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)

Colonization with group B beta-hemolytic streptococci (GBS) at any time during pregnancy is an important risk factor for neonatal sepsis. To determine which groups of pregnant women are at high risk for GBS, a retrospective chart review was conducted on 608 pregnant women who had recorded data on prenatal charts and were seen between October 1995 and December 1997 at a family practice-run prenatal clinic. A total of 543 subjects were studied after exclusion of women who had no results of GBS colonization recorded. Demographically, the study population comprised 91.1% white non-Hispanic, 4.8% African-American, 1.5% Asian, and 2.6% white Hispanic women; 28.9% were primiparas, 38.9% unmarried; 60.0% low income; 31.1% smokers, 7.7% with a history of drug or alcohol use; 8.4% with a history of sexually transmitted disease; and 27.2% with fewer than 11 prenatal visits. The mean age was 26.4 years (range, 14 to 42 years). Seventy-six (14.0%) of the study subjects were colonized with GBS. White non-Hispanic women had a GBS colonization prevalence of 13.6%; for all others, prevalence was 18.7%. No statistically significant differences were found in regard to age, weight, number of prenatal visits, income level, marital status, history of drug use, or parity. The GBS colonization rate for smokers was 33.1% versus 16.4% for nonsmokers (P = .012). Maternal colonization of GBS was not found to be associated with any of the risk factors studied, other than smoking. This study identified smoking as a possible risk factor for GBS infection. Routine screening for GBS infection during pregnancy may be beneficial because no strong risk factors for colonization exist.
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PMID:Risk factors for maternal colonization with group B beta-hemolytic streptococci. 1061 53

Our objective was to describe clinical features and predisposing factors attributed to lactic acidosis in 4 HIV-infected patients on long-term nucleoside reverse transcriptase inhibitor (NRTI) therapy. All patients had received at least 6-20 months of NRTI-containing antiretroviral therapy: all used stavudine (d4T), in one combined with lamivudine (3TC), in the other 3 with didanosine (ddI); in one hydroxyurea was added. In all, the initial symptoms were gastrointestinal (nausea and vomiting), followed by tachypnoea preceding the lactic acidosis; death followed 6-22 days after admission (liver failure and uncontrollable arrhythmias). Treatment with riboflavin was unsuccessful in one patient. The only definite risk factor in all cases was NRTI-induced mitochondrial toxicity; one patient was concomitantly treated for Kaposi's sarcoma (with bleomycin and vinblastine) and one just recovered from pneumococcal sepsis. None of the patients had a history of chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. In all patients, some sort of toxicity to other previously used NRTIs had occurred earlier. Lactic acidosis occurred after months of NRTI therapy in patients who had already suffered other forms of NRTI toxicity. Concomitant diseases or comedication might have aggravated the mitochondrial toxicity of the NRTIs. Screening methods to detect mitochondrial toxicity are necessary, since lactic acidosis occurs rather unexpectedly, with a rapid, fatal course.
Int J STD AIDS 2000 Sep
PMID:Clinical features and risk factors of lactic acidosis following long-term antiretroviral therapy: 4 fatal cases. 1099 8

Severe lactic acidosis has been increasingly reported as a potentially fatal complication of HIV treatment. We report on an asymptomatic HIV-infected woman treated with stavudine, lamivudine and indinavir for one year. She was hospitalized because of progressive dispnoea, oedema, cyanosis and severe lactic acidosis. Arterial blood pH was 6.98, bicarbonate 4.4 mmol/l (normal value 22-26), blood lactate: 29.7 mmol/l (normal value <2.2). Hepatic function was normal. She had an impressively rapid response (within a few hours) to empirical treatment with thiamine (100 mg i.v.). No evidence of sepsis or malabsorption were identified and vitamin B1 level was not tested before thiamine infusion. Three months later she was re-started successfully on nelfinavir plus nevirapine. The rapid response to thiamine infusion deserves a careful attention and such an approach should be considered in similar cases as a support treatment of this potentially life-threatening complication of HIV therapy.
Int J STD AIDS 2001 Jun
PMID:Severe lactic acidosis and thiamine administration in an HIV-infected patient on HAART. 1136 26

Pelvic inflammatory disease (PID) is a spectrum of inflammatory disorders of the female genital tract involving at least the endrometrium and may include the fallopian tubes, ovaries, and pelvic cavity. Over 1 million women each year are treated for PID in the United States, and it is one of the most serious infections diagnosed in women due to its sequelae. Women with PID acutely experience pain and are at risk for sepsis; however, the significant increases in ectopic pregnancy and infertility are the most disturbing long-term complications. It most often is initiated with an infection by a sexually transmitted disease, but can also involve a variety of pathogenic aerobes and anaerobes secondarily.
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PMID:Outpatient management of pelvic inflammatory disease. 1211 50

