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)

The systemic inflammatory response syndrome (SIRS) in acute liver failure (ALF), in which infection is common, has not been studied. In this study, SIRS components were recorded on admission and during episodes of infection, in 887 ALF patients admitted to a single center during an 11-year period. Overall, 504 (56.8%) patients manifested a SIRS during their illness, with a maximum of 1, 2, and 3 concurrent SIRS components in 166, 238, and 100 patients, respectively. In 353 (39.8%) patients who did not become infected, a SIRS on admission was associated with a more critical illness, subsequent worsening of encephalopathy, and death. Infected patients more often developed a SIRS and one of greater magnitude. The magnitude of the SIRS in 273 patients with bacterial infection correlated with mortality, being 16.7%, 28.4%, 41.2%, and 64.7% in patients with 0, 1, 2, and 3 maximum concurrent SIRS components, respectively. Similar correlations with mortality were seen for SIRS associated with fungal infection, bacteremia, and bacterial chest infection. Fifty-nine percent of patients with severe sepsis died, as did 98% of those with septic shock. A significant association was found between progressive encephalopathy and infection. Infected patients with progressive encephalopathy manifested more SIRS components than other infected patients. For patients with a SIRS, the proportions of infected and noninfected patients manifesting worsening encephalopathy were similar. In ALF, the SIRS, whether or not precipitated by infection, appears to be implicated in the progression of encephalopathy, reducing the chances of transplantation and conferring a poorer prognosis.
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PMID:The systemic inflammatory response syndrome in acute liver failure. 1100 17

In patients with inflammatory conditions such as infection, cytokines induce the production of C-reactive protein(CRP) and serum amyloid A protein(SAA) in hepatic cells. It has been reported that upon viral infection, the serum SAA level increases by a greater degree than the serum CRP level. Procalcitonin (PCT), the precursor of calcitonin, is a new type of inflammatory marker that is specifically induced by bacterial infection, sepsis and lethal multiple organ failure, but not by viral infection, autoimmune diseases, tumors or surgical stress. To evaluate the immunoluminometric assay(LUMI test PCT; Brahms Diagnostics, Berlin, Germany) procedure for determining the PCT level and to study the clinical significance of the serum PCT level, we determined the serum levels of PCT, CRP and SAA in patients with various inflammatory diseases and normal subjects. The serum PCT level in the normal subjects was < 0.3 ng/ml. Among the patients with inflammatory disease who had a high CRP level(CRP > 20000 micrograms/dl), the PCT level was elevated only in those patients with severe bacterial infection. These results suggest that determining the PCT level may be useful in the differential diagnosis of severe bacterial infection. The patients who had a low CRP level(CRP < 150 micrograms/dl), had a PCT level within the normal range. The patients with autoimmune disease, viral infection, and fungal infection did not have an elevated PCT level.
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PMID:[Assay for determination of the serum procalcitonin level: biochemical and clinical evaluation]. 1121 85

