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)

We report a 3-year analysis (1986 to 1989) of the management of 63 home parenteral nutrition patients, 40 with short-bowel syndrome and 23 with chronic intestinal obstruction with or without intestinal resection. Intravenous fluid requirements varied from 0.9 to 6 L/day, and the content of glucose varied between 46 and 531 g/day, protein varied from .0 to 85 g/day, fat from .0 to 100 g/day, sodium from 37 to 695 mEq/day, potassium from 30 to 220 mEq/day, chloride from 60 to 760 mEq/day, and acetate from 0 to 200 mEq/day. Body weight was normalized and well maintained in the majority of patients, but using the strict definition of deficiency as the presence of one abnormal value during 3 years, more than half had abnormal plasma chloride, glucose, alkaline phosphatase, serum glutamic oxaloacetic transaminase, total protein, albumin, selenium, and iron concentrations, and more than a third had low calcium, magnesium, vitamin D, and vitamin C levels. Normochromic anemia was seen in 73% and high blood creatinine associated with low urine volumes in 42%. Most (78%) returned to relatively normal lifestyles, but employability was occasionally impaired by loss of third-party insurance coverage resulting from a therapy that may cost $100,000 per year. Overall mortality was low (5% per year), but 73% needed readmission to hospital, mainly for suspected catheter sepsis. The results indicate that home parenteral nutrition has allowed many patients to survive gut failure and return to work but problems with chronic fluid, electrolyte and micronutrient deficiencies, catheter sepsis, and insurance coverage often restrict optimal rehabilitation.
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PMID:Home parenteral nutrition--a 3-year analysis of clinical and laboratory monitoring. 850 44

After a general discussion of the factors contributing to maternal mortality and morbidity, a solution to both of these problems is suggested for India: an initiative at the district level to improve support, supervision, training, essential midwifery and obstetric care. The general causes of the 200 or more times higher maternal morality risks in developing countries act throughout the woman's lifetime: powerlessness, illiteracy, malnutrition, deficiency of calcium, vitamin D and iron, heavy physical labor, unchecked fertility, lack of prenatal and obstetric care and illegal abortion. The most common causes of maternal morality and morbidity, eclampsia, obstructed labor, hemorrhage and sepsis, have been prevented in developed countries and in China. We know how to prevent them, by technical support and management at the district level. 4 elements are required: 1) adequate primary health care, food and universal family planning; 2) prenatal care and nutrition with referral if needed; 3) assistance of a trained person at every childbirth; 4) access to obstetric care for those at high risk. Rather than spend money or urban specialized hospital centers, half to 2/3 of all fatal complications of childbirth can be eliminated by local hospitals with the ability to do basic obstetrics such as caesareans and blood transfusions. There is a need for further health systems research in the given locale, but what we need now is an initiative on making pregnancy and childbirth safe for all women.
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PMID:On safe motherhood. 342

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

Moderate hypercalcaemia occurred in a 17-year-old male who was immobilized with abdominal and right hip sepsis for 9 months after a motor vehicle accident. The hypercalcaemia was due to bone resorption, with a urine hydroxyproline:creatinine ratio of 0.203 (normal less than 0.017) and a urine calcium loss of 22.9 mmol/24 hr, associated with impaired renal function. There was radiological evidence of severe bone demineralization in the pelvis over 42 weeks. Radiocalcium absorption, using 47Ca, was decreased (0.17, normal range 0.35-1.30), renal tubular maximum for calcium reabsorption was decreased (1.61 mmol/1 glomerular filtrate, normal range 1.8-2.2), the serum parathyroid hormone concentration was in the low normal range (3.2, 3.6 u/l, normal range 2-6) and the plasma 1,25-dihydroxy-vitamin D concentration was decreased despite a normal 25-hydroxy-vitamin D concentration, indicating suppression of the parathyroid, 1,25-dihydroxy-vitamin D axis. The patient was found to be hypogonadal at 41 weeks after admission and testosterone therapy was begun, with associated improvement in mobilization and a reduction of the hypercalcaemia.
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PMID:Immobilization hypercalcaemia with severe bone mineral loss and hypogonadism. 646 82

The effects of prolonged home total parenteral nutrition on growth and psychomotor development were studied in eight infants during a two-year period. Each patient was begun on HTPN in the first 60 days of life, using a Broviac silastic catheter for venous access. Normalization of somatic growth has been observed in all patients during the study period. Six of eight patients have normal psychomotor development following discharge from the hospital into the home environment. Catheter-related complications in this group have been infrequent; one episode of sepsis was documented during 121 patient-months. The major metabolic complication observed was the development of rickets despite provision of recommended doses of vitamin D. HTPN appears to be useful in providing nutritional support for selected infants during the first two years of life.
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PMID:Home parenteral nutrition in infants. 676 67

