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)

The natural history of hypertrophic obstructive cardiomyopathy (HOCM) is usually characterized by development of mitral insufficiency, congestive heart failure (CHF) and sudden death. In patients (pts) belonging to at least clinical class III (NYHA) after failed medical therapy (beta-blocking agents and calcium-antagonists) surgery should be considered (by means of transaortic subvalvular myectomy). The history and development of different surgical techniques and procedures has been described in detail since 1958, when Cleland performed the first transaortic subvalvular myotomy. Our surgical series (1963-May 31, 1986) consists of 212 pts (mean age 40 years, range 6-73 years) with typical and atypical HOCM. The total hospital mortality rate was 6.6% (n = 14), which was reduced to 3.8% (n = 6), if only transaortic subvalvular myectomy (TSM) was performed (n = 160). In the group of 52 pts with additional surgical procedures the mortality rate was 15.4% (n = 8). The main problems occurred in pts with additional mitral valve replacement (MVR) (n = 15, three deaths). The rate of HOCM-related complications (secondary VSD, total AV-block, cerebral embolism, intraoperative re-myectomy) and those related to surgery (bleeding, pulmonary embolism, wound dehiscence, septicemia) was low. Therefore TSM for HOCM is a low-risk surgical procedure with a good long-term prognosis. However, in pts with a need for additional surgical procedures, the risk is considerably increased. Subjective impression of the pts and hemodynamic data indicate a clear clinical improvement postoperatively. Concerning long-term survival and reduction of the sudden death rate, our data do not allow a final judgement at the moment.
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PMID:Techniques and complications of transaortic subvalvular myectomy in patients with hypertrophic obstructive cardiomyopathy (HOCM). 343 68

Two cases of coexisting septic and crystalline joint disease are reported. In one patient polyarticular septic arthritis occurred simultaneously with gout and pseudogout. In a second patient septic arthritis preceded the appearance of calcium pyrophosphate dihydrate (CPPD) crystals in the joint fluid, supporting an earlier postulate that lysosomal enzymes released during sepsis lead to shedding of crystals from cartilage and synovium into the joint space. This sequence was demonstrated in a rat air pouch model of synovium, in which CPPD crystals embedded in facsimile synovial tissue were released after injection of pyogenic bacteria. Coexisting septic arthritis should always be considered when crystals are identified in inflamed joints, particularly in elderly patients with concurrent infections.
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PMID:Crystal shedding in septic arthritis: case reports and in vivo evidence in an animal model. 346 9

Eleven patients with Hodgkin's disease refractory to chemotherapy were treated with six cycles of intermediate-dose methotrexate with calcium leucovorin rescue, followed by cyclophosphamide, doxorubicin, vincristine, and prednisone (MTX-CHOP). Three other patients were treated with a similar program of treatment minus doxorubicin (MTX-COP). The overall response rate was 57%, with four (29%) patients achieving a complete response and four patients achieving a partial response. None of the three patients treated with MTX-COP had a complete remission (CR); thus the complete remission rate with MTX-CHOP was somewhat higher (36%). Only one of the CR's is in continuous complete remission and free of disease at 99+ months. One patient died of overwhelming sepsis and pancytopenia during treatment. Hematologic toxicity in the other patients was acceptable. The overall median survival was 18 months. The search for an effective treatment program for this group of patients remains a major challenge.
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PMID:Salvage chemotherapy for advanced Hodgkin's disease. 349 84

Platelet consumption is a prominent feature of disseminated intravascular coagulation. We investigated whether monocyte procoagulant activity (PCA) might play a role in platelet consumption associated with gram-negative septicemia. Human mononuclear cells exposed in vitro to lipopolysaccharide demonstrated parallel dose-dependent increases in PCA and ability to induce platelet aggregation. Induction of platelet aggregation required the generation of thrombin dependent on coagulation Factors VII, X, and II, and calcium. This is consistent with monocyte tissue factor initiating thrombin generation. A specific monoclonal antimonocyte antibody was used to identify monocytes via indirect immunofluorescence, and demonstrated that all monocytes were included in platelet aggregates. Mononuclear cells that did not express PCA did not induce platelet aggregation and monocytes were not surrounded by platelet clumps. These data suggest that monocytes induced to express tissue factor on their surface may be important mediators of endotoxin-induced platelet, as well as fibrinogen, consumption.
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PMID:Human platelet aggregation is initiated by peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide in vitro. 353 97

Rats were treated with Escherichia coli endotoxin (ET) either acutely or chronically or rendered septic by cecal ligation and puncture. At 6 h after ET injection, at various intervals of continuous ET infusion, and at 17-18 h after the onset of peritonitis, animals were killed and hepatocytes were isolated. Cytosolic [Ca2+] ([Ca2+]c) was measured by quin 2 during the resting state and after stimulation with epinephrine and vasopressin. Basal and epinephrine-, vasopressin- and glucagon-stimulated glycogen phosphorylase activity were also determined. In hepatocytes from acutely ET-treated rats, resting levels of [Ca2+]c were decreased 46% from 245.8 +/- 11.0 to 131.0 +/- 8.5 nM (n = 4-6, P less than 0.05). In septic rats a 39.5% decrease was noted [i.e., from 154.0 +/- 17.7 (n = 4, sham) to 93.3 +/- 91 nM (n = 5, septic, P less than 0.05)]. These decreased [Ca2+]c levels were associated with changes of glycogen phosphorylase activity in a manner suggesting a cause and effect relationship; e.g., acute ET treatment resulted in greater than 80% depression of phosphorylase a activity, whereas sepsis induced a 58% decrease in the activity of this enzyme. In ET-infused rats the resting level of [Ca2+]c and its response to hormonal stimulation were not different from hepatocytes of saline-infused rats, although glycogen phosphorylase activity was less responsive to these hormones. The effect on the enzyme's response to Ca2+-mobilizing hormones was more marked than to glucagon. This is consistent with the concept that information flow in the Ca2+-messenger system is a site of metabolic lesions produced by endotoxicosis and sepsis.
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PMID:Rat liver free cytosolic Ca2+ and glycogen phosphorylase in endotoxicosis and sepsis. 353 41

