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1/13. Invasive Group C streptococcus infection associated with rhabdomyolysis and disseminated intravascular coagulation in a previously healthy adult.

    Infections with Group C Streptococci can lead to severe disease, particularly in individuals with underlying illnesses such as cardiovascular disease, malignancy or immunosuppression. We report the first case of rhabdomyolysis and disseminated intravascular coagulation secondary to Group C streptococcus in a previous healthy male. A toxic shock-like syndrome associated with Group C and Group G Streptococci has been reported. However, unlike with Group A Streptococci, production of endotoxins by these organisms is less well defined. We tested the patient's isolate for its ability to produce superantigenic toxins and to induce a mitogenic response. Although it is not known whether Group C Streptococci require special growth conditions for the production of superantigens, we could not demonstrate either the production of exotoxins or the induction of a mitogenic response.
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2/13. Selective decontamination of the digestive tract contributes to the control of disseminated intravascular coagulation in severe liver impairment.

    A premature neonate with severe Coxsackie B1 hepatitis acquired in utero developed disseminated intravascular coagulation a few days after birth. The neonate did not respond to conventional treatment. Eradication of aerobic gram-negative bacilli (enterobacteriaceae) from the gut with oral nonabsorbable polymyxin E and tobramycin (selective decontamination of the digestive tract) was followed by clinical improvement; disseminated intravascular coagulation was controlled. After an unstable convalescence, the neonate recovered and was discharged in good general condition. A correlation between oral feeding, gut carriage of enterobacteriaceae, fecal endotoxin pool, and platelet counts was observed. The eradication of gut carriage of aerobic gram-negative bacilli was associated with a significant decrease of the intestinal endotoxin pool and paralleled the recovery from thrombocytopenia. Selective decontamination is discussed as a method of possible value for controlling systemic endotoxin-induced symptoms in the critically ill with intestinal endotoxemia.
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3/13. Elevated serum beta-D-glucan level and depressed neutrophil phagocytosis in a heatstroke patient.

    endotoxemia has been reported as a mechanism for the fatal sequela after heatstroke. Subsequent disseminated fungal infection in a heatstroke patient has been also described. Beta-D-glucan, a constituent of the fungal cell wall, is an early diagnostic measure for fungal infection. In a heatstroke case, we examined for the first time levels of serum beta-d-glucan and endotoxin. A 34-year-old man with a body temperature of 43.5 degrees C was admitted in a state of shock. Prior to the development of disseminated intravascular coagulopathy (DIC), a remarkable elevation of serum beta-D-glucan level to 116 pg/mL (normal level<6.0 pg/mL) was revealed on the first day of admission. However, serum endotoxin was not detected when using a method that excluded beta-D-glucan contamination from endotoxin measurement (normal level<1.0 pg/mL). This change of beta-D-glucan level was accompanied by a depressed neutrophil function, especially in phagocytosis of 34% (normal range 70-90%) but not in bacterocidal function (81% versus a normal range of 70-100%). After intensive care including continuous hemodiafiltration, the patient regained consciousness but remained ataxic due to cerebellar infarction, which might have resulted from DIC, and subsequent bilateral fungal oculitis were revealed 45 days after admission. This case report demonstrates the elevation of serum beta-D-glucan but normal endotoxin levels after heatstroke, which may prompt further study to re-examine the serum levels of endotoxin in such catastrophic insults.
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4/13. disseminated intravascular coagulation in an ambulatory young woman.

    We are reporting the case of an ambulatory young woman with a 10-year history of recurrent venous thrombosis who presented to us with diffuse intravascular coagulation (DIC). After excluding the recognized causes of DIC, we examined the possibility that her clinically quiescent ulcerative colitis might be the underlying stimulus. We documented sepsis-range endotoxemia in this patient at a time when she was afebrile and had a normal c-reactive protein level. in vitro her serum upregulated tissue factor in cultured endothelial cells. We postulate that she had become tolerant to the systemic effects of endotoxin leaking from her inflamed colon but that the endotoxin stimulated her endothelium and/or monocytes to produce tissue factor that made her intensely hypercoagulable. Her prothrombotic state may have been compounded by the fact that she was heterozygous for prothrombin G20210A and that her plasma clotting time demonstrated resistance to activated protein c.
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5/13. hypotension and disseminated intravascular coagulation following intralesional bacillus Calmette-Guerin therapy for locally metastatic melanoma.

    Four patients developed serious hypotension and signs of disseminated intravascular coagulation shortly after a second round of Tice bacillus Calmette-Guerin (BCG) injections into locally recurrent cutaneous melanoma satellite nodules. Each of these patients survived following intensive therapy with isoniazid, pyridoxine, steroids, pressors, antibiotics, and cardio-renal support including, in one case, three acute hemodialyses. Plasma specimens from two of the four patients caused gelation of lysate from the amebocytes of Limulus polyphemus, indicating the presence of endotoxin or an endotoxin-like substance. in vitro studies on the BCG preparations led us to conclude that this endotoxin activity in the plasma is not the result of direct injection of endotoxin with the BCG preparation, but rather from release of endotoxin from endogenous sources, such as the intestinal tract during a period of relative hypotension following an allergic reaction. Prior immunity appeared to be the consistent factor in the toxic reactions reported herein. Finally, we present recommendations for serial monitoring of these patients and discuss the use of an alternative agent for intralesional therapy.
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6/13. The proteinase inhibitor complexes (antithrombin iii-thrombin, alpha 2antiplasmin-plasmin and alpha 1antitrypsin-elastase) in septicemia, fulminant hepatic failure and cardiac shock: value for diagnosis and therapy control in DIC/F syndrome.

