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)

A subpopulation of human lymphocytes bearing receptors for the Fe portion of IgG causes lysis of nucleated target cells in the presence of antibody. The reaction is known as antibody-dependent cellular cytotoxicity (ADCC) and the effector cells have been called killer (K) cells. We have measured K cell activity quantitatively in the peripheral blood of cancer patients using 51Cr labeled murine mastocytoma target cells and hyperimmune rabbit antimastocytoma antibody. ADCC was the same in males and females, was not affected by eating, smoking or the presence of infections, but was decreased in those over 65 years, during pregnancy, and in those with cachexia, or severe sepsis associated with nonmalignant diseases. It was normal in those with cancers being treated for cure and in those with benign diseases, but was decreased in those with advanced cancers. Operation did not produce a significant change in those who were not immunodepressed; in those who were immunodepressed before operation it caused a significant decrease maximal by the fifth day with recovery by the 15th day. Radiotherapy caused a decrease in K cell activity, maximal at 4 weeks, that persisted for 12 weeks with recovery after that time in those who did not have residual tumor. The values did not return to normal in those who had persistent tumor or distant metastases.
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PMID:Effect of operation and radiotherapy on antibody-dependent cellular cytotoxicity. 31 42

Subphrenic abscess is reported in two patients, one previously operated on for pancreatic carcinoma and the other for clear cell carcinoma of the left kidney. The subphrenic abscess presented with cachexia and low grade fever six months and one year after surgery. Metastatic carcinoma was erroneously diagnosed in both patients. Despite massive antibiotic treatment, both patients succumbed to sepsis. Because of the inherent diagnostic challenge, delineation of a subphrenic abscess in cancer patients without clear-cut evidence of a metastatic spread is crucial.
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PMID:Subphrenic abscess simulating metastatic carcinoma. 47 41

Infantile transmural ulcerative enteritis is a disorder of early infancy characterized by feeding difficulties, intermittent and progressive diarrhea, cachexia, anemia, abdominal distention, and small-bowel dilation which may progress to intestinal obstruction. The pathologic process, of unknown etiology, involves a transmural enteritis with deep undermining mucosal ulceration, not unlike that seen in Crohn's disease, except that granulomas are usually not present. The early stages of the diseases may be reversible if the bowel is simply placed at rest by use of intravenous nutrition. In the later stages of the illness, there is progressive mechanical and functional intestinal obstruction due to inflammatory constriction of the distal small bowel and lack of effective peristalsis through the inflammed segments. The terminal stages are characterized by marked abdominal distention, complete obstruction, septicemia, and death. It is during the period of abdominal distention due to progressive intestinal obstruction that surgical intervention is of benefit. A cutaneous enterostomy proximal to the involved segments of small intestine serves to decompress the bowel, to minimize bacteremia, and to allow the distal inflamed intestine to heal. Total intravenous nutrition is mandatory for a period of several weeks until there is healing of the distal small bowel and closure of the enterostomy. In all surviving infants, bowel function has returned to normal and there have been no long-term sequelae or recurrences.
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PMID:Surgical management of infantile ulcerative enteritis. 80 75

Intralipid was used as the main source of calories in the long-term therapy of a patient with severe nutritional failure and cachexia. The treatment was tolerated well for 64 days. The patient died of sepsis after a second therapeutic course which lasted 16 days adn was preceded by an impairment in liver function apparently related to starvation. At autopsy, free fat droplets and extreme foamy swelling of the cytoplasm of the reticuloendothelial cells were found in all examined organs. These findings constitute an unusual example of iatrogenic lipidosis. It is suggested that caution be exerted in the administration of Intralipid to patients with impaired liver function and that serum lipids be maintained regularly during therapy.
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PMID:Latrogenic lipidosis following prolonged intravenous hyperalimentation. 81 19

A case of Hodgkin's disease confined to the spleen is described. A picture of sepsis with rapidly progessive cachexia was present from the outset. Necrosy revealed no gross evidence of the disease and diagnosis was solely dependent on the histological evidence.
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PMID:[On a case of exlusively splenic Hodgkin's disease, with histological detection alone]. 108 22