Some 250 million cases of sexually transmitted disease (STD) occur each year, and in some countries 1 or even 2 women in every 10 are infected with an STD. STDs are likely to reach an advanced stage before women notice them. The consequences of STDs are devastating, according to a report by the Population Information Program of the Johns Hopkins School of Public Health, and they include stillbirths, blinding eye infections in the newborn, chronic female abdominal pain, ectopic pregnancy, and infertility. There are social consequences for women such as divorce, and husbands may abandon infertile wives. Gonorrhea and chlamydia can cause both severe inflammation of the pelvis with acute pain and possible infertility. Pelvic inflammatory disease can permanently scar the fallopian tubes, increasing the risk of ectopic pregnancy, which can be fatal when the fallopian tube ruptures. Babies born to mothers with gonorrhea and chlamydia are likely to develop eye infections that may make them blind. Chlamydia infection in pregnant women may also cause premature rupture of the membranes, sepsis, and the death of premature neonate. Infection may spread to the lungs of newborns, leading to chlamydial pneumonia. Syphilis can cause spontaneous abortion, stillbirth, neonatal death, or congenital syphilis in the infant. Trichomoniasis and herpes can also be transmitted from mother to fetus. And infection with an STD increases the risk of infection with the human immunodeficiency virus (HIV). The World Health Organization (WHO) recommends that prenatal care should always include checks for STDs. A WHO Technical Working Group on Care of Mother and Baby has stressed the importance of detecting and treating STDs in pregnant women. The working group urged training of health workers to distinguish between STDs and other infections. The group, which met July 5-9, 1993, outlined health center strategies for prevention and treatment.
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PMID:STDs infect 250 million a year. 1234

Neisseria meningitidis and Neisseria gonorrhoeae are Gram-negative pathogenic bacteria responsible for bacterial meningitis and septicemia, and the sexually transmitted disease gonorrhea, respectively. Porins are the most represented outer membrane proteins in the pathogenic Neisseria species, functioning as pores for the exchange of ions, and are characterized by a trimeric beta-barrel structure. Neisserial porins have been shown to act as adjuvants in the immune response via activation of B cells and other antigen-presenting cells (APCs). Their effect on the immune response is mediated by upregulation of the costimulatory molecule B7-2 (CD86) on the surface of APCs, an effect that is Toll-like receptor 2- and MyD88-dependent. The effect of neisserial porins on the immune system also involves interaction with components of the complement cascade. Furthermore, neisserial porins co-localize with mitochondria of target cells, where they appear to modulate apoptosis.
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PMID:The role of porins in neisserial pathogenesis and immunity. 1259 31

To identify prognostic indicators of survival at different CD4 cell levels, independent of highly active antiretroviral therapy (HAART), among injection drug users (IDUs). A community-recruited cohort of injection drug users followed semiannually from 1988 through 2000. Five partially overlapping subcohorts were defined by when participants first reached a CD4 cell level of 351 to 500, 201 to 350, 101 to 200, 51 to 100, or </=50 cells/microL. Prognostic factors were measured at entry into each category. Kaplan-Meier survival estimates for HIV-related death and Cox regression models were constructed by CD4 category. Among the 1030 HIV-infected IDUs, survival improved in the HAART-era with hazard ratios 0.42, 0.36, 0.24, 0.21, and 0.25, respectively, for CD4 cell groups of 500 to 351, 350 to 201, 200 to 101, 100 to 51, and </=50 cells/microL. Shorter survival was associated with prior hospitalization, AIDS, and sexually transmitted disease, with similar effects in the pre-HAART and HAART eras. For the lowest CD4 cell level, prior sepsis or endocarditis, outpatient/emergency room visits, and alcohol use provide additional prognostic value. Survival among HIV-infected IDUs improved since the introduction of HAART, even though utilization of HAART was incomplete. Clinical and behavioral variables provided prognostic information about survival, including substance use indicators.
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PMID:Prognostic factors for survival differ according to CD4+ cell count among HIV-infected injection drug users: pre-HAART and HAART eras. 1560 29

A profoundly immunosuppressed HIV-infected man developed sepsis syndrome with multi-organ failure. A septic screen failed to identify a bacterial or fungal cause and despite empirical treatment for these pathogens the patient remained unwell. Investigations revealed disseminated tuberculosis. With specific anti-tuberculosis therapy the patient rapidly recovered. Although most cases of sepsis syndrome in HIV-infected patients are due to bacteria, tuberculosis should be added to the differential diagnosis of this presentation.
Int J STD AIDS 2006 Aug
PMID:Septic shock and multi-organ failure in HIV infection-'sepsis tuberculosa gravissima'. 1692 7

A 30-year-old HIV-infected intravenous drug user presented with sepsis, acute renal failure, oedema, proteinuria and iron deficiency anaemia. After extensive investigation, a diagnosis of reactive systemic AA (amyloid, serum amyloid A protein) amyloidosis was made on the basis of renal, gastric and duodenal biopsies.
Int J STD AIDS 2007 May
PMID:Renal and gastrointestinal amyloidosis in an HIV-infected injection drug user. 1752 3

Kaposi's sarcoma (KS) usually presents with typical skin lesions. We report two cases that presented with illnesses suggesting major sepsis, but were found to have disseminated KS at postmortem with little in the way of cutaneous involvement.
Int J STD AIDS 2007 Nov
PMID:Septic illness and Kaposi's sarcoma. 1800 17


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