Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Meningococcal sepsis is a good model to study the dynamic response of cytokines and other soluble factors in vivo in the early stages of the disease. Levels of soluble CD14, interleukin-6 (IL-6), IL-6 receptor (IL-6R), and C-reactive protein (CRP) have been measured in plasma from 26 children with septic shock (nine of whom had disseminated intravascular coagulation) and from ten control children. All samples were collected at the onset, before treatment, and, when possible, 24 and 48 hours later. At admission, patients had significantly higher levels of IL-6 (p < 0.001) and CRP (p < 0.001), and lower levels of IL-6R (p < 0.005) than normal controls. After 24 hours, there was a significant increase of sCD24 (p < 0.05) and CRP (p < 0.001). Although IL-6 showed a progressive decline since the onset, its levels were always higher than controls. There was an inverse correlation between IL-6 and both IL-6R (p < 0.001) and CRP (p < 0.001), probably due to the later increase of CRP. Nevertheless, sCD14 did not correlate with IL-6 levels. We have confirmed the finding of IL-6 as a sensitive and reliable inflammatory marker in septic shock. Moreover, the ratio IL-6/IL-6R may have a prognostic value, given a putative role of IL-6R in modulating the effects of IL-6 in meningococcal sepsis.
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PMID:Lack of correlation between soluble CD14 and IL-6 in meningococcal septic shock. 955 85

Severe alcoholic liver injury has been relatively rare, but is gradually increasing in Japan. The clinical features and prognostic factors in severe alcoholic liver injury were retrospectively investigated in 105 patients, consisting of 3 with severe alcoholic hepatitis (SAH), 43 with cirrhosis with superimposed alcoholic hepatitis [liver cirrhosis (LC)+alcoholic hepatitis (AH)], 38 with AH, and 21 with alcoholic cirrhosis. Seven of the 105 patients (6.7%, 2 with SAH and 5 with LC+AH) died of hepatic failure. Patients with SAH showed severe hyperbilirubinemia, reduced hepatic biosynthetic capacity, and marked acute inflammatory reactions, and developed multiple organ failure, such as disseminated intravascular coagulation (DIC), renal failure, acute pancreatitis, or pneumonia. Two SAH patients died within 1 month, whereas five with LC+AH died within 77 days during the second episode of AH. In these nonsurvivors, the serum total bilirubin (T.Bil) level was not normalized, and the hepaplastin test (HPT), serum albumin, cholesterol, and platelet count were not markedly improved after the first episode of AH. In the survivors, elevation of AST lasted longer, and the improvement of T.Bil, hepatic biosynthetic capacity, and the platelet count were much less in patients with LC+AH than in those with AH. Multivariate analysis using the Cox proportional hazards model showed serum C-reactive protein (CRP) and DIC as significant independent prognostic factors among SAH, LC+AH, and AH groups. When factors related to multiple organ failure, such as DIC and renal failure, were excluded, T.Bil and CRP were selected as independent prognostic factors. In patients with LC+AH and AH, CRP, and HPT were shown to be significant independent prognostic factors. These results suggest that SAH with multiple organ failure, and another episode of AH in advanced LC with hyperbilirubinemia and reduced hepatic biosynthetic capacity, are indicative of an extremely poor prognosis in chronic alcoholics.
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PMID:Prognostic factors in severe alcoholic liver injury. Nara Liver Study Group. 1023 76

Release of toxins in the organism trigger a cascade of biological and chemical events. The process involves a large number of molecules produced under genetic control in a perfectly regulated chronological order. Certain molecules (TNFx, IL-1, Il-2.) have inflammatory proprieties, generally producing systemic Inflammatory Response Syndrome (SIRS). Other less numerous molecules (IL-4, IL-10) have antiinflammatory actions. Finally, soluble receptors and these cytokines contribute to the decrease in the quantity of active cytokines at the receptor level. Dozens of other molecules, many of which remain to be fully understood, are also found in the blood stream. They can, for example, facilitate white cell adhesion (ICAM, VCAM, selectins.). Some of them (G-CSF. CM-CSF. IL-5) stimulate production of granulocytes, monocytes, eosinophils. More recently, certain peptides, like macrophage inhibiting factor (MIF) and procalcitonin (PCT) have been added to the list of molecules involved in bacterial infections. Coagulation factors are also very rapidly released in response to toxinic aggression triggering disseminated intravascular coagulation. Later, acute-hase inflammation proteins, such as C-reactive protein (CRP), haptoglobin, serum amyloid A, etc. are found in largely increased quantities. All these molecules are potential markers of inflammation. Only a few have however been retained for routine assay due to their fragility and their short-half life or due to analytical difficulties. CRP and PCT can however be used to differentiate viral infections from bacterial infections and are thus routinely used in clinical applications. In the second part of this review, we briefly discuss therapeutic perspectives for severe infections and septic shock. There have been many attempts to neutralize different cytokines but results have been disappointing to date. There are however many possibilities currently under study, particularly neutralization of endotoxins, immunomodulation, use of recombinant C and S proteins, etc.
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PMID:[Inflammatory cascade response to toxin release: therapeutic perspectives]. 1142 20

