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)

In summer 1996, a 31-year-old woman developed arthralgia, subfebrility, and papular efflorescences on the skin, clinically and histologically suspect of vasculitis, to be followed by severe lung edema and anuria, with serum creatinine up to 1182 mol/L in the autumn 1996. The administration of high dose corticosteroids, plasmapheresis and hemodialysis resulted in regression of the clinical symptoms and considerable improvement of the kidney function. Kidney biopsy revealed sclerosing extracapsular glomerulonephritis with extensive fibrocellular crescents. Thereafter, the patient felt well, however, renal insufficiency showed gradual progression, so the patient was continuously treated with hemodialysis from January 1998. Two more episodes of severe lung edema occurred at the beginning of 1998 and in the autumn 1998, with rapid symptom regression upon the administration of high dose corticosteroids. In April 1998, during the episode of staphylococcal sepsis, multiple nodose shadows of the lungs were detected, to persist asymptomatically for the next six months. Toward the end of November, nodal enlargement and disruption, with the formation of cavitations occurred. The patient's general condition deteriorated gradually, and she died from respiratory arrest in February 1999. The patient received corticosteroids during most of the disease course, and cyclophosphamide only once, during the first episode of lung edema. On autopsy, a number of cavitations were observed in the lungs, with necrotic areas of a varying size and numerous cicatrices in the rest of pulmonary parenchyma. Besides fibrosis and areas of necrosis, histology showed palisading granulomas, with erythrocytes, macrophages and siderophages within the alveoles. Apart from candidal colonization of the airways, which developed in the terminal stage of the disease, all tests for fungi, Staphylococcus aureus and Mycobacterium tuberculosis were repeatedly negative. ANCA and other immunoassays were also negative on several occasions. Differential diagnosis of multiple nodose lesions of the lungs is discussed. The authors believe the patient suffered from Wegener's granulomatosis.
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PMID:[Multiple nodose shadows of the lungs as a differential diagnosis problem]. 1693 41

Emergency plasma exchange therapy is life saving in many cases. Therefore, clinicians must be aware of the indications at which any delay in initiating therapy may prove to be fatal. Different hematological (Moschkowitz-, hyperviscosity- and catastrophic antiphospholipid syndrome; massive haemolysis [e.g Wilson's disease]), neurological (myasthenic), endocrine (thyrotoxicosis) and nephrological (rapidly progressive glomerulonephritis) crisis situations and for prevention of them; certain poisonings, fulminant liver failure, severe pancreatitis due to chylomicronaemia, meningococcus sepsis and iatrogenic or suicidal drug-overdose. In this latter, it is of fundamental importance that the protein binding of the drug should be high (>80%), whereas the volume of its distribution should be relatively low (<0,2 l/kg body weight) and the endogenous clearance of it should be less, than 500 ml/min. Urgent leukocytapheresis should be performed above 50.000 blasts/microl, in acute or chronic myeloid leukemia if symptoms of leukostasis are present (if blasts are above 100.000/microl, cytoreduction is mandatory even without symptoms). Similarly, urgent thrombocytapheresis should be administered above platelet numbers 1000 G/l, when there is concomitant thrombophilia or clinical symptoms of thrombostasis are present.
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PMID:[Indications of urgent plasma exchange and cytapheresis therapies--a review based on literature data and personal experience]. 1706 1

TLR4 is the receptor for the Gram-negative bacterial cell wall component LPS. TLR4 signaling is controlled by both positive and negative regulators to balance optimal immune response and potential sepsis. Unchecked TLR4 activation might result in autoimmune diseases, a hypothesis that has not been formally resolved. In this study, we found that TLR4 signaling to LPS can be positively enforced by expressing gp96 on cell surfaces through the chaperone function of, but not the direct signaling by, gp96; TLR4 as well as the commensal flora are essential for the production of anti-dsDNA Ab and the immune complex-mediated glomerulonephritis in transgenic mice that express surface gp96. Moreover, a similar constellation of autoimmunity was evident in mice that encode multiple copies of tlr4 gene. Our study has revealed that increased TLR4 signaling alone without exogenous insult can break immunological tolerance. It provides a strong experimental evidence for TLR4 dysregulation as an etiology of lupus-like renal disease.
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PMID:TLR4 up-regulation at protein or gene level is pathogenic for lupus-like autoimmune disease. 1708 2

