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)

We retrospectively studied 42 patients hospitalized for Stevens-Johnson syndrome at the Veterans General Hospital-Taipei between 1979 and 1991. Twenty-seven patients were males and 15 females; the ages ranged from 7 months to 82 years old with a mean age 50. The most common precipitating factor was drugs among which diphenylhydantion was the leading offender followed by nonsteroidal anti-inflammatory agents and allopurinol. Sixteen cases might be etiologically associated with infection, including 13 with upper respiratory infection, one with acute hepatitis B, one with pulmonary tuberculosis, and one with fever of unknown origin that was suspected to be viral infection. Although mycoplasma infection was thought in the literature to be a common etiologic factor of Stevens-Johnson syndrome, it was scarcely found in our study. Four patients were not treated with systemic steroids but still recovered uneventfully. Systemic steroid as a whole was not proved to be necessary, but early large-dose steroid therapy might abbreviate the course of the disease. The mortality rate was 11.9% which differs unremarkably from the reported rate (5-15%). Two patients died of pneumonia with sepsis, one of hemorrhagic shock (bleeding of adenocarcinoma of stomach), one of aspiration pneumonia, and one of sepsis with disseminated intravascular coagulation, upper gastrointestinal bleeding, and hyperglycemic hyperosmolar nonketotic coma.
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PMID:[Stevens-Johnson syndrome: a review of 42 cases]. 849 Jul 98

In ischemic hepatitis, which is not rare, there is a marked but transient increase in serum aminotransferase activity to at least 20 times the upper limit of normal, without any other cause for hepatic necrosis. It is generally preceded by an acute cardiac complication, usually pulmonary edema or a tachyarrhythmia, causing decrease in cardiac output, or may follow acute respiratory failure. The typical histological lesion is centrilobular hepatic necrosis. We present 2 cases of ischemic hepatitis due to hypotension following rapid atrial fibrillation, sepsis and acute respiratory failure, highlighting the different etiologies, laboratories results, and the relative benign course, described in the literature. The patients were a woman aged 80 and a man aged 76. Awareness of the place of this disorder in the differential diagnosis of acute hepatitis may save needless, dangerous investigations.
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PMID:[Ischemic hepatitis]. 884 54

As with most liver diseases, the symptoms of hepatitis in dogs are nearly always aspecific: the dogs eat less, are apathetic, sometimes have polyuria/polydipsia, and sometimes have diarrhoea. Hepatoencephalopathy and ascites only occur with these symptoms in very advanced stages of chronic hepatitis. Only a part of the dogs have jaundice. Because of these aspecific symptoms, the diagnosis hepatitis is often not taken into consideration, even though the presence of a liver disease can be easily detected by measuring plasma concentrations of alkaline phosphatase and bile acids, one or both of which are elevated. The diagnosis is confirmed by histological examination of a liver biopsy sample. The most common forms of hepatitis are non-specific reactive hepatitis, acute hepatitis, and chronic hepatitis. Non-specific reactive hepatitis is a reaction against endotoxin as a result of sepsis or an increased gastrointestinal absorption. Treatment is directed to the primary process. Leptospirosis also causes non-specific reactive hepatitis, but then renal insufficiency is the most prominent feature. The diagnosis is made not on the basis of a liver biopsy but on the basis of increased IgM titres against Leptospira. Immediate treatment with antibiotics and infusions at the first signs (jaundice and uraemia) can save the animal's life. Acute hepatitis can develop as a result of infection, toxins, or liver hypoxia. There is no specific treatment, but adequate recovery often occurs with supportive treatment. Corticosteroids are contraindicated. Chronic hepatitis, which can lead to cirrhosis, is the most common form of hepatitis. It is an autoimmune inflammatory reaction that is usually caused by a virus infection but sometimes by poisoning (intoxication). Long treatment with prednisolone or azathioprine is usually successful, but early recognition of the disease increases the likelihood of success. Nowadays, chronic hepatitis due to hepatic copper accumulation in Beddlington terriers can be detected by DNA tests. Such tests make it possible to distinguish between carriers and non-carriers. Affected animals can be kept symptom-free by life-long treatment with zinc gluconate or penicillamine.
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PMID:[Hepatitis in dogs; a review]. 958 48