Common variable immunodeficiency (CVI) is a primary immunodeficiency characterized by deficient antibody production. The cause of this immunodeficiency is unknown; several in vitro studies have revealed a significant number of alterations that could explain the hypogammaglobulinemia present in this syndrome. Among those described are primary B cell alterations, numerical and functional T cell abnormalities, and defects in the interaction between accessory cells. The alteration typical of CVI is the failure of B lymphocytes to differentiate from antibody-producing cells, resulting in deficient immunoglobulin secretion. Among the T cell abnormalities described are a diminished proliferative response to mitogens and antigens, alterations in the level of production of several cytokines, especially reduction in the production of IL-2, diminished antigen-specific T cells and increase basal apoptosis after stimulation. Antigen presenting cells, monocytes and dendritic cells can also present alterations and contribute to deficient antigen response. The clinical manifestations of these patients is variable; most present recurrent bacterial infections due to encapsulated bacteria, especially sinusitis, otitis, bronchitis, and pneumonias. A few patients can present mycobacterial or fungal infection and occasionally Pneumocystis carinii. Viral infection is uncommon in these patients although some suffer recurrent herpes zoster infection. Clinical features of septicemia and central nervous system infections are less frequent. The incidence of digestive tract infections in these patients is high. The most common cause of diarrhea is Giardia lamblia; Salmonella, Shigella and Campylobacter are also common pathogens. Autoimmune disease is also more prevalent in these patients than in the general population. The most frequently associated diseases are hemolytic anemia, idiopathic thrombocytopenic purpura and autoimmune neutropenia. Cancer is also frequently associated with CVI, the most common forms being lymphoproliferative syndromes, especially non-Hodgkin's lymphoma. Granulomas are a unusual manifestation in some patients with CVI; their localization varies but the most commonly affected organs are the spleen and lungs. Some authors have compared these granulomas with those characterizing sarcoidosis, especially when appearing in the lung. Diagnosis of CVI is usually by exclusion of other diseases, such as cystic fibrosis, immotile cilia syndrome or allergic processes. CVI should be suspected in all patients with recurrent bacterial infections especially those localized in the respiratory tract. Other primary immunodeficiencies which present clinical findings similar to CVI and which should be ruled out are selective IgG subclass deficiency, IgA deficiency and selective deficiency in the response to polysaccharide antigens with normal immunoglobulin levels. The serum hypogammaglobulinemia present in all patients with CVI provides the diagnostic key. The age at which clinical manifestations appear, the absence of familial antecedents and the presence of circulating B lymphocytes form the basis of the differential diagnosis between X-linked agammaglobulinemia and autosomal recessive forms. The treatment of choice of patients with CVI is treatment with human gamma-globulin. Currently, the most common route of administration is intravenous; these molecules have a half-life of approximately 21 days and a high degree of safety concerning the possible transmission of viral infections. Adverse reactions are generally few and clinically unimportant. The most frequently used doses oscillate between 200 and 400 mg/kg body weight every 2-4 weeks. Both the dose and its frequency should be personalized for each patient. Early diagnosis of patients with CVI, application of treatment with appropriate antibiotics for infections and treatment with gamma-globulins prevent long-term complications of this disease and dramatically improve the quality of life and life expectancy of these patients.
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PMID:[Common variable immunodeficiency. Review]. 1143 84

In a prospective study, 132 patients were investigated for yeast infection of burn wounds. Ten patients (7.6%) were infected with Candida species. All patients with yeast infections were also infected with bacteria with the exception of one patient who was infected with Candida tropicalis alone. The predominant yeast recovered was Candida krusei. Yeast infection was found to be more common in the younger age group. The isolation of a Candida species alone from one patient and Candida isolation from patients with sepsis in burn wounds indicate a significant role for yeasts in the production of infection in burn wounds. Therefore, special cultures for yeasts are recommended for all cases of burn wound infection.
Mycoses 2001
PMID:Yeast infection of burns. 1148 51

Fungi cause 8% of nosocomial infections. This is caused, in part, by the increasing pool of immunocompromised patients. Elderly, transplant and HIV patients, as well as premature infants, have become prime candidates for invasive fungal infections. The widespread use of broad spectrum antibiotics plays a role. Utilisation of appropriate antifungal treatment modalities requires an understanding of the pathogenesis of infection. This is a challenging problem as fungi can cause different clinical manifestations that depend on the type of fungal species and patient response to the infection. Although Candida spp. are the most frequent pathogen, other species such as Aspergillus and Cryptococcus have become major pathogens. Environmental fungi which include Blastomyces, Coccidioides and Histoplasma have become more aggressive in the vulnerable patient. The genitourinary system can be a source or target of disseminated fungal infection. Diagnosis depends on clinical awareness, utilisation of appropriate diagnostic modalities, imaging modalities and a thorough clinical assessment. The treatment of primary (Blastomyces, Coccidioides, Histoplasma) infection generally requires amphotericin B (AmpB). The opportunistic infections (Aspergillus, Cryptococcus and Candida) may respond to the triazoles although AmpB remains the 'gold standard'. Infections caused by Candida spp. represents the greatest challenge to the clinician. The presence of Candida spp. in the urine may indicate colonisation or infection. Untreated, Candida can remain as a 'saprophyte' or develop ascending infection, sepsis or death. The prophylactic use of fluconazole may in itself result in resistant infection, hence the 'conundrum'.
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PMID:Genitourinary fungal infections: a therapeutic conundrum. 1158 89