Scabies is a worldwide disease and a major public health problem in many developing countries, related primarily to poverty and overcrowding. In remote Aboriginal communities in northern Australia, prevalences of up to 50% among children have been described, despite the availability of effective chemotherapy. Sarcoptic mange is also an important veterinary disease engendering significant morbidity and mortality in wild, domestic, and farmed animals. Scabies is caused by the ectoparasitic mite Sarcoptes scabiei burrowing into the host epidermis. Clinical symptoms include intensely itchy lesions that often are a precursor to secondary bacterial pyoderma, septicemia, and, in humans, poststreptococcal glomerulonephritis. Although diagnosed scabies cases can be successfully treated, the rash of the primary infestation takes 4 to 6 weeks to develop, and thus, transmission to others often occurs prior to therapy. In humans, the symptoms of scabies infestations can mimic other dermatological skin diseases, and traditional tests to diagnose scabies are less than 50% accurate. To aid early identification of disease and thus treatment, a simple, cheap, sensitive, and specific test for routine diagnosis of active scabies is essential. Recent developments leading to the expression and purification of S. scabiei recombinant antigens have identified a number of molecules with diagnostic potential, and current studies include the investigation and assessment of the accuracy of these recombinant proteins in identifying antibodies in individuals with active scabies and in differentiating those with past exposure. Early identification of disease will enable selective treatment of those affected, reduce transmission and the requirement for mass treatment, limit the potential for escalating mite resistance, and provide another means of controlling scabies in populations in areas of endemicity.
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PMID:Problems in diagnosing scabies, a global disease in human and animal populations. 1742 86

End-stage renal disease (ESRD), due to its high morbidity and mortality as well as social and financial implications, is a major public health problem. Outcome depends not only on different modalities of treatment like hemodialysis and peritoneal dialysis, but also on existing co-morbidities, age, duration on dialysis, supportive therapies and infection control strategies. Thus, a detailed study becomes necessary to improve health care delivery, provide medical care and to establish a geographical reference. The present study was undertaken to characterize the ESRD patients by their demographic and co-morbid conditions and relate this to the morbidity and mortality trends. The medical records of 110 ESRD patients seen over a five-year period (June 1995 to December 1999) in two tertiary-care hospitals in Riyadh, Saudi Arabia were studied retrospectively. There were 79 (64.5%) males and 31 (35.5%) females; their age ranged from 17 to 92 years (mean age 53.8 +/- 17.8 years). Diabetes was the commonest cause of ESRD seen in 26 (26.6%) followed by nephrosclerosis, unknown etiology, lupus nephritis, pyelonephritis and primary glomerulonephritis. Diabetes mellitus was the most prevalent co-morbidity seen during the study period and occurred in 65 patients (59%) followed by heart disease in 36 (32.7%), liver disease in 30 (27.3%), cerebrovascular accidents in 13 (11.8%) and neoplasm in 11 (10%). Seven (6.3%) patients only were smokers. Hemodialysis was the most frequent treatment choice as renal replacement therapy. Among the causes of hospitalization, cardiovascular conditions were the leading single cause (19.1%), followed by access related reasons and infections (11.5% each). The overall hospitalization rate was 11.2 days/year. The overall mortality rate was 8.07 deaths/year. The leading cause of death was cardiovascular in 15 (51.7%) followed by unknown/sudden death in eight (27.5%). Other causes of death included fluid overload, gastrointestinal hemorrhage, septicemia, liver disease and pulmonary embolism. Diabetes was the commonest co-morbid cause among the deceased. Old age, diabetes mellitus, prolonged duration on dialysis and cardiac diseases were the common causes of mortality. Our findings are consistent with worldwide reports. The study provides a reference data and will hopefully be helpful in improving the medical care.
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PMID:Morbidity and mortality in ESRD patients on dialysis. 1766 Jun 70

Renal transplantation is the optimal treatment for children with ESRD. We undertook this study to establish the outcome of pediatric renal transplants in a resource-constrained environment in a developing country. A retrospective analysis on 90 pediatric renal transplants (age at transplant </=18 yr) done at our center over a 15 yr period was analyzed. The mean age of the recipients was 15 yr (range 6-18 yr) accounting for 6.1% of all the renal transplants done at our center (90/1472). Ninety-six percent of patients received kidneys from live-related donors. The major causes of ESRD were glomerulonephritis (28%) and urological abnormalities (17%), while the etiology was unknown in 50%. Immunosuppression was based on a triple drug regimen consisting of prednisolone, CsA and azathioprine in 98% of children. Amongst complications, any acute rejection episodes (46.7%), UTI (26.7%) and CMV disease (16.7%) predominated. The mean duration of follow-up was 42 +/- 33 month (range 3-159 month). Graft loss occurred in nine (10%) children at a mean duration of 25 +/- 22 month (range 6-70 month). Overall 1-, 5-, and 10-yr graft survival was 98%, 84% and 76%. Overall 1-, 5-, and 10-yr patient survival was 95%, 87%, and 79%. The significant predictors of graft loss were CMV disease (p = 0.018) and >2 rejection episodes (p = 0.05), while sepsis (p = 0.01) was the most important contributor to patient loss. Pediatric renal transplantation in India can be accomplished successfully. The graft and patient survival in our study, the largest from India, is comparable to those published from developed countries and is encouraging given the limited resources.
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PMID:Pediatric renal transplantation--a single center experience of 15 yr from India. 1797 18