A 79-year-old man with herpes zoster was referred to our hospital for pain control. He was a survivor of the atomic bombing of Hiroshima, and had a history of cerebral infarction and hypertension. A cervical epidural catheter was placed for continuous analgesic infusion. After 20 days of catheterization, he gradually developed a high fever and confusion, and complained of nausea and headaches. An urgent blood examination revealed a white blood cell count of 15,200 mm-3 and a C-reactive protein of 32.4 mg.dl-1. The catheter was removed and antibiotic therapy was started. Repeated magnetic resonance imaging could not confirm epidural abscess formation. The bacterial culture of the cerebrospinal fluid was negative, but the cultures of the blood, the catheter tip, and the nasal cavity swab were positive for methicillin-resistant Staphylococcus aureus. Although intravenous vancomycin was administered, systemic inflammation persisted. The patient consecutively suffered varied disorders such as acute renal failure, disseminated intravascular coagulation, and gastrointestinal bleeding. Although symptomatic treatment had been prolonging his life, 58 days after the catheter removal, the patient suddenly developed cerebellopontine infarction, which made mechanical ventilation necessary. He remained unconscious until his death 117 days after the catheter removal. We discussed the possible pathogenetic mechanisms of the present case.
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PMID:[The development of methicillin-resistant Staphylococcus aureus sepsis in a patient with herpes zoster during treatment with continuous epidural infusion]. 1192 98

A decrease in light transmittance before clot formation, manifesting as a biphasic waveform (BPW) pattern in coagulation assays, was previously correlated with the onset of disseminated intravascular coagulation (DIC). In this study of 1187 consecutive admissions to the intensive care unit, the degree of this change on admission predicts DIC better than D-dimer measurements. Additionally, the BPW preceded the time of DIC diagnosis by 18 hours, on average, in 56% (203 of 362) of DIC patients. The BPW is due to the rapid formation of a precipitate and coincident turbidity change on recalcification of plasma. The isolated precipitate contains very-low-density lipoprotein (VLDL) and C-reactive protein (CRP). The addition of CRP and Ca(++) to normal plasma also causes the precipitation of VLDL and IDL, but not LDL or HDL. The K(d) of the CRP/VLDL interaction is 340 nM, and the IC(50) for Ca(++) is 5.0 mM. In 15 plasmas with the BPW, CRP was highly elevated (77-398 microg/mL), and the concentration of isolated VLDL ranged from 0.082 to 1.32 mM (cholesterol). The turbidity change on recalcification correlates well with the calculated level of the CRP-VLDL complex. Clinically, the BPW better predicts for DIC than either CRP or triglyceride alone. The complex may have pathophysiological implications because CRP can be detected in the VLDL fraction from sera of patients with the BPW, and the VLDL fraction has enhanced prothrombinase surface activity. The complex has been designated lipoprotein complexed C-reactive protein.
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PMID:Biphasic transmittance waveform in the APTT coagulation assay is due to the formation of a Ca(++)-dependent complex of C-reactive protein with very-low-density lipoprotein and is a novel marker of impending disseminated intravascular coagulation. 1223 65

A 72-year-old man was admitted to the emergency ward in our hospital on July 20, 2001, because of consciousness disturbance, fever, generalized skin eruption, and severe general weakness beginning 7 days previously. Physical examination on admission revealed marked systemic cyanosis, erythema, and purpura. Laboratory findings indicated disseminated intravascular coagulation (DIC) and multiorgan failure (platelet count, 0.9 x 10(4)/micro l; fibrin degradation product, 110 micro g/ml; C-reactive protein, 22.6 mg/dl). Soluble interleukin 2-receptor (sIL-2R) was markedly increased to 14 710 U/ml. Blood gas analysis demonstrated severe metabolic acidosis. He was diagnosed with multiorgan failure due to DIC. Administration of heparin and sodium bicarbonate was started immediately, but respiratory failure was exacerbated and systemic spasm caused by encephalitis was noted. Although he was supported by an artificial ventilator, deterioration of metabolic acidosis occurred, and the blood pressure decreased to less than 60 mm Hg. He died 5.5 h after admission. The serological test showed no positive antibody titers against Orientia tsutsugamushi, Rickettsia japonica, or Rickettsia typhi. However, a specific DNA band derived from R. japonica was detected by the polymerase chain reaction (PCR) method using a primer from a blood clot. Therefore, he was definitively diagnosed as having Japanese spotted fever. The PCR method may be markedly useful for establishing a definitive diagnosis of Japanese spotted fever during the critical stage.
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PMID:Fulminant Japanese spotted fever definitively diagnosed by the polymerase chain reaction method. 1237 93