The clinical outcome of 61 patients with renal amyloidosis treated with chronic dialysis was reviewed. Eighteen patients, 4 with primary or AL amyloidosis and 14 with reactive or AA amyloidosis, died within one month from starting treatment. The other 43 patients were treated with dialysis for 3 to 199 months and are the object of this study. Sixteen patients had AL amyloidosis and 27 had AA amyloidosis. Thirty-five patients were treated with hemodialysis (HD) for a mean period of 40 +/- 47 months and 8 were treated with continuous ambulatory peritoneal dialysis (CAPD) for 20 +/- 15 months. Patient survival rate at 1 and 5 years was 68% and 30% respectively. There was no difference in survival rate between patients treated with HD and those treated with CAPD, while patients younger than 45 had a better 5-year survival rate. Twenty four (60%) patients achieved a satisfactory rehabilitation with dialysis. At the last follow-up, 15 patients (14 on HD, 1 on CAPD) were alive 61 +/- 58 months after starting dialysis. Twenty-eight patients died after 30 +/- 20 months. The main causes of death were: cardiovascular accident (11), stroke (3), sepsis (5) and cachexia (5). The most important extra-renal complications of amyloidosis were related to cardiovascular involvement (heart failures, arrhythmias, hypotension) and gastrointestinal involvement (malabsorption). Intra-dialytic hypotension in patients on HD and peritonitis in patients on CAPD were the main problems related to dialytic procedure. his study confirms that life expectancy and the quality of life of dialysis patients with systemic amyloidosis are poorer than those of general dialysis population.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic dialysis in patients with systemic amyloidosis: the experience in northern Italy. 151 84

Among 625 patients with squamous cell carcinoma and 134 patients with adenocarcinoma of the esophagus and cardia, a one stage resection was performed upon 375 patients of the squamous carcinoma group (excluding pharyngolaryngoesophagectomy) and 92 patients in the adenocarcinoma group. The patients formed the basis of the current analysis. Male to female ratio was 7:1 for those with squamous carcinoma compared with 3.6:1.0 for those with adenocarcinoma (p = 0.037). Most squamous carcinomas were located in the middle one-third (56.3 percent) and lower one-third (33.0 percent) of the esophagus. Adenocarcinomas were predominantly found at the cardia (91.3 percent) and lower one-third (6.5 percent). Postoperatively, respiratory complications occurred in 34.4 percent of patients in the group with squamous carcinoma and in 19.6 percent of patients in the group with adenocarcinoma (p = 0.01). Cardiac complications occurred in 28.3 percent of patients in the group with squamous carcinoma and in 16.3 percent of patients in the group with adenocarcinoma (p = 0.03). Anastomotic leaks were uncommon for both groups (4.3 and 5.4 percent, respectively). Anastomotic recurrence occurred in 6.1 and 7.6 percent of patients, respectively. Respiratory complications, malignant cachexia and sepsis accounted for most of the deaths in the hospital. The 30 day mortality rates for patients with squamous carcinoma and adenocarcinoma were comparable (4.8 and 6.5 percent, respectively) (p = 0.33). After 30 days, mortality rates differed significantly (11.7 and 3.3 percent, respectively) (p = 0.026). The overall hospital mortality rates, however, were comparable (16.5 and 9.8 percent, respectively) (p = 0.14). The overall five year survival rate for both groups was 15 percent. For patients with squamous carcinomas, the five year survival rate after curative resection was 31 percent compared with 5 percent for palliative resection. For patients with adenocarcinomas, the respective five year survival rates were 35 and zero percent. It was concluded that the two types of tumor differ significantly in the incidence of postoperative morbidity, but mortality and the long term survival rates were similar.
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PMID:A comparison of outcome after resection for squamous cell carcinomas and adenocarcinomas of the esophagus and cardia. 163 32

