Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article has provided an overview of the effects of HIV on renal function. Most transmission of the virus occurs by sexual, blood, and perinatal contact. CD-4 positive cells, especially those that are integral components of the immune system, serve as the reservoir for the reproduction of the virus. The resulting effect is destruction of the immune system with eventual multisystem failure and death. Renal complications arise from several factors, notably the compounding effects of chronic dehydration, malnutrition, infection, and use of nephrotic agents. Acute renal complication can be reversible with prompt assessment, and management directed at maintaining hydration, preventing sepsis, and carefully monitoring drugs. A chronic, irreversible renal disease in HIV is due, in large part, to a syndrome known as AIDS nephropathy, characterized by glomerular sclerosis and nephrotic-type symptoms, which ultimately lead to the need for dialysis. Aids nephropathy is seen most often in intravenous drug users, Haitians, and blacks with HIV. End-stage disease complicates the course of HIV and contributes to early mortality. A small, but significant number of renal patients acquires HIV infection as a result of multiple blood transfusions or through organ donation. Concentrated exposure to blood and body fluid during dialysis necessitates implementation of meticulous infection control procedures to protect both staff and patients. Guidelines by the CDC suggest that universal precautions adequate to prevent the spread of hepatitis B will suffice for HIV as well. HIV infection presents special challenges for those involved with renal management. Prevention and management of renal complication are made possible by thorough understanding of the complex network and interaction of the disease process.
 ...
PMID:Renal system complications in HIV infection. 219 22

Fibronectin is a large-molecular-weight glycoprotein present on most cell surfaces, in extracellular fluids, and in plasma. Both cell-associated and soluble fibronectin are thought to have important roles in the inflammatory response and host defense and may contribute to the maintenance of microvascular integrity during septic episodes. Newborn infants have levels of fibronectin in plasma that are one-third to one-half those found in the healthy adult. In addition, neonates with respiratory distress syndrome, perinatal asphyxia, bacterial sepsis, intrauterine growth retardation, or postnatal malnutrition have a further depression in their plasma levels of fibronectin. The low plasma concentration of fibronectin in newborn infants may contribute to the hypofunction of the neonatal reticuloendothelial system and predispose to the development of sepsis. Rates of synthesis of plasma fibronectin are diminished in the neonate, and an inverse correlation between fibronectin half-life and gestational age exists. The role of fibronectin in treatment or prophylaxis of neonatal sepsis remains to be determined.
 ...
PMID:Role of fibronectin in diseases of newborn infants and children. 219 69

In a prospective study including 60 patients with esophageal carcinoma the nutritional status was evaluated by means of anthropometric, biochemical and immunological data. As a first measure of malnutrition the diminuation of each single parameter was estimated in a 10%-scale, according to this a linear rising number of points given and the sum for all 11 parameters expressed as a score (Gofferje and Fekl). Second the nutritional status was judged by the prognostic nutritional index (Buzby and Mullen). Both score and index were correlated with serious postoperative complications (wound infection, anastomotic leakage, sepsis, organ failure, death). The results show that it was not possible to assess the risk of esophagectomy preoperatively on the ground of nutritional parameters solely. The reason could be that the nutritional status was rather normal in most cases and its risk burden therefore low. In conclusion performing preoperative nutritional therapy routinely seems not to be justified.
 ...
PMID:[Nutritional status in esophageal cancer: assessment and significance for preoperative risk assessment]. 249 40

Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS), a visceral myopathy causing intestinal obstruction in the newborn, is a generally fatal condition, with death being secondary either to sepsis or to malnutrition if long-term intravenous feeding is not provided. A patient with MMIHS is described who has been raised by total parenteral nutrition (TPN) for seven years since her birth. Severe hepatic dysfunction was encountered in early infancy, which gradually cleared after the initiation of milk feeding by mouth, although the milk could not be absorbed because of the high-output jejunostomy. The patient also experienced a bone disease similar to scurvy but caused by copper deficiency at the age of 9 months. The central venous catheter now in situ is the 25th one for the patient. When these catheters were evaluated, the Broviac proved more efficacious than the traditional Silastic for use in long-term TPN. The patient does not yet have normal bowel function and still requires TPN.
 ...
PMID:Successful nutrition management of megacystis-microcolon-intestinal hypoperistalsis syndrome--a case report. 252 Mar 38

