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)

Fever was unchanged by chemotherapy in ten patients with bacteriologically positive pulmonary tuberculosis. Blood cultures were positive for Gram-positive organisms in six patients and for Gram-negative organisms in four patients. The same organism was present in sputa and blood in six patients and in urine and blood in two patients. Leukocytosis was not found, and roentgenographic findings did not suggest superinfection. Nine of the ten patients survived. Blood cultures must be obtained in patients with pulmonary tuberculosis whose fever is not altered by antituberculous chemotherapy, so that concomitant septicemia is not neglected.
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PMID:Occurrence with bacteriologically positive pulmonary tuberculosis. 41 Sep 59

Sera from 103 fasting individuals 3 to 76 years of age and free of clinical infectious disease and sera from 183 patients with infectious disease were assayed for serum total non-esterfied fatty acids (tNEFA) and compared. Data were also separated into five groups according to age of donor: 3--7, 8--19, 20--35, 36--60, and 61--76 years. The mean group serum levels of tNEFA increased with age. Among patients with infectious diseases sixty-five were diagnosed as having hepatitis, 41 with infectious mononucleosis, 18 with cellulitis, 12 with pulmonary tuberculosis, 11 with non-pneumococcal pneumonia, 9 with pneumococcal pneumonia, 8 with pharyngitis, 6 with pyelonephritis, 6 with aseptic meningitis, 4 with Gram-negative sepsis, and 3 with encephalitis. The sera from 23 non-fasting patients with gonorrhea were also tested. The serum tNEFA levels were found to be altered, in fact depressed from normal group values, only in patients with pneumonia or tuberculosis. This depression may be related to aberrant pulmonary metabolism during pneumonia.
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PMID:Reduced level of non-esterified fatty acids in sera from patients with infectious respiratory disease. 69 41

Two cases of pneumococcal sepsis, meningitis and unilateral endophthalmitis after total splenectomy are described. The first patient, a 9-year-old girl, had severe panuveitis complicated by traction retinal detachment, eventually requiring vitrectomy. Due to large chorioretinal scars the visual recovery was poor. Minor residual neurological signs remained. The second patient, a 39-year-old man, showed endophthalmitis of the right eye. The recovery of the pneumococcal meningitis was complicated by severe neurological impairment. The right eye progressed to phthisis bulbi. The importance of early recognition of postsplenectomy sepsis (PSS) is emphasised since the survival rate is poor and the risk of visual loss high.
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PMID:Endogenous pneumococcal endophthalmitis after splenectomy: report of two cases. 130 44

This study was conducted in a subdivisional hospital of eastern Himalayan region among 5,273 pregnant women over a period of 8 years. There were 29 deaths, the maternal mortality rate was 55 per 10,000. Septic abortion was encountered in 4 among them. Direct obstetric cause was responsible in 72.41% of cases and indirect cause in 27.59% cases. Sepsis, both puerperal and postabortal resulted in 24.14% followed by postpartum haemorrhage in 20.69%. Two of these cases were associated with inversion of the uterus. Preeclampsia caused 10.34% and eclampsia 6.9% of the deaths. Among the indirect causes severe anaemia and pulmonary tuberculosis accounted for 10.34% and 6.9% respectively. Infective hepatitis was the cause in 6.9% cases. Only 17% of the cases were booked and the rest were unbooked. Majority of the cases (62.07%) belonged to the age group of 20-30 years. Primigravida constituted 41.38% of the cases.
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PMID:Maternal mortality in a subdivisional hospital of eastern Himalayan region. 151 13

The experience of surgeons in Africa with patients infected with human immunodeficiency virus (HIV) suggests 5 trends: 1) an increased incidence of surgical sepsis--most commonly in the female genital tract, the pleural cavity, large joints, and the anorectal area--in HIV-infected patients; 2) an increase in surgical tuberculosis of spine, bone joints, lymph nodes, and the peritoneal cavity concomitant with an increased incidence of pulmonary tuberculosis in high-incidence countries; 3) impaired healing of wounds, wound breakdown, and the development of skin lesions and ulcers; 4) tumors whose aggressiveness is accelerated by HIV infection; and 5) new pathologies such as nonspecific cystitis, chronic osteitis, and vascular disease. In many cases, HIV infection has not been identified until after hospital patients have demonstrated a rapid, progressive decline after routine surgery. To date, only 1 study has attempted to determine the extent to which HIV infection influences the outcome of surgery. Mortality in an intensive care unit at the University Teaching Hospital in Lusaka, Zambia, differed significantly between HIV-positive and seronegative patients only in terms of pneumonia; however, seropositive patients also have an elevated, albeit nonsignificant, risk of mortality from severe gynecologic sepsis.
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PMID:Surgical pathology of HIV infection: lessons from Africa. 755 18

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)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

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.
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PMID:The non-immune inflammatory response: serial changes in plasma iron, iron-binding capacity, lactoferrin, ferritin and C-reactive protein. 378 68