    Thrombin (Thr), plasmin (Pl) and elastase (ELP) are serine proteinases which are quickly inactivated by their specific inhibitors (AT III, alpha 2AP, alpha 1AT), if intravascular activation of coagulation and fibrinolytic system or if release from PMN granulocytes by different stimuli (F.I., endotoxin, activated factor xii, a.o.) occurs. The immunological determination of the developing proteinase inhibitor complexes (PIC) AT III-Thr, alpha 2AP-Pl and alpha 1AT-ELP gives information as to whether intravascular coagulation, hyperfibrinolysis or unspecific proteolysis induced by elastase have taken place. Despite the high antiprotease activity in the plasma the a.m. serine proteinases may exert their proteolytic activity towards their specific substrates in vivo. In infectious diseases, fulminant hepatic failure and cardiac shock a complex consumption of coagulation factors and inhibitors may cause severe coagulation defects, microcirculatory disturbances and bleeding tendency. The PICs behaviour was determined in more than 80 patients with infectious diseases, in 5 patients with fulminant hepatic failure (FHF) and 7 patients with cardiac shock. Only in infectious diseases, mainly in septic complications, and septic complications during FHF and cardiac shock, are alpha 1AT-ELP levels found to be highly elevated. After cardiac shock, in FHF and in infectious diseases coagulation and fibrinolysis may additionally be activated. In this case AT III-Thr and alpha 2AP-Pl complexes could be detected in the patients plasma. This indicates that intravascular coagulation and hyperfibrinolysis has additionally taken place. To prevent bleeding complications a replacement therapy with plasma derivatives (AT III, plasminogen concentrate, PPSB and FFP) has been successfully performed in several patients with septic complications and in the 5 patients with FHF and the 7 patients with cardiac shock. No bleeding complication occurred, and the haemostatic balance could be maintained in the treated patients. AT III replacement therapy is necessary to stop DIC, PPSB improves severe coagulation defects, only FFP may additionally provide alpha 1AT, alpha 2AP and factor v. In acute renal failure sometimes plasminogen replacement is necessary to maintain a normal activity of the fibrinolytic system. The complex consumption of coagulation proteins in infectious diseases, FHF and cardiac shock cannot successfully be treated with an anticoagulant such as heparin alone.
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7/13. Non-septic endotoxemia in cirrhotic patients.

    We have found that endotoxemia detected by conventional LCT (limulus colorimetric test) in patients with liver diseases could not be detected by endotoxin-specific LCT at all, and proposed that this beta-glucan like activity (BGLA) should be termed as non-septic endotoxemia, distinguishing it from septic endotoxemia seen in gram-negative sepsis. In this study, we investigated non-septic endotoxemia through the clinical course of 8 cirrhotic patients. Non-septic endotoxemia appeared at the onset of DIC but tended to decline in level in the late terminal stage. This phenomenon cannot be consistent with the "spillover" theory which explains the mechanism of endotoxemia without sepsis in liver disease. We think it is an urgent problem to elucidate the nature of BGLA in liver disease, without recourse to the "spillover" theory.
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8/13. A case of liver cirrhosis complicated with endotoxemia and disseminated intravascular coagulation: a case report.

    A 59-year-old female was admitted to our hospital because of massive ascites and increasing jaundice, suggesting a severe decompensated state of liver cirrhosis. On the third hospital day, she was diagnosed as disseminated intravascular coagulation (DIC) from a coagulofibrinolytic study and developed renal failure. Continuous drip infusion of gabexate mesilate, a synthetic inhibitor of serine-protease, was found to be successful in managing DIC, followed by the restoration of renal function. During the clinical course, blood endotoxin, assayed by the chromogenic method, was initially 11 pg/ml and increased, in accordance with the elevation of serum FDP, to a level of 110 pg/ml when renal failure occurred. A proportional relationship was observed between changes in blood endotoxin and serum FDP throughout the course. This finding may be an important clue in studying the mechanism of DIC and non-septic endotoxemia both developing in liver cirrhosis.
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9/13. plasmapheresis and haemodialysis in a case of septic cholangitis complicated by hepatic and renal failure. Case report.

    plasmapheresis was used as a complement to conventional therapy in a patient with multiorgan failure and disseminated intravascular coagulation (DIC) following biliary obstruction and septic cholangitis. The patient's remarkable improvement after plasmapheresis suggests a beneficial influence on the pathophysiologic mechanisms. plasmapheresis is concluded to inhibit DIC and eliminate endotoxins.
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10/13. disseminated intravascular coagulation and hypotension after intravasation of barium.

    Prolonged hypotension and disseminated intravascular coagulation were seen in a patient after intravasation of barium sulfate contrast medium during a barium enema examination. High endotoxin levels were measured in the contrast material. in vitro, this material induced generation of bradykinin. The clinical features observed may be explained by contact activation of the Hageman factor-dependent pathways caused by the contrast material and/or by circulating endotoxins. Treatment of this rare but severe complication occurring during a barium enema procedure should be directed against the endotoxic shock.
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keywords = endotoxin
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