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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute sore throat is a very common pathology, but should not because of this be considered as banal. In effect, the beta-haemolytic streptococcus A, which is responsible for most of the bacteriological etiologies is not only responsible for distant inflammatory complications, acute articular rheumatism (RAA) and glomerulonephritis, which are re-appearing in the United States, but also a fulminating septicemia and a syndrome of visceral failure that makes a grave prognosis for life. Moreover, today, streptococcus A is one of the factors involved in a series of fatal fasciites and necrosing myosites seen in several European countries. Understanding of these complications gives better definition of the causative immunological mechanisms and particularly the adverse role of the "superantigens" of streptococci in the start of an increase in the responses of immunocompetent cells and pro-inflammatory and prothrombic mediators. Finally, availability now of rapid diagnostic tests with monoclonal antibody techniques confirms the presence of streptococci A in acute sore throat and should help the physician to make an etiological diagnosis that takes into account the clinical signs. Unfortunately, these tests are not widely available in France and are not subject to reimbursement. All these factors justify the introduction of an antibiotherapy targetted at streptococcus A in the context of bacterial sore throat. Oral penicillin V (phenoxymethyl penicillin, Oracilline) is always the reference, with an excellent anti-bacterial and clinical activity and without risk of production of strains of streptococcus that are of reduced sensitivity or resistant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Targetted antibiotic therapy. Acute sore throat: streptococcus A update]. 786 18

To identify the demographic, clinical, and pathologic features and the prognosis of renal disease in a series of patients with infectious or postinfectious proliferative glomerulonephritis (GN), data were collected from records of 76 adult patients admitted from 1976 to 1993 to 2 neighboring suburban hospital nephrology units, whose catchment population consists of patients living in a suburban borough of Paris with a below-average socioeconomic status. Thirty-four patients (45%) were alcoholics, diabetics, or intravenous illicit-drug users. Sixty-six patients presented with acute nephritic and/or nephrotic syndrome. Acute renal failure was present in 56 (76%) and required dialysis in 14. The diagnostic workup comprised at least 1 renal biopsy in each case. The patient's background, site of infection, clinical course, laboratory variables, and, when available, bacteriologic findings were analyzed in each case to interpret the evolution of the disease. Initial renal biopsy disclosed endocapillary GN in 44 patients, crescentic GN in 26, and membranoproliferative GN in 6. Ten patients had endocarditis. Staphylococci and Gram-negative strains, not streptococci, were the most common bacteria identified. The origin of sepsis was mainly the oropharynx (21), the skin (19) and the lung (14); 19 cases involved multiple sites of infection. Eight patients died (11%), and 20 (26%) recovered renal function, but GN followed a chronic course in 38 (50%), rapidly requiring maintenance dialysis in 6. Poor prognostic factors included age over 50 years, purpura, endocarditis, and glomerular extracapillary proliferation. Twenty-six patients underwent repeat renal biopsy 1 month to 11 years after the initial presentation. The main finding, irrespective of the interval since the first biopsy, was that ongoing or new iatrogenic infection acquired during hospitalization was almost invariably acquired during hospitalization was almost invariably associated with developing glomerular proliferative changes. This study shows that infectious proliferative GN remains common, but that its epidemiology has changed from what was observed until 2 decades ago. The responsible bacteria, when identified, now comprise a majority of staphylococci and Gram-negative strains, in contrast to the streptococci which predominated 3 decades ago. Infectious GN affects with increasing frequency patients with an underlying condition responsible for immunosuppression, especially alcoholism, even in the absence of cirrhosis. Destructive glomerular proliferation persists, especially but not exclusively until infection has been eradicated, and despite rescue treatment with corticosteroids and/or cytostatic drugs. Thus, the prognosis is poor, and infectious GN often ends in renal death. Infection continues in this decade to represent a frequent and probably often overlooked cause of end-stage renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The current spectrum of infectious glomerulonephritis. Experience with 76 patients and review of the literature. 789 44

