcuma longa L., on ICAM-1 expression in tumour necrosis factor-alpha-stimulated EA.hy926 cells and lungs of lipopolysaccharide-treated mice. Both, in vitro and in vivo curcumin induced HO-1 and curcumin-elicited induction of HO-1 was associated with inhibition ICAM-1 expression. Moreover, curcumin significantly inhibited pulmonary sequestration of leucocytes in response to lipopolysaccharide as evidenced by decrease of myeloperoxidase activity in lung tissue. Both in vitro and in vivo effects of curcumin were reversed by an inhibitor of HO activity, chromium (III) mesoporphyrin IX chloride. We conclude that induction of HO-1, via decrease of endothelial ICAM-1, plays a pivotal role in curcumin-dependent prevention of pulmonary sequestration of neutrophils in a mouse model of endotoxaemia.
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PMID:The role of haem oxygenase-1 in the decrease of endothelial intercellular adhesion molecule-1 expression by curcumin. 1797 99

Trace elements (TEs) are required by both humans and bacterial pathogens. Although metal ion homeostasis is tightly controlled in humans, growing evidence suggests that pathogens utilize a variety of means designed to circumvent the sequestration of TEs. Colonizing pathogenic microorganisms employ a variety of strategies to sense, acquire, store, and export metal ions in the vertebrate host which include the biosynthesis and utilization of siderophores, and the expression of high-affinity metal-ion transporters. For iron, selenium, and zinc, significant correlations have been shown between TE levels in plasma, serum, or tissues, and the prevention or treatment of a variety of infectious diseases; fewer such data exist for copper, chromium, or manganese. TEs are often employed as antioxidants, and as supplements in patients with TE-deficient states. The role of TE supplementation in humans as antioxidants remains controversial, but has demonstrated significant benefit in the role of selenium for patients with sepsis, and of zinc for the prevention of several infectious diseases.
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PMID:Metal ions and infectious diseases. An overview from the clinic. 2447 87


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