The cytokine TNF mediates many of the pathologic signs of cachexia, inflammation, and sepsis. The current work describes the regulation of TNF in human myelomonocytic cell lines after PMA stimulation. The cell lines exhibit a low level of constitutive TNF mRNA expression. Within 2 to 4 h of PMA exposure, steady state levels of TNF mRNA are markedly elevated in all myelomonocytic cell lines studied. This rise is due to increased mRNA stability, which increased by almost twofold, and to an overall increase in transcription, which rises by more than sixfold. At the level of the genomic TNF gene, a DNase I hypersensitive site is detected within the TNF promoter between -200 to -100 bp relative to the transcription initiation site. Although absent in nonexpressing erythroleukemia cell lines, the DNase I site is present in uninduced myelomonocytic cell lines and is not changed after PMA induction. The PMA induction of c-fos mRNA correlated well with TNF gene induction; expression of genes encoding other proteins in the AP-1 complex (junB and junD) were also induced by PMA. The nuclear extracts from resting and induced ML-1 cells contain proteins binding specifically to the AP-1, AP-2, and NF kappa B sequence located within the TNF promoter. PMA induction increases the level of a number of specific binding complexes relative to the resting cells. The regulatory mechanisms of the human and murine TNF genes are discussed.
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PMID:Tumor necrosis factor-alpha mRNA accumulation in human myelomonocytic cell lines. Role of transcriptional regulation by DNA sequence motifs and mRNA stabilization. 190 40

It is currently hypothesized that the mechanisms of cancer cachexia involve the host's production of inflammatory cytokines, which in turn orchestrate a series of complex interrelated steps that ultimately lead to a chronic state of wasting, malnourishment, and death (see Fig. 1). The metabolic changes seen in the tumor-bearing host are similar, but not identical, to those seen in sepsis and inflammation and appear to result from a generalized response of the host to the stimulus of invasion--the tumor. Although there are likely to be several humoral factors, of either host or tumor origin (see Fig. 1), involved in cancer cachexia, recombinant DNA methodology has provided sufficient amounts of only a few cytokines to enable careful investigation of their cachectic potential. TNF/cachectin has been most extensively studied and appears to play a clear role, because administration of low-dose continuous or escalating doses simulates changes associated with cancer cachexia. In addition, these cachectic changes have been blocked by a specific antisera. IL-1, IL-6, and interferon-gamma all have potential as mediators of cancer cachexia and more work is clearly indicated. It is possible that, given our current understanding of the mechanisms of cancer cachexia, it can be theorized that TNF, which causes many of the manifestations of cancer cachexia, and IL-1 are released by macrophages in response to tumor (see Fig. 1). Interferon-gamma appears to potentiate these effects and may also be necessary for the complete syndrome of cancer cachexia. IL-6 probably is released as another mediator, principally mediating the acute phase response seen in cancer cachexia. Other factors are certain to be involved. Further study into the mechanisms and possible treatment of cancer cachexia is needed, because a large proportion of cancer patients who are incurable by current therapies continue to suffer from this lethal wasting diathesis. Furthermore, specific strategies to reverse the cachectic changes associated with cancer will likely improve antitumor treatment.
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PMID:Mechanisms of cancer cachexia. 202 66

Cachexia in tumour-bearing patients involves loss of skeletal muscle proteins. In order to elucidate the mechanisms underlying this phenomenon, we tested the hypothesis of the presence of a circulating proteolytic factor (possibly interleukin-1, acting through an increased PGE2 release) in the plasma of cancer patients, because such a mechanism has been demonstrated in patients with sepsis or trauma and in animals with bacteraemia or viraemia. The effect of plasma from 13 malnourished cancer patients and 14 controls on PGE2 release and protein degradation (assessed as Tyr release) in rat diaphragm in vitro was evaluated; human recombinant interleukin-1 alpha (IL-1) was used for comparison. IL-1 increased PGE2 release (+44% at 5 U/ml), but did not greatly affect proteolysis. On the contrary, human plasma (125 microliters/ml) from both control and tumour-bearing individuals did not affect PGE2 release significantly, but greatly reduced Tyr release. The decrease in Tyr release by plasma was dose-dependent. In conclusion, our data indicate that, at variance with what was demonstrated in patients with trauma or sepsis, loss of skeletal muscle proteins in cancer patients is not mediated by a circulating factor. In addition, evidence is provided of dissociation between PGE2 and Tyr release and of lack of proteolytic activity for IL-1.
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PMID:Effect of plasma from cancer patients on rat skeletal muscle protein degradation and PGE2 release in vitro. 233 Mar 45


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