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Query: UMLS:C0036690 (
sepsis
)
59,461
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Non-O1 Vibrio cholerae produced two distinct colony types, designated as opaque and translucent. NRT36S, a clinical isolate shown to be virulent in volunteers, produced predominantly opaque colonies, but translucent colonies appeared on subculture. Opaque variants were recovered exclusively following exposure to normal human serum or animal passage. A nonreverting translucent mutant of NRT36S, JVB52, was isolated following mutagenesis with the transposon Tn5 IS50L::phoA (TnphoA). Only translucent colonies were produced by a nonpathogenic environmental isolate, A5. Electron microscopic examination of the opaque form of NRT36S revealed thick, electron-dense, fibrous capsules surrounding polycationic
ferritin
-stained cells. The
ferritin
-stained material around translucent NRT36S or A5 was patchy or absent. JVB52 had a thin but contiguous capsular layer. The amount of
ferritin
-stained capsular material correlated with the amount of surface polysaccharide determined by phenol-sulfuric acid assay: opaque NRT36S had approximately three times as much polysaccharide as translucent NRT36S or A5 and four times as much as JVB52. The encapsulated, opaque variant of NRT36S was protected from serum bactericidal activity, while translucent non-O1 V. cholerae was readily killed. The encapsulated form also had increased virulence in mice. Our data provide the first indication that non-O1 V. cholerae strains can have a polysaccharide capsule. This capsule may be important in protecting the organism from host defenses and may contribute to the ability of some non-O1 V. cholerae strains to cause
septicemia
in susceptible hosts.
...
PMID:Non-O1 Vibrio cholerae NRT36S produces a polysaccharide capsule that determines colony morphology, serum resistance, and virulence in mice. 131 6
Six of 14 patients with acute myeloblastic leukemia (AML) complicated reactive histiocytosis during initial remission induction therapy. All six patients had a high fever without signs of infection during initial chemotherapy, and periods of myelosuppression were prolonged. Histiocytes with a mature appearance, some of which phagocyted erythrocytes, thrombocytes or neutrophils, increased in the bone marrow. All of 3 patients tested showed high serum levels of
ferritin
. Two of 3 patients treated with 125 mg/day methylprednisolone achieved complete remission. In the remaining 3 patients, one patient achieved complete remission, but the others died of fungal pneumonia or
sepsis
. Thus, reactive histiocytosis is one of the severe complications in patients with AML undergoing chemotherapy.
...
PMID:[Reactive histiocytosis during initial remission induction therapy for acute myeloblastic leukemia]. 147 93
Serum
ferritin
level was studied in 158 adult patients with different forms and variants of leukemia, and it was found to be elevated in 85.4% of cases. A number of factors influencing
ferritin
concentration in the blood serum have been established: a high degree of serum iron deficiency, leukemic intoxication, infectious complications (pneumonia,
sepsis
, necrosis, etc.), hemolytic syndrome. All these factors should be taken into consideration in evaluating serum
ferritin
levels in acute leukemia patients.
...
PMID:[Factors influencing the serum ferritin level in acute leukemia patients before chemotherapy]. 161 76
The use of recombinant human erythropoietin (rhuEPO) has revolutionized the treatment of renal anemia, but the dose regimens have not been established. We studied the effects of subcutaneous rhuEPO given 4,000U (1 vial) every 5-10 days in 9 patients on continuous ambulatory peritoneal dialysis (CAPD). Ten stable CAPD patients (6 females and 4 males; mean age +/- SEM, 54.4 +/- 5.6 years; mean baseline hemoglobin concentration 7.3 +/- 1.2g/dL) were commenced on s.c. rhuEPO. None of the patients had a history of gastrointestinal bleeding, aluminum overload,
sepsis
nor receiving androgens. Seven patients were receiving 4,000 U rhuEPO weekly, one patient each was receiving 4,000 U every 5 and 10 days (range, 66.7-89.3 U/kg/week). The dose was adjusted every 4 weeks according to response by altering the dose interval. The mean hemoglobin concentration increased from 7.3 +/- 1.2 g/dL to 10.3 +/- 1.1 g/dL over 8 weeks. There was no significant changes in the serum
ferritin
, urea, creatinine and potassium levels. One patient required an increase in antihypertensive therapy. We feel that s.c. rhuEPO 4,000 U given on an intermittent basis is effective in the treatment of anemia in CAPD patients. The administration of a single vial each time is convenient and cost sparing. The gradual rise in hematocrit avoids complications.
...
PMID:Subcutaneous recombinant human erythropoietin in patients on CAPD. 168 Apr 47
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)
...