In a retrospective cohort of more than 4 million white and black male United States (US) veterans, we explored the role of specific prior autoimmune, infectious, inflammatory, and allergic disorders in the etiology of multiple myeloma (MM) and monoclonal gammopathy of undetermined significance (MGUS). Patients were selected from computerized inpatient discharge records at US Veterans Affairs hospitals. The analysis included 4641 patients (3040 white, 1601 black) and 2046 patients (1312 white; 734 black) with a discharge diagnosis of MM and MGUS, respectively. Using Poisson regression, we calculated age-adjusted relative risks (RRs) and 95% confidence intervals (CIs) for the relationship between MM, MGUS, and specific prior medical conditions. Significantly elevated risks of MM were associated with broad categories of autoimmune (RR, 1.15; 95% CI, 1.02-1.28), infectious (RR, 1.29; 95% CI, 1.20-1.38), and inflammatory disorders (RR, 1.18; 95% CI, 1.10-1.27) and specific prior autoimmune (polymyositis/dermatomyositis, systemic sclerosis, autoimmune hemolytic anemia, pernicious anemia, and ankylosing spondylitis), infectious (pneumonia, hepatitis, meningitis, septicemia, herpes zoster, and poliomyelitis), and inflammatory (glomerulonephritis, nephrotic syndrome, and osteoarthritis) disorders. Risks for MGUS were generally of similar magnitude. Our results indicate that various types of immune-mediated conditions might act as triggers for MM/MGUS development.
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PMID:Risk of multiple myeloma and monoclonal gammopathy of undetermined significance among white and black male United States veterans with prior autoimmune, infectious, inflammatory, and allergic disorders. 1823 85

Review of literature revealed no studies about the predominant causes and risk factors of acute renal failure in Jordan. This study identifies the most common causes of acute renal failure and the possible risk factors among hospitalized Jordanian population. A total of 111 patients were admitted to both King Abdullah University Hospital and Princess Basmah Teaching Hospital from December 2005 to April 2006 with a diagnosis of acute renal failure or developed acute renal failure in hospital during their stay. A written form was filled from the patients and their files. Results showed that 31.5% of patients were diabetic, 44.1% were hypertensive, and 40.5% had preexisting chronic renal failure. On admission, creatinine blood levels were high in 97 patients (87.4%), while at discharge, they were high in 61 patients (55%). Urgent dialysis was done for 20 patients (18%). In all, 95 patients (85.6%) were discharged home, and 16 patients (14.4%) died in hospital. Causes of acute renal failure included dehydration, diuretics, sepsis, contrast media, nonsteroidal anti-inflammatory drugs, glomerulonephritis, systemic lupus erythematosus, stones, and others. In conclusion, one-third of the causes of acute renal failure in this sample of hospitalized Jordanian patients were due to drugs, which makes this problem preventable. Mortality was affected by the age of patients and the duration of hospitalization.
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PMID:Etiologies of acute renal failure in a sample of hospitalized Jordanian patients. 1856 9

The term cardiorenal syndrome (CRS) increasingly has been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of heart-kidney interactions, we present a new classification of the CRS with 5 subtypes that reflect the pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction. CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g., acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS comprises chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing progressive chronic kidney disease. Type 3 CRS consists of an abrupt worsening of renal function (e.g., acute kidney ischemia or glomerulonephritis) causing acute cardiac dysfunction (e.g., heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g., chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction. Biomarkers can contribute to an early diagnosis of CRS and to a timely therapeutic intervention. The use of this classification can help physicians characterize groups of patients, provides the rationale for specific management strategies, and allows the design of future clinical trials with more accurate selection and stratification of the population under investigation.
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PMID:Cardiorenal syndrome. 2665 22

The term 'cardiorenal syndrome' (CRS) has increasingly been used in recent years without a constant meaning and a well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the CRS today includes 5 subtypes whose etymology reflects the primary and secondary pathology, the time frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can generally be defined as a pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical derangements, to make the rationale for management strategies and to design future clinical trials with accurate selection and stratification of the studied population.
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PMID:The cardiorenal syndrome. 1916 27


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