Fungal infection is an uncommon complication after renal transplantation. We describe a rare form of mucormycosis in the renal graft. Our method was to review chart data and to perform medline searches. The patient was a 42-year-old man who underwent living-unrelated kidney transplantation in Egypt and returned to Israel on POD 8. Within the ensuing 4 weeks he experienced acute rejection which responded to treatment with steroids. Few days after discharge he was readmitted because of fever and graft dysfunction. An infected large perigraft collection was drained, but the patient became anuric and septic. Kidney biopsy showed infarcted necrotic tissue infiltrated by fungi which grew Mucor species. Despite initial improvement following graft nephrectomy and antifungal treatment the patient died of sepsis. Literature review revealed only three additional cases of graft infection due to Mucorales. We conclude that Renal graft infection due to Mucorales is an extremely rare and potentially lethal complication. Living unrelated donation in third world countries might be a possible risk factor. Fungal colonization may occur during transplantation. A high index of suspicion, leading to early diagnosis and initiation of antifungal treatment, in addition to graft nephrectomy, are keys to a more favorable outcome.
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PMID:Mucormycosis of the renal allograft: case report and review of the literature. 1179 42

A common complication of the intensive therapy that children with cancer receive is infection. The Oncology Unit of The Children's Hospital at Westmead maintains a comprehensive database of all admissions for suspected sepsis. From July 1994 to June 1999 broad-spectrum antibiotics were commenced in 2331 episodes. With early and aggressive use of empirical amphotericin B, 545 courses were given. Bacteraemia was documented in 701 episodes and invasive fungal disease in 73. Trends seen during the study included: (i) the proportion of febrile neutropenic patients receiving granulocyte colony stimulating factor increased from 40% to 60%; (ii) the mean neutrophil count at cessation of antibiotics fell from 0.97 to 0.63 x 10(9) cells/L for patients not receiving growth factors; (iii) the proportion of non-albicans Candida species infections increased. In addition, an outbreak of infection caused by Scedosporium sp. was documented; (iv) first-line empirical antibiotic combinations containing vancomycin fell from 20% to 7%; and (v) the ability to maintain or escalate anti-fungal therapy with reduced nephrotoxicity through use of lipid formulations of amphotericin was increasingly apparent in high-risk patients. During the study, infection was the primary cause of death in 11 non-bone marrow transplant (BMT) patients (five fungal, four viral, one bacterial infection and one sepsis syndrome) and five BMT patients (two bacterial and three viral). A prospective randomized study of toxicity due to amphotericin B given in either lipid emulsion or dextrose showed no significant difference, but both groups showed a lower incidence of amphotericin B intolerance in comparison with the adult series. The inability to reduce toxicity of amphotericin B by simple mixing with lipid emulsion has led to increasing use of commercially available lipid formulations of amphotericin B.
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PMID:Suspected infection in children with cancer. 1180 84

Tumour necrosis factor-alpha (TNF-alpha) is related to some other factors in addition to being the essential cytokine of the sepsis which results from Candida infections. In our study, we investigated serum TNF-alpha levels, measured by enzyme-linked immunosorbent assay (ELISA), and platelet-activating factor (PAF)-like activity, measured by high-pressure liquid chromatography (HPLC) of the mice infected with Candida species. The PAF antagonist, ginkgolide BN 52021 was used to evaluate the possible interaction between TNF-alpha and PAF. The average TNF-alpha levels were found to be 396, 489, 699 and 803 pg ml(-1) on the 4th, 5th, 6th and 19th days of Candida albicans infection, respectively (P<0.05). There was no statistically significant difference between the serum TNF-alpha levels of the groups infected with other Candida species, such as C. kefyr, C. krusei and C. tropicalis (P>0.05). Serum TNF-alpha levels were found to be more significantly different in mice with C. albicans infection that were injected with PAF antagonists on the 6th day (23 pg ml(-1)). It was therefore thought that PAF antagonists have an inhibitory effect on TNF-alpha production. No significant difference was found between PAF levels in the three groups: healthy control mice, C. albicans-infected mice and C. albicans-infected mice given PAF antagonists (466 milli-absorbance unit (mAU), 475 mAU and 329 mAU, respectively). It was noticed that the positive interaction between PAF and TNF-alpha was not important after the first 4 days of the infection had passed.
Mycoses 2002 Apr
PMID:The role of tumour necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) interaction on murine candidosis. 1200 May 5