Cytokines, released by T cells, participate in inflammation and produce tissue injury. Excess production of cytokines such as interleukins (ILs) and tumor necrosis factor (TNF) is believed to be involved in the pathobiology of conditions such as septicemia and septic shock, collagen vascular diseases, glomerulonephritis etc. On the other hand, prostaglandins (PGs) are known to modulate inflammation, immune response, and T-cell response to antigens. But relatively little information is available on the effects of PGs and PG precursors on the release of cytokines. Here the authors present data which suggests that PGs including thromboxane B2 (TXB2) and their precursors such as dihomo-gamma linolenic acid (DGLA), arachidonic acid (AA) and eicosapentaenoic acid (EPA) can inhibit T-cell proliferation and influence their ability to secrete IL-2, IL-4, IL-6 and TNF in vitro. These results may have relevance to the use of PG-precursors in various inflammatory conditions including collagen vascular diseases.
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PMID:Effect of prostaglandins and their precursors on the proliferation of human lymphocytes and their secretion of tumor necrosis factor and various interleukins. 793 85

Idiopathic membranoproliferative glomerulonephritis (MPGN) has a poor prognosis, with 90% of patients requiring dialysis treatment after 20 years regardless of therapy. Up to 34% of patients may die due to thrombotic complications or sepsis. This study investigates the influence of aspirin plus dipyridamole on proteinuria and renal function in nephrotic MPGN patients with moderately reduced glomerular filtration rate. Eighteen patients with biopsy-proven MPGN (15 type I, 3 type II) and nephrotic syndrome were randomly assigned to receive protein restriction, antihypertensive therapy (control group) or in addition aspirin and dipyridamole (treatment group). Patients were prospectively followed for a mean of 36 months. Serum creatinine remained unchanged after 36 months compared to baseline in both groups. In the treatment group proteinuria was reduced from 8.3 +/- 1.4 to 1.6 +/- 0.7 g/day (P < 0.05). In control patients proteinuria decreased from 7.1 +/- 1.6 to 4.3 +/- 1.1 g/day. After 36 months proteinuria was significantly lower in the treatment group compared to control (P < 0.02 Mann-Whitney rank sum test). In conclusion, aspirin plus dipyridamole may be of value in reversing nephrotic syndrome and associated risks in patients with MPGN and moderately reduced renal function.
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PMID:Effect of aspirin and dipyridamole on proteinuria in idiopathic membranoproliferative glomerulonephritis: a multicentre prospective clinical trial. Collaborative Glomerulonephritis Therapy Study Group (CGTS) 797 86

Prognostic significance of various clinical and laboratory indices for predicting the course and outcome of infectious endocarditis (IE) has been analyzed for 139 IE patients aged 15-68 (77 males and 62 females). The unfavourable prognosis was associated with uncontrollable sepsis, persistence of circulating immune complexes and developing glomerulonephritis. The latter had also prognostic signs unfavourable for IE: moderate or severe proteinuria and/or cylindruria, reduced renal function, diffuse proliferation, pronounced extracapillary and/or tubulointerstitial components.
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PMID:[The prognosis of the nature of the course and outcome of infectious endocarditis]. 801 29

If the skin's protective mechanisms are disrupted, cutaneous infection may result. Diagnosis is based on recognition of clinical signs. Accurate assessment of these signs and prompt initiation of appropriate treatment can help patients avoid serious complications, such as glomerulonephritis occurring with impetigo contagiosa or gangrene and sepsis occurring with cellulitis. Recurrence of skin infections is difficult to prevent, but patients should be encouraged to practice good hygiene and to avoid irritants and predisposing factors nonetheless.
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PMID:Common infections of the skin. Characteristics, causes, and cures. 804 84

One hundred and twenty patients with a mean age of 38 years (range 12-85 years; M 91, F 37) were studied over a period of 5 years in a teaching hospital in Dhaka. Sixty-two patients presented with probable anuria with 1-4 days' duration, 63 patients presented with oliguria, and 3 were nonoliguric. The causes of acute renal failure were medical (94), surgical (22), obstetrical (13). Of the medical cases, the causes were gastroenteritis in 42 cases, gastroenteritis with CNS involvement in 11 cases, rapidly progressive glomerulonephritis in 10 cases, acute viral hepatitis in 8 cases, and septicemia in 8 cases. Of 22 surgical cases, postoperative acute renal failure was the cause in 9, road traffic accident in 6, and renal calculus disease in 7. There were 13 cases in the obstetrics group, of whom 9 were due to abortion, 2 were due to preeclampsia, and the other 2 were postoperative. The mean blood urea of all cases was 35 mmol/L and serum creatinine was 988 mumol/L. Dialysis was required in 105 cases; of these, 72 were medical cases, 21 were surgical cases, and 12 were obstetric cases. The overall survival rate was 75%. The improved survival is probably due to timely referral and prompt medical management.
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PMID:Outcome of acute renal failure in adults in a teaching hospital in Bangladesh. 829 Jul 6