Burn injury-induced changes at the neuromuscular junction include muscle weakness and altered response to neuromuscular blocking drugs. Protein malnutrition and sepsis can concomitantly occur with burn trauma. The role of pure malnutrition or sepsis, in the absence of burn injury, in inducing neuromuscular changes was studied in the mouse gastrocnemius muscle. Additionally, cAMP levels in muscle were evaluated to reflect metabolic activity. Sepsis was studied using doses of endotoxin at one-fourth or one-third the dose evoking 50% lethality. Diets of 5% protein and 5% protein + 35% fiber achieved protein and protein/calorie malnutrition, respectively. In each model neuromuscular function was evaluated by maximal tension developed. Pharmacologic responses were measured through effective dose to paralyze active tension by either 50 or 95%. Protein and protein/calorie malnutrition leading to an approximate 8% body weight loss caused a depression of maximal tension developed; this depression in tension was associated with a 10-fold increase in cAMP levels. Effective doses of d-tubocurarine for twitch inhibition during malnutrition were not significantly different from controls. Sepsis at 2 weeks caused an approximate 8% body weight loss, a significant decrease in maximal tension and at least a 3- to 5-fold shift to the right in dose-response curves to d-tubocurarine. In contrast to malnutrition, cAMP levels were significantly decreased (P less than .001) in sepsis to 1/400 of controls. The altered neuromuscular function and pharmacology observed in sepsis are similar to changes observed in burn injury. Protein malnutrition common to these two states may be important in functional but not pharmacological changes at the neuromuscular junction.
 ...
PMID:Intraperitoneal endotoxin but not protein malnutrition shifts d-tubocurarine dose-response curves in mouse gastrocnemius muscle. 254 58

Hypoglycemia associated with renal failure is more common than generally thought. Its occurrence is often a marker of multisystem failure and has an ominous prognostic implication. Its pathogenesis is frequently complex and involves one or several mechanisms. In the evaluation of uremic hypoglycemia, the first step should be the exclusion of obvious causes such as insulin, oral hypoglycemic agent therapy, and the use of drugs known to cause hypoglycemia. Propranolol, salicylates, and disopyramide are among the most commonly implicated agents. Additional triggering events are alcohol consumption, sepsis, chronic malnutrition, acute caloric deprivation, concomitant liver disease, congestive heart failure, and an associated endocrine deficiency. When no obvious cause can be demonstrated, the hypoglycemia is referred to as spontaneous. Spontaneous uremic hypoglycemia has been attributed to deficiency of precursors of gluconeogenesis, that is, alanine, deficient gluconeogenesis, impaired glycogenolysis, diminished renal gluconeogenesis and impaired renal insulin degradation and clearance, poor nutrition, and, in a few cases, deficiency in an immediate counterregulatory hormone such as catecholamine and glucagon. However, the mechanism(s) seems to differ from one patient to the other. Dialysis also predisposes to hypoglycemia in uremia, possibly because of the chronic state of malnutrition. Postdialysis hypoglycemia is secondary to glucose-induced hyperinsulinemia, which is caused by the high glucose content in the dialysate. In uremic hypoglycemia, neuroglycopenic manifestations predominate because of frequent autonomic nervous system dysfunction and lack of catecholamine release in response to hypoglycemia. Its severity and duration are variable. Hypoglycemia should be suspected in any patient with renal failure who exhibits any change in mental or neurologic status. Detection of hypoglycemia should rely on frequent and careful glucose determinations in any patient with uremia.
 ...
PMID:Hypoglycemia associated with renal failure. 264 22