94 maternal deaths and 1546 fetal and neonatal deaths were registered among 28,706 births at the CHU Averroes in Casablanca between 1978-80. 45% of women who deliver at the clinic are very poor and only 10% are relatively well off. Obstetrical antecedents were noted in 27% of the fetal deaths. 70% of the maternal deaths occurred in women aged 20-34. 32 maternal deaths occurred among 16,232 women with 1-2 children, 30 among 6514 women with 3-5 children, and 32 among 5960 women with 6-14 children. 11,027 of the 28,706 were primaparas. Perinatal mortality was 4.46% among primaparas, 8.24% among grand multiparas, and 4.1% among secondiparas. In 58 of the 94 cases of maternal mortality the woman was hospitalized after attempting delivery at home or in a village clinic. Among women with 1 or 2 children, hemorrhage was the cause of death in 8 cases, infection in 7 cases, eclampsia in 3 cases, thromboembolism in 2 cases, uterine inversion in 2 cases, pulmonary tuberculosis in 1 case, embolism in 5 cases, and other causes 1 case each. Among women with 3-5 children hemorrhage was the cause of death in 10 cases, septicemia in 3 cases, uterine rupture in 3 cases, eclampsia in 3 cases, uterine inversion in 2 cases, viral hepatitis in 2 cases, emboli in 2 cases, and other reasons 1 case each. Among grand multiparas hemorrhage was the cause of death in 11 cases, uterine rupture in 12 cases, peritonitis in 2 cases, eclampsia in 2 cases, emboli in 2 cases, and other causes 1 case each. 19 of the maternal deaths were judged to have been avoidable with better management. Prematurity and birth weight of 1000-2500 g associated or not with other pathology were found in 714 of 1546 perinatal deaths. Of 390 cases of death in utero with retention and maceration, 68 were caused by reno-vascular syndromes, 76 by maternal infections, 33 by maternal syphilis, 26 by fetal malformation, 18 by maternal diabetes, 10 by Rh incompatability, and 159 by indeterminate causes. In 795 cases of intrapartum mortality without maceration, 114 were caused by retroplacental hematomas, 61 by placenta previa, 74 by uterine rupture, 119 by prolapse of the cord, 51 by fetal malformation, 45 by dystochia, 53 by twin pregnancies, 104 by fetal distress, 44 by obstetrical trauma, 55 by prematurity, and 75 by undetermined causes. In 361 cases of early neonatal mortality, 88 were caused by renovascular syndromes, 24 by diabetes, 13 by Rh incompatibility, 34 by placenta previa, 94 by prematurity, 28 by fetal malformation, 35 by fetal infections, 31 by fetal distress, and 14 by obstetrical trauma. The rates of maternal and perinatal mortality are very high compared to those of European countries.
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PMID:[Maternal mortality and perinatal mortality]. 720 85

Autopsy or biopsy findings in 10 human immunodeficiency virus (HIV)-positive persons from Bangalore, India, revealed a wide spectrum of pathological changes. Patients' mean age was 33.4 years and the mean duration between symptom onset and death was 27.13 days. Nine patients had evidence of neuro-acquired immunodeficiency syndrome (AIDS) and 8 of them succumbed to various opportunistic infections. Histologic examination showed diffuse cryptococcal meningitis in 5 cases; 2 cases showed disseminated systemic cryptococcosis. Pulmonary tuberculosis was present in 3 patients. Despite no signs of associated neurotuberculosis in any patient, 4 autopsied and 1 biopsied case showed evidence of systemic tuberculosis. Toxoplasma encephalitis was present in 2 cases; observed in this series was the first case, in India, of co-existent toxoplasma and acanthamoeba. Other bacterial infections such as meningococcal meningitis and psudomonas septicemia were found in 3 cases; pneumocystis carinii pneumonia was present in 1 case. Evidence of early HIV leukoencephalopathy was observed in the only asymptomatic HIV-positive individual (who died in a traffic accident). AIDS-associated bacterial infections caused by organisms other than Mycobacterium tuberculosis are often underdiagnosed and should be considered in developing countries. In cases of cryptococcal and tuberculosis meningitis or multiple parasitic infections, patients should be screened for associated HIV infection.
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PMID:Pathological lesions in HIV positive patients. 775 Oct 41

A review of 1,069 total admissions of 537 systemic lupus erythematosus (SLE) patients during a 10-yr period at Ramathibodi Hospital showed that 220 episodes which occurred in 137 patients (25.5%) were motivated by infection. Skin was the most common site (23%) with Herpes zoster being the most common organism (15.5%) found in our lupus patients. However, if we considered only major infections, pulmonary tuberculosis, salmonella septicemia and urinary tract infection by E. coli would be the most frequent complications respectively. In the absence of immunosuppressive therapy, infections coincided with the initial manifestation of SLE in 25 patients and were associated with exacerbation of the disease in 20 patients. Mean SLEDAI score in these patients was 8.8, suggesting that active lupus link together with infection. Steroid therapy influenced the rate of opportunistic infections (p = 0.006). Infections were determined to be the cause of death in 23 of 77 patients (29.9%). Opportunistic pathogens played an equal role as other common bacterial organisms in these fatal cases. SLE patients who died from infections were treated with cyclophosphamide in higher proportion than those with no infectious complication (p = 0.025). Our study demonstrated the rate, nature and predisposing factors of infection in SLE which may lead to better anticipation and diminution of morbidity and mortality related to infection in hospitalized patients with SLE.
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PMID:Infection in systemic lupus erythematosus. 796 23


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