Invasive fungal infections (IFI) parallel the explosive increase in the immunocompromized patient population, and are characterized by diagnostic difficulties and extreme mortality. Candidemia in a tertiary referral hospital in the Middle East confirms the current epidemiologic shift in this common blood stream pathogen towards non-malignancy cases (38%) and antifungal prophylaxis failure (20%), high presentation sepsis scores and attributable mortality (32%). Invasive aspergillosis (IA) is also associated with high mortality. Use of non-invasive computerized tomographic (CT) radiologic scanning linked to early administration of high dose liposomal amphotericin B (LAB) is associated with a reduced mortality of 9.5% compared to historical experience of 28%.Life threatening invasive aspergillosis also occurs in patients who are less obviously immunocompromized. Investigations may reveal subtle immune deficits which could place the patient at some risk for an invasive mycosis. Antifungal treatment used in combination with progenitor cell growth factors and gamma-interferon has proved successful in such situations of progressive fungal disease unresponsive to antifungal therapy alone. Pharmacologic remodeling of existing compounds by lipidisation reduces both the toxicity denominator and the efficacy numerator of the therapeutic index when compared to the parent drug. A comparative dose study of liposomal amphotericin B in aspergillosis has demonstrated equi-efficacy, generated debate over the ability of the controlled clinical trial to be capable of assessing antifungal efficacy, and illustrated that recovery from an invasive fungal infection may require maximum tolerated doses and immunomanipulation. Several new antifungal strategies are under clinical investigation. These include reformulating existing antifungals, exploitation of the growing knowledge of virulence factors to synthesize antagonists, immune reconstitution and immunoprotection. An interim analysis of an ongoing placebo controlled study of recombinant interleukin-11 to assess its efficacy in reducing sepsis in leukemia patients through prevention of chemotherapy induced gut epithelial cell apoptosis, has demonstrated a difference in the two study arms in sepsis rates and preservation of gastrointestinal epithelial cell integrity. The unique and special challenges presented by the dynamic epidemiologics of invasive fungal infections are demanding and attracting considerable responses, in the fields of diagnosis and therapeutics. Current strategies need considerable improvement, yet ongoing collaborative efforts will have a positive impact on our understanding of the fungus-host interaction and ultimately our ability to offer better care for our patients with invasive mycoses.
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PMID:Invasive fungal infections: evolving challenges for diagnosis and therapeutics. 1200 73

Approximately 30% of patients with diabetes mellitus will have disease-related dermatological problems. Dry skin can be associated with autonomic neuropathy and may be fragile, promoting bacterial invasion. Any potentially infected 'diabetic foot' must be taken seriously, and non-painful deep sepsis suspected if there is evidence of sensory loss. Consideration should be given to eliminating nasal carriage of staphylococci if recurrent superficial sepsis occurs in the presence of poor diabetic control. Fungal infections, both of skin and nails, are common but usually not serious in the absence of immunosuppression. Treatment with topical antifungals may need to be combined with systemic therapy for successful eradication. Systemic antifungal therapy should be carefully considered as treatment needs to be prolonged and is potentially toxic, particularly in individuals with diabetes mellitus who often have co-morbidities. Varicose eczema should be treated by physical therapies intended to improve venous return and prevent peripheral edema and tissue injury. Allergic dermatitis is commonly associated with topical treatments and other sensitizers. Many reactions are not apparent from history, and patch testing for sensitivity is recommended. There are several diabetes mellitus-specific conditions that dermatologists must be aware of, including, necrobiosis lipoidica diabeticorum, granuloma annulare, diabetic dermopathy (spotted leg syndrome or shin spots), diabetic bullae (bullosis diabeticorum), and limited joint mobility and waxy skin syndrome. Ulceration, due to varying combinations of peripheral vascular disease and sensory neuropathy, is the province of the specialist team dealing with the diabetic foot and should ideally be referred to an appropriate multidisciplinary team.
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PMID:Dermatological care of the diabetic foot. 1218 Aug 94


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