Hypocalcemia has been documented in critically ill patients, including those with sepsis and shock. However, its incidence and significance in bacteremic patients without shock has not been established. In the present study the presence of hypocalcemia was evaluated in a group of 67 consecutive bacteremic patients, as compared with 64 infected but nonbacteremic patients. After correction of serum calcium level for serum protein, 25 of the bacteremic patients (37.3%) had "corrected" hypocalcemia (less than 8.5 mg/dL [2.12 mmol/L]), compared with only three in the nonbacteremic group (4.5%). The incidence and magnitude of hypocalcemia in gram-positive and gram-negative infections was similar. In hypocalcemic patients, the "corrected" calcium level was found to be inversely correlated with day of disease and attained a nadir on day 6 to 8 of bacteremia. This nadir was significantly lower in male than in female subjects. Hypocalcemic patients had a significantly higher maximal temperature than normocalcemic ones, but hypocalcemia was unrelated to serum levels of albumin, transaminase, and creatinine.
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PMID:Bacteremic hypocalcemia. A comparison between the calcium levels of bacteremic and nonbacteremic patients with infection. 354 15

To learn about the pathogenesis of sepsis-associated hypocalcemia, we measured serum ionized calcium concentrations in 60 critically ill patients with bacterial sepsis; 12 (20%) had hypocalcemia. The mortality rate in the hypocalcemic patients with sepsis (50%) was higher than that in the normocalcemic patients with sepsis (29%). Only patients with gram-negative sepsis became hypocalcemic, and hypocalcemia contributed to hypotension in 7 of the 12 hypocalcemic patients. Serum calcium concentrations returned to normal in each of those patients with sepsis who survived. Hypocalcemia during sepsis occurred in previously normocalcemic patients and was multifactorial in origin, resulting from acquired parathyroid gland insufficiency, renal 1 alpha-hydroxylase insufficiency, vitamin D deficiency, and acquired calcitriol resistance. We conclude that the hypocalcemia of sepsis is associated with a high mortality rate and usually occurs in previously normocalcemic patients who acquire a defect in the parathyroid-vitamin D axis.
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PMID:The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone-vitamin D axis. 359 47

A synthesis of the postulated sequence of events for development of the inappropriate response of the myocardium to a demand for increased cardiac index is schematically represented in Fig. 10. In sepsis, bacteremia and/or the release of endotoxin activate the macrophages which release a spectrum of mediators. Some of these mediators (and possibly also endotoxin itself) have a negative influence on myocardial contractile function either directly and/or through altering cellular calcium flux. This results in impaired myocardial function manifested initially by decreased stroke volume. Subsequently, stroke volume will be either partially or completely restored to normal through the action of circulating catecholamines, the concentration of which is markedly elevated due to the presence of endotoxin and/or macrophage-produced mediators. Endotoxin and/or these mediators also act on the SA node increasing its sensitivity to beta-adrenergic stimulation. This will result in elevated heart rates. The latter, combined with the restored stroke volume, will yield an increased cardiac index which is the hallmark of the hyperdynamic phase of sepsis. In the cecal ligation and puncture model of sepsis, where cardiac index is maintained at the original level, the partially restored stroke volume and the elevated heart rate will combine to maintain cardiac index. Although this mechanism of increasing cardiac index through tachycardia is not energy efficient, the myocardium is able to cope with these changes and also to maintain its high energy phosphate concentrations, since the utilization of the three major myocardial substrates (fatty acids, lactate and glucose) is not affected by sepsis. Although this putative sequence of events is consistent with the observed experimental findings, further work is needed to substantiate its applicability to the etiology of myocardial dysfunction in man during sepsis.
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PMID:Myocardial dysfunction in sepsis. 361 52

Life-threatening human sepsis is often treated using bolus intravenous aminoglycoside injections with transient deafness as a reported side effect. Young adult cats were given various high dosages of gentamicin in bolus injections (1 ml in 30 s). Scala vestibuli calcium and gentamicin, blood gentamicin and compound action potentials of the VIII nerve were measured shortly after the injections and 45 min later. An obvious relationship could be demonstrated between levels of gentamicin, decreased calcium content and acoustic thresholds elevation. Even after a high dose of 175 mg/kg that abolished action potentials at t = 2 min, recovery invariably occurred. It is believed that the reported transient hearing loss in humans may be partly attributable to a temporary blockage of calcium by gentamicin.
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PMID:Perilymphatic calcium and VIII nerve action potentials during gentamicin bolus i.v. injections. A preliminary study. 361 67

A patient with septic arthritis of the wrists was noted to have concurrent calcium pyrophosphate crystals in synovial fluid aspirated from both joints. These were present in unusually large numbers and were associated with destructive changes of the joints. It seemed likely that the complete dissolution of calcified cartilage accounted for the liberation of such numerous crystals. Previous reports of pseudogout associated with septic arthritis have noted the presence of abundant calcium pyrophosphate crystals in synovial fluid. It is suggested that this feature should always raise the possibility of concurrent sepsis.
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PMID:Diagnosis of pseudogout and septic arthritis. 366 64


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