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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A lethal case of septicemia caused by Yershia enterocolitica serotype 3 is described. A 59-year-old male, previously healthy, presented with 6 weeks of fever, abdominal pains and gradual prostration ending in overhelming septicemia and death before a conclusive diagnosis was established. Necropsy showed cirrhosis, haemochromatosis and numerous abscesses in the liver.
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PMID:Fulminant septicemia caused by Yersinia enterocolitica. 90 87

Vibrio vulnificus is an extremely invasive gram-negative bacillus that causes bacteremia and shock. It should be suspected in any patient who is immunocompromised or has liver disease or hemochromatosis. Reduced gastric acidity may also increase the risk of infection if a patient presents with a history of ingesting raw shellfish (especially oysters) or trauma in brackish waters and skin lesions. Patients most commonly present with one of three clinical syndromes: primary septicemia, wound infection, or gastroenteritis. Treatment includes aggressive wound debridement, antibiotic therapy, and supportive care. Rapidly diagnosing and promptly initiating therapy are critical because V vulnificus infection is rapidly progressive and mortality approaches 100% if septic shock occurs.
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PMID:Vibrio vulnificus. Hazard on the half shell. 177 90

Hemochromatosis, or primary iron overload, is a variably expressed genetic metabolic disorder greatly modified by sex, age, diet, and alcohol consumption. Although a diagnosis has been made at the bedside by careful documentation of the slow resolution of subcutaneous iron pigment, clinical diagnosis is frequently overlooked, and even autopsy may fail to reveal hemochromatosis as the cause for cirrhosis. Genetic linkage studies have confirmed the extremely high prevalence of this disorder. Untreated patients may succumb to sepsis caused by organisms such as Vibrio vulnificus, Yersinia species, and others whose virulence is altered by iron availability.
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PMID:Hemochromatosis and infection: alcohol and iron, oysters and sepsis. 248 33

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

We present a patient with idiopathic liver hemochromatosis and mild secondary cirrhosis complicated by Yersinia sepsis and miliary liver abscesses proven by echography and CT.
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PMID:Ultrasound and CT of multifocal liver abscesses caused by Yersinia enterocolitica. 267 27

A fatal case of Yersinia enterocolitica septicemia which was complicated by unique hemosiderosis is reported. On admission, the patient had diabetes and showed unusual hyperferritinemia. Postmortem examination revealed that the liver was studied with abscesses, and Yersinia antigen was expressed in foamy macrophages within these abscesses. Moreover, the cadaver showed generalized hemosiderin deposition, which was mainly observed in the liver and, to lesser degrees, in the pancreas, spleen, lymph nodes, brain, thyroid and kidneys. Since there was no apparent cause of the hyperferritinemia and generalized hemosiderosis, consideration was given to possible primary hemochromatosis. However, no liver or pancreatic fibrosis was demonstrated. Kupffer cells were also loaded with hemosiderin, and therefore it was considered that these cells had lost their ability to phagocytize the microorganism adequately, leading to major liver involvement. Interestingly, hemosiderin deposits in the kidneys were mostly present in glomerular epithelial cells. To our knowledge, this unique presentation has not been previously described in humans.
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PMID:Fatal Yersinia enterocolitica septicemia complicated by unique hemosiderosis. A case report. 306 9

A case of fatal septicemia caused by Vibrio vulnificus and Clostridium bifermentans in a patient with subclinical liver disease is described. The patient appeared to recover from the infection initially after antibiotic therapy but finally succumbed to rapidly developing hepatic failure. Postmortem examination revealed hemochromatosis. The pathogenesis of the polymicrobial septicemia and hepatic failure is discussed in the light of the published literature.
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PMID:Acute hepatic failure precipitated in a patient with subclinical liver disease by vibrionic and clostridial septicemia. 321 97

A 67-year-old man with Escherichia coli bacteremia and meningitis was found to have hemochromatosis. To my knowledge this is the first documented case of E coli meningitis occurring in the setting of hemochromatosis. The case raises issues regarding the role of chronic liver disease in the pathogenesis of gram-negative sepsis and the impact of iron loading on host immunocompetence and bacterial virulence.
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PMID:Escherichia coli bacteremia, meningitis, and hemochromatosis. 389 40

Acute abdomen, irreversible shock and sudden death are a typical although infrequent complication in patients with hemochromatosis. The author presents a further case of this syndrome and discusses the two leading pathogenetic interpretations described in the literature: sudden release of ferritin, and endotoxin shock. Clinical and post-mortem findings from this patient and a review of 19 cases from the literature suggest that most patients with this syndrome die from a primary bacterial peritonitis with gram negative sepsis and endotoxin shock.
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PMID:[Acute abdomen with irreversible shock, a rare but typical complication of hemochromatosis]. 390 80

We analyzed the clinical data and liver histology for iron overload in 74 renal allograft recipients. Twenty of the 74 patients had histological evidence of hemosiderosis. Four patients had hemochromatosis. Of the 2 noninvasive diagnostic tests the serum ferritin level was more reliable than percent saturation of transferrin in predicting the histological diagnosis of hemosiderosis. Of the 20 patients with hemosiderosis 14 died either from liver failure or concomitant sepsis. Female patients and those who received long-term dialysis had higher susceptibility for developing hemosiderosis. Of the 6 patients treated with phlebotomies, the response was good in 4 and incomplete in 2. Hemosiderosis and hemochromatosis should be considered in the differential diagnosis of posttransplant liver disease. Intermittent phlebotomies if carried out early may prevent the progression of hemosiderosis to micronodular cirrhosis.
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PMID:Hemosiderosis and hemochromatosis in renal transplant recipients. Clinical and pathological features, diagnostic correlations, predisposing factors, and treatment. 390 17


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