Surveillance for scrub typhus was conducted in Japan in 1998 using a questionnaire. A total of 462 cases were reported. Scrub typhus occurred in both the fall and spring in the northern part of Honshu (the main island), and in the fall in the central part of Honshu and on the island of Kyushu. The occurrence of the disease varied with age, gender, and activity. Seventy-six percent of the patients were more than 51 years old, and 36% and 16% of the patients were engaged in farm work and forestry, respectively. Fever, rash, and eschar were detected in 98%, 93%, and 97% of the patients, respectively. Elevated levels of C-reactive protein, aspartate transaminase, and alanine transaminase were detected in 96%, 87%, and 77% of the patients, respectively. Disseminated intravascular coagulation developed in 34 cases and had a unique regional distribution. This study shows the status of scrub typhus in Japan in 1998 and provides important information for diagnosis and prevention.
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PMID:Scrub typhus in Japan: epidemiology and clinical features of cases reported in 1998. 1238 41

Several cases of granulomatous phlebitis of small hepatic veins are reported in the literature, though the etiology remains unclear. We experienced a similar case of granulomatous phlebitis involving terminal hepatic venules and this case will be reported in comparison with two previous cases presenting in our laboratory. A 39-year-old-female had a long course of medical treatment for epilepsy. She suffered from acute liver injury after prolonged fever for more than 1 week. Leukocytosis (11,100/ micro L) without eosinophilia, and inflammatory reactions such as C-reactive protein (21.0 mg/dL) were pointed out. She suffered from transient disseminated intravascular coagulation, but these abnormalities recovered with antibiotic and steroid therapy. Liver biopsy revealed granulomatous lesions mainly involving terminal hepatic venules. The possibility of tuberculosis was excluded by a negative Thiel-Nielsen stain and a negative molecular study for bacterial deoxyribonucleic acid of Mycobacteria species. Extrahepatic involvements were not clear clinically. This case and the previous two cases shared granulomatous phlebitis of the intrahepatic small hepatic veins, as well as clinical features suggestive of bacterial infection. Clinicians should be aware of such a rare clinicopathological entity.
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PMID:Granulomatous phlebitis of small hepatic vein. 1242 83

Twenty-eight patients with Japanese spotted fever were clinically investigated. The diagnosis was determined by confirming an increase of specific antibody. All patients were treated with minocycline, and all recovered, excluding one patient with a fulminant course. Fever and exanthema were observed in all patients, and an eschar was pointed out in 20 (71%) patients. The platelet count was 10 x 10(4)/microl or lower in 8 (28%) patients. The fibrin degradation product (FDP)-level was abnormally high, 10 microg/ml or more, in 16 (57%) patients. The creatine kinase (CK) value was high in 14 of 22 patients, suggesting the presence of myositis. The leukocyte count, FDP, C-reactive protein, and soluble interleukin 2 receptor (sIL2-R) levels were significantly higher in severe cases. In the group without concomitant steroid therapy, mean times of 54.7 h and 101.4 h were required to reduce the temperature to 38 degrees C and 37 degrees C or lower, respectively, after the initiation of tetracycline treatment. There were 6 severe cases: 1 with disseminated intravascular coagulation, 2 with multiorgan failure, 1 with acute respiratory distress syndrome, and 2 with meningoencephalitis. These severe cases formed a group that required 6 or more days to initiate therapy after the onset (P < 0.005 vs non-severe group), showing that delay in diagnosis and therapy is the major cause of aggravation. In the 2 patients complicated by multiorgan failure, the sIL2-R level, produced by activated lymphocytes, was 10,000 U/ml or higher, suggesting that an sIL2-R level of more than 10,000 U/ml can be used as a marker of poor prognosis. It may be better that moderate to severe cases are treated with minocycline plus short-term steroid therapy.
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PMID:Clinical study of Japanese spotted fever and its aggravating factors. 1267 13

A 50-year-old woman with a 15-year history of type 2 diabetes mellitus was admitted to our hospital due to high fever and a skin lesion with severe pain, swelling and a sensation of heat in the right thigh. Laboratory examination showed elevated C-reactive protein (CRP), thrombocytopenia, nephrotic syndrome and renal dysfunction. Her blood glucose level had been well controlled. Streptococcus agalactiae was detected in both the skin lesion and blood culture, and pathological examination revealed neutrophil infiltration in the fascia and muscle layer. The patient was diagnosed with necrotizing fasciitis, septic shock and disseminated intravascular coagulation. A combination therapy of antibiotics and surgical debridement resulted in the improvement of symptoms as supported by laboratory findings, and the skin lesion also showed improvement. Although group A streptococcus is well known to be implicated in the pathogenesis of necrotizing fasciitis, only S. agalactiae, belonging to group B streptococcus, was isolated from the tissue and blood cultures in this case. Although this organism is not virulent and rarely causes a necrotizing fasciitis, both the superficial fascial layer and underlying muscle were affected in this case. There have been only a few reports of necrotizing fasciitis due to S. agalactiae in patients with diabetes mellitus. Although the blood glucose level was well controlled in our patient, this disease might be caused by other factors, including diminished sense of touch and pain, abnormality of microcirculation and hypogammaglobulinemia due to nephrotic syndrome.
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PMID:Successful treatment of necrotizing fasciitis associated with diabetic nephropathy. 1275 84


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