Fourteen mares and their foals were attended at parturition. After mare-foal bonding, 8 colostrum-deprived (CD) foals were removed from their dams, deprived of colostrum, and provided with an alternative milk source for the first 24 h of life. The mares were milked out every 2-4 h during this period to remove colostrum, after which the CD foals were returned to their mares and allowed to nurse. Six colostrum-fed (CF) foals were allowed to suck colostrum in the normal manner. Foal serum IgG concentration was determined by single radial immunodiffusion (means, CD = 0 mg/dl; CF = 1,508 mg/dl). Accepted methods were used to minimise infections in the neonatal foals. Of the 8 CD foals, 7 demonstrated clinical signs of sepsis. Septicaemia was confirmed in 5 of the 7 septicaemic CD foals by ante-mortem blood culture or by culture of tissue at necropsy. Organisms isolated included: Actinobacillus equuli, Escherichia coli, undifferentiated coliforms, Pseudomonas spp., and Actinomyces pyogenes. Clinically ill foals were treated with antimicrobial drugs, intravenous fluid therapy, flunixin meglumine, and anti-endotoxin hyperimmune serum. Three septicaemic CD foals survived. Four of 7 septicaemic CD foals died or were destroyed. Post-mortem lesions included bacterial embolic pneumonia, glomerulonephritis/nephritis, lymphoid depletion/atrophy, splenic and lymphoid necrosis, hepatitis, septic arthritis, and systemic bacterial embolism. None of the CF foals became septicaemic. One CF foal had foal heat diarrhoea and 1 CF foal had a serum IgG concentration of 160 mg/dl (i.e. failure of passive transfer), but both foals were otherwise normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective study of septicaemia in colostrum-deprived foals. 822 85

Group A streptococci (S. pyogenes) possess a number of capsule and cell wall associated components and release many extracellular proteins (toxins and hydrolytic enzymes) that are known or thought to contribute to the virulence and pathogenicity of the microorganism. Groupe A streptococci cause a wide array of infections, the most frequent of which are acute pharyngitis and pyoderma with two severe sequelae (acute rheumatic fever and glomerulonephritis). Other manifestations are scarlet fever and various soft tissue infections as well as sepsis and the recently characterized streptococcal toxic shock syndrome. The somatic components of group A streptococci include cell wall M protein, capsular hyaluronic acid, lipoteichoic acid, peptidoglycan, fibronectin binding protein, C5a peptidase and receptors for various human plasma proteins particularly IgA and IgG. The extracellular products are numerous and consist of among others the hemolytic toxins streptolysins S and O, hyaluronidase, streptokinase and cysteinyl proteinase as well as the superantigens erythrogenic toxins A and C also known as pyrogenic exotoxins.
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PMID:[Cellular constituents and extracellular proteins involved in the pathogenic capacity of Streptococcus group A]. 873 28

We report here a case of Cogan's syndrome associated with systemic vasculitis as well as myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis. A 71-year-old woman with the diagnosis of aortitis syndrome and pulmonary fibrosis for 7 years, complained of vertigo and hearing impairment. A diagnosis of serous otitis media was made. Although steroid therapy was effective, the symptoms relapsed several times. Seven months after the first manifestation of aural symptoms, she developed painful red eyes bilaterally and proteinuria. On admission, perinuclear ANCA without cytoplasmic ANCA was detected by indirect immunofluorescence assay and MOP-ANCA was detected by enzyme linked immunosorbent assay using the 363 ELISA Unit. Renal biopsy showed necrotizing crescentic glomerulonephritis without immune deposits. A diagnosis of atypical Cogan's syndrome with systemic vasculitis and pulmonary fibrosis was made from the clinical and histological findings. As nephrotic syndrome progressed after admission, she was started on high-dose corticosteroid administration. Urinary protein and other symptoms, except for hearing acuity, improved in parallel with a decrease in the MPO-ANCA titer to normal values. While tapering the dose of corticosteroid, the MPO-ANCA titer increased again and dyspnea occurred. Although pulse methylpredonisolone therapy was performed, the patient died of respiratory failure complicated with sepsis. Postmortem lung biopsy showed pulmonary fibrosis and massive alveolar hemorrhage. The findings of this case study suggest that MPO-ANCA may be closely related to the pathogenesis of Cogan's syndrome.
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PMID:[A case of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis associated with Cogan's syndrome]. 891 96


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