Circulating interleukin-6 (IL-6) concentrations correlate with disease activity in severe inflammatory conditions, in sepsis and in some hematological malignancies. On the other hand, IL-6 is a potent stimulator of osteoclastogenesis and has been implicated as a contributory factor in the genesis of osteopenic conditions. We measured circulating IL-6 levels by a sensitive (detection limit of 10 U/ml) and specific bioassay in 103 patients with advanced cancer, including 41 with tumor-induced hypercalcemia before any specific hypocalcemic therapy. We related IL-6 concentrations to clinical features and to biochemical parameters of bone metabolism, including blood Ca, Ca2+, Pi, intact parathyroid hormone, parathyroid hormone-related protein, osteocalcin, 1,25-(OH)2-vitamin D and, as markers of bone resorption, the fasting urinary excretion of calcium (Ca/creatinine) and hydroxyproline. IL-6 levels were increased, i.e. detectable, in 23% of the patients, 8/41 (20%) hypercalcemic and 16/62 (26%) normocalcemic patients (NS); the distribution of the values was similar in the two groups. The presence of increased IL-6 concentrations was not related to any clinical characteristic, notably not to the survival nor to the existence of bone metastases, whether in hypercalcemic or normocalcemic patients; e.g., only 3/12 (25%) hypercalcemic subjects without bone metastases had elevated IL-6 levels. We found no significant correlations between IL-6 concentrations and any of the biochemical parameters studied. Hypercalcemic subjects with increased IL-6 had higher urinary Ca/creatinine levels than patients with normal IL-6 levels (P < 0.005) but this was not the case in normocalcemic subjects. Mean concentrations of inflammatory or other bone metabolism markers were not significantly different between patients with normal or with elevated IL-6 levels. In summary, circulating IL-6 levels were increased in 23% of 103 patients with advanced cancer, but the frequency of increased IL-6 concentrations was not related to the presence of hypercalcemia or to any marker of calcium metabolism or bone turnover. The pathogenic importance of circulating IL-6 in patients with solid tumors remains to be demonstrated and our data indicate that increased circulating levels of IL-6, possibly reflecting the activation of the immune system, only contribute in a minor way to the osteolytic process in patients with tumor-induced hypercalcemia.
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PMID:Circulating concentrations of interleukin-6 in cancer patients and their pathogenic role in tumor-induced hypercalcemia. 798 59

After a near total small bowel resection for an acute thrombosis of the mesenterial artery, a 61 year-old man was treated with total parenteral nutrition at home for five years. The treatment was complicated by episodes of sepsis, anaemia and uremia. After four years he developed pain in long bones and the back and grave hypercalcuria. Roentgenogram showed demineralisation. There was no hyperparathyroidism and serum phosphate and serum calcium were normal. His chronic metabolic acidosis was treated continuously with enteral acetate. He received basal amounts of vitamin D and amino acids. By administering calcitonin we were able to cure his progressive bone pains and normalize his calcium urinary output. No side effects were observed. Therefore, calcitonin may contribute to the treatment of bone disease associated with total parenteral nutrition.
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PMID:[Calcitonin treatment of metabolic bone disease induced by parenteral nutrition]. 832 48

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

Infections remain among the major causes of disease, hospitalization and death in uremic patients, especially in those treated by dialysis. Several pathophysiologic factors enhance this infectious risk: (1) breakdown of protective barriers; (2) affinity of bacteria for foreign materials; (3) bioincompatibility; (4) uremic toxin retention; (5) deficiency and resistance to vitamin D; (6) carriership of germs, and (7) malnutrition. Twenty to 30% of dialysis patients develop infection, and 20-30% of these die from their infection. Sepsis is significantly more frequent, and mortality secondary to sepsis is 50 times higher than in the normal population. Bacteremia (prevalence 1 episode/100 patient-months) is mainly caused by Gram-positive species, especially in vascular access-related infection and infection of unknown origin. Among these Gram-positive germs, staphylococci play a predominant role. The most frequent and most morbid viral infections are associated with hepatitis. Whereas the incidence of hepatitis B decreases, hepatitis C has become the major variant. The incidence of tuberculosis has increased up to 15 times, and in the Western world it mainly affects patients who immigrated from endemic areas. Fungal infections are also frequent, especially in the setting of peritoneal dialysis. In conclusion, infections remain a frequent and morbid problem in dialysis patients. Preventive measures should be applied more vigorously.
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PMID:Incidence of infectious morbidity and mortality in dialysis patients. 1220 97

Exposure of blood to tissue factor (TF) sets off the coagulation cascade. TF is a transmembrane protein that serves as an essential cofactor for activated coagulation factor VII (FVIIa). TF may be exposed locally by vascular injury (such as balloon angioplasty) or by spontaneous rupture of an atherosclerotic plaque. Expression of TF may also be induced on monocytes and endothelial cells in conditions like sepsis and cancer, causing a more generalised activation of clotting. TF may thus play a central role in thrombosis in a number of settings, and attention has turned to blocking TF as a means to prevent thrombosis. Inhibiting the inducible expression of TF by monocytes can be achieved by 'deactivating' cytokines, such as interleukin (IL)-4, -10 and -13, or by certain prostanoids; by drugs that modify signal transduction, such as pentoxifylline, retinoic acid or vitamin D(3), or by antisense oligonucleotides. Such approaches are for the most part at a preclinical stage. The function of TF can be blocked by antibodies that prevent the binding of FVIIa to TF; by active site-inhibited FVIIa, which competes with native FVIIa for binding; by antibodies or small molecules that block the function of the TF/FVIIa complex; and by molecules, such as TF pathway inhibitor or nematode anticoagulant peptide C2, which inhibit the active site of FVIIa in the TF/FVIIa complex after first binding to activated factor X. The latter two agents have entered Phase II clinical trials. Perhaps most intriguing is the use of anti-TF agents locally, which holds the promise of stopping thrombosis at a specific site of injury without the bleeding risk associated with systemic anticoagulation.
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PMID:Tissue factor - a therapeutic target for thrombotic disorders. 1222 78


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