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

We have discussed the relationship between systemic illness, infection, and lung disease. As we have seen, patients with a wide variety of disease states, including advanced age, diabetes mellitus, alcoholism, collagen vascular disease, cancer, heart failure, and organ transplantation are potentially at increased risk for pneumonia because of disease-related impairments in host defenses. In addition, two virtually ubiquitous conditions in hospitalized patients, malnutrition and therapeutic interventions (especially with common medications), frequently add to the risk of airway invasion by bacterial pathogens. Systemic illness not only makes lung infection more common, but may adversely affect outcome and resolution, as well as determine the clinical presentation of pneumonia. In one particular population, the intubated and mechanically ventilated patient, the risk of infection is particularly high, and nosocomial pneumonia is a major cause of mortality. To the extent that the host response itself leads to the symptoms and signs of infection, systemically ill individuals may have subtle clinical features when serious bacterial invasion is present. Many components of the host defense system can become abnormal with serious illness, but a common mechanism that ties many systemic diseases to pneumonia is an alteration in airway epithelial cell receptivity for bacteria, namely, bacterial adherence, a process that mediates airway colonization, the first pathogenetic step on the road to pneumonia. The impetus for understanding how serious illness promotes lung infection is that once these mechanisms are identified, potential preventative strategies to minimize infection risk in the individual with systemic disease may be developed. The relationship among systemic illness, the lung, and infection also exists in a different direction: infection of a systemic nature (the septic syndrome) can lead to disease in the lung (ARDS). We have described the features of the septic syndrome and identified how it may lead to lung injury, usually by indirect means, through activation of inflammatory mediators that are carried to the lung via the vasculature. Although it is frequently impossible to predict which specific patient with systemic sepsis will develop acute lung injury, the current state of knowledge does permit us to identify high-risk individuals. Surprisingly, clinical assessment rather than biochemical testing is the best predictor of the development of acute lung injury. Patients with severe injury, profound shock and multiple systemic insults are most prone to acute lung injury in the presence of systemic sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Respiratory infections and acute lung injury in systemic illness. 268 63

Hepatic transplantation is the only therapeutic choice for end-stage pediatric liver diseases. The survival improvement, registered in the last few years is mainly due to the employment of cyclosporine in therapy, but also to new and sophisticated surgical techniques and immunosuppressive drugs. The indications in children are: biliary atresia after unsuccessful Kasai procedure, paucity of intrahepatic bile ducts (of syndromic and not syndromic type), some metabolic diseases (alfa1 antitrypsine deficiency, hereditary tyrosinemia), post infective cirrhosis, acute fulminant hepatic failure, hepatic malignancies. Absolute contraindications include severe systemic illness, severe cardiac or kidney failure, thrombosis or abnormalities of caval and portal veins, systemic sepsis, HIV infection. Other drawbacks are mental deficiency and the inability of family to care for the child and follow therapy after discharge. Relative contraindications are: HBsAg positivity, HIV positivity without infection, malnutrition. Finally the scarcity of donors of liver of adequate size is an important limitation for transplant especially in childhood.
 ...
PMID:[Liver transplant in children. I]. 269 3

To determine the susceptibility to sepsis in newborn infants deficient in glucose-6-phosphate dehydrogenase (G6PD), we screened 33,943 Saudi Arab infants. Deficiency of G6PD was found in 18%. Sepsis was determined by the presence of clinical signs of sepsis and confirmed by positive blood cultures. Sepsis was documented in 75 infants (2.2/1000). The incidence of sepsis was significantly higher in 6138 G6PD-deficient infants (3.4/1000) than in the 27,805 with normal G6PD activity (1.9/1000; p less than 0.02). The incidence of catalase-positive organism sepsis was higher in G6PD-deficient infants (2.9/1000) compared with those with normal G6PD activity (1/1000; p less than 0.0002), whereas the incidence of catalase-negative organism sepsis did not differ (p less than 0.2). Deficiency of G6PD was more common in infants with late sepsis (46%) than in those with early sepsis (21%) and in all infants screened (18%) (p less than 0.03 and p less than 0.001, respectively). We conclude that neonates with G6PD deficiency are more susceptible to late sepsis and to infection with catalase-positive organisms. The exact mechanism for the increased susceptibility is not clear, but a partial explanation could be lack of leukocyte bactericidal activity associated with G6PD deficiency, and an increased susceptibility to infection caused by hyperferremia resulting from lysis of G6PD-deficient erythrocytes.
 ...
PMID:Incidence and causes of sepsis in glucose-6-phosphate dehydrogenase-deficient newborn infants. 271 88


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>