PMID:Clinical pharmacokinetics of iron preparations. 267 7
During a 19-month period we determined the incidence of bacterial infection among 39 patients treated with desferrioxamine who had end-stage renal disease and were undergoing maintenance hemodialysis. Twenty-three received desferrioxamine because of aluminum-related bone disease, and 16 because of iron overload. A control group of 193 patients on maintenance hemodialysis but without desferrioxamine was used. No difference was found in the incidence of
septicemia
or of all bacterial infections between the patients with aluminum-related bone disease treated with desferrioxamine and the control patients (0.12 vs. 0.12
septicemia
per patient-therapy-year, p greater than 0.05; 0.23 vs. 0.26 bacterial infections per patient-therapy-year, p greater than 0.05). The incidence of
septicemia
in patients treated with desferrioxamine for iron overload, however, was almost three times that in the control patients (0.36 vs. 0.12
septicemia
per patient-therapy-year, p less than 0.01). To assess the effect of iron overload itself, we determined the frequency of bacterial infection in patients on regular hemodialysis who have never received desferrioxamine. These were subdivided into three groups according to serum
ferritin
level which indicated normal or low iron stores (Group I: serum
ferritin
10-330 micrograms/l, n = 125), moderate (Group II: serum
ferritin
331-1000 micrograms/l, n = 49) or more advanced iron overload (Group III: serum
ferritin
1001-2000 micrograms/l, n = 10). Compared to patients with normal or low serum
ferritin
levels (Group I), we found a significantly higher rate of bacterial infection among patients in Group II compared with Group I (0.18 vs. 0.34 infections per patient-therapy-year, p less than 0.05) and Group III compared with Group I (0.18 vs. 0.58 infections per patient-therapy-year, p less than 0.01). These results suggest that treatment with desferrioxamine does not favour the development of
septicemia
or bacterial infection independently of iron overload and that iron overload itself may predispose patients on regular hemodialysis to bacterial infection.
...
PMID:Iron overload, but not treatment with desferrioxamine favours the development of septicemia in patients on maintenance hemodialysis. 345 53
The capsular polysaccharide (CP) of Bacteroides fragilis is an important virulence factor in the formation of experimental intraabdominal abscesses. Incubation of this organism with subinhibitory doses of clindamycin induced morphological changes in the bacteria, including elongation and loss of CP, detected by
ferritin
-labeled antibody to capsule. Pretreatment of bacteria with subinhibitory doses of clindamycin, however, did not affect the ability of live or heat-killed organisms to produce intraabdominal abscesses in a mouse model of intraabdominal
sepsis
. Dose-response experiments with purified CP as well as lipopolysaccharide (LPS) from B. fragilis ATCC strain 23745 mixed with sterile cecal contents as adjuvant revealed that both surface components of the organism were capable of causing abscesses in the mouse model. The dose of LPS required to induce abscesses was five times higher than the required dose of CP. Nevertheless, these studies suggested that B. fragilis LPS is another virulence factor in the formation of intraabdominal abscesses.
...
PMID:Effect of subinhibitory doses of clindamycin on the virulence of Bacteroides fragilis: role of lipopolysaccharide. 371 90
The interrelationships between various components of the non-immune inflammatory response (white cell count, plasma lactoferrin, C-reactive protein,
ferritin
, iron and iron-binding capacity), were studied serially in a variety of inflammatory conditions including acute lobar pneumonia, active pulmonary tuberculosis, rheumatoid arthritis on gold therapy and
sepsis
in the face of marrow hypoplasia induced by chemotherapy. Lactoferrin concentrations paralleled the white count in all groups. They were highest in pneumonia and tuberculosis, mildly elevated in rheumatoid arthritis and markedly decreased in neutropenic
sepsis
. Very high initial lactoferrin concentrations were associated with a poor prognosis in acute pneumonia. C-reactive protein and
ferritin
concentrations remained elevated through the period of study in acute pneumonia and neutropenic
sepsis
, while they gradually normalised over weeks in subjects with tuberculosis or rheumatoid arthritis on therapy. In pneumonia and tuberculosis moderate hypoferraemia and a reduced iron-binding capacity were evident. In contrast, a raised percentage saturation was present in neutropenic
sepsis
, probably related to erythroid marrow suppression. Comparisons between
ferritin
, lactoferrin and C-reactive protein in the various groups supported the concept that
ferritin
behaves in part as an acute phase reactant and that hypoferraemia in inflammation is due to deviation of iron into
ferritin
stores. The suggestion that lactoferrin is responsible for the hypoferraemia and hyperferritinaemia was not supported by the present data. Iron deficiency appeared to limit the hyperferritinaemic response in rheumatoid arthritis, while erythropoietic inhibition by chemotherapy dampened the hypoferraemic response in neutropenic
sepsis
.
...
PMID:The non-immune inflammatory response: serial changes in plasma iron, iron-binding capacity, lactoferrin, ferritin and C-reactive protein. 378 68
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.
...
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.
...
PMID:Hemosiderosis and hemochromatosis in renal transplant recipients. Clinical and pathological features, diagnostic correlations, predisposing factors, and treatment. 390 17
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