Acute hepatic failure (AHF) in India almost always presents with encephalopathy within 4 weeks of the onset of acute hepatitis. Further subclassification of AHF into hyperacute, acute and subacute forms may not be necessary in this geographical area, where the rapidity of onset of encephalopathy does not seem to influence survival. Viral hepatitis is the cause in approximately 95-100% of patients, who therefore constitute a more homogeneous population than AHF patients in the West. In India, hepatitis E (HEV) and hepatitis B (HBV) viruses are the most important causes of AHF; approximately 60% of cases are caused by to these viruses. Hepatitis B virus core mutants are very important agents in cases where hepatitis B results in AHF in this country. Half of the patients with AHF admitted to our centre are female, one-quarter of whom are pregnant. Therefore, pregnant females who contract viral hepatitis constitute a high-risk group for the development of AHF. However, the outcome of AHF in this group is similar to that in non-pregnant women and men. No association with any particular virus has been identified among sporadic cases of AHF. In our centre, approximately one-third of AHF patients survive with aggressive conservative therapy, whereas two-thirds of deaths occur within 72 h of hospitalization. Cerebral oedema and sepsis are the major fatal complications. Both fungal and gram-negative bacteria are major causes of sepsis. Among patients with AHF, despite the presence of sepsis, its overt clinical features (i.e. fever, leucocytosis) may be absent and objective documentation of the presence of sepsis in such patients is achieved by repeated culture of various body fluids. It should be possible to develop simple, clinical prognostic markers for AHF in this geographical region, in order to identify patients suitable for liver transplantation.
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PMID:Acute hepatic failure in India: a perspective from the East. 1084 29

Acute hepatitis is a common disease of young adults worldwide. Mortality is generally low, as most cases are self-limiting. Fatality does occur in a few and certain factors are responsible. A retrospective review and analyses of complications contributing to deaths due to acute hepatitis (AH), in hospitalised patients, over a five-year period, at the University College Hospital, Ibadan, Nigeria, is here presented. Mortality was very high at 48%. This was much higher than the overall mortality recorded in the hospital during the same period. Liver failure was the commonest complication associated with mortality and was present in all the patients. Other complications which may have contributed to mortality in acute hepatitis were, gastrointestinal haemorrhage(39%), acute renal failure(22%), disseminated intravascular coagulopathy(12%), sepsis(17%), anaemia(17%), hypovolaemic shock(17%), sickle cell hyperhaemolytic crisis(11%), and hypoglycaemia(6%).
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PMID:Complications contributing to mortality in acute hepatitis at the University College Hospital, Ibadan, Nigeria. 1180 12

We report an 18-year-old boy with severe acute pancreatitis developing during acute hepatitis E and complicated by sepsis and acute renal failure. The patient recovered on supportive management.
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PMID:Severe acute pancreatitis in acute hepatitis E. 1187 40

Research on the free radical gas, nitric oxide (NO), during the past twenty years is one of the most rapid growing areas in biology. NO seems to play a part in almost every organ and tissue. However, there is considerable controversy and confusion in understanding its role. The liver is one organ that is clearly influenced by NO. Acute versus chronic exposure to NO has been associated with distinct patterns of liver disease. In this paper we review and discuss the involvement of NO in various liver diseases collated from observations by various researchers. Overall, the important factors in determining the beneficial versus harmful effects of NO are the amount, duration, and site of NO production. A low dose of NO serves to maximize blood perfusion, prevent platelet aggregation and thrombosis, and neutralize toxic oxygen radicals in the liver during acute sepsis and reperfusion events. NO also demonstrates antimicrobial and antiapoptosis properties during acute hepatitis infection and other inflammatory processes. However, in the setting of chronic liver inflammation, when a large sustained amount of NO is present, NO might become genotoxic and lead to the development of liver cancer. Additionally, during prolonged ischemia, high levels of NO may have cytotoxic effects leading to severe liver injury. In view of the various possible roles that NO plays, the pharmacologic modulation of NO synthesis is promising in the future treatment of liver diseases, especially with the emergence of selective NO synthase inhibitors and cell-specific NO donors.
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PMID:Nitric oxide in liver diseases: friend, foe, or just passerby? 1207 81

The seminar on maternal morbidity and mortality in the Philippines held in 1991 is described. The objective of the meeting was to define the status of women's health in the country and to prepare for a more comprehensive and developed implementation of local reproductive health services. The seminar honored the International Day of Action for Women's Health. Maternal mortality statistics show a rate of 1.1.1000 live births since 1988 vs. 2.1/1000 live births in 1980. Maternal mortality is greater among young 1st time mothers, among those with 5 children, and among those 40 years regardless of the number of children. Obstetric deaths account for 85% of all maternal deaths. The common causes in 1985-89 were hemorrhage, infection, and hypertensive disorders. Pulmonary disease and acute hepatitis account for indirect obstetric mortality. The prior period from 1984 to 1985 in Manila showed the leading causes to be puerpural sepsis, septic induced abortion, postpartum hemorrhage, and eclampsia. In Manila 33% deliver at home. 65% of hospital emergency cases involve women without prenatal care, and 1 out of 4 are dying upon admission and 1 out of 5 die within 5-6 hours. 58% died within 2 days after admission. 80% of these deaths were preventable. Lack of health education and inadequate diet due to poverty account for a major predisposing role. Confounding factors are anemia, tuberculosis, and parasitism. Broad risk factors are the inadequacy of health services and socioeconomic conditions. Proposals to reduce maternal mortality by 50% include focusing health programs on both mother and child, improving knowledge about prenatal care, improving the quality of prenatal care, and improving the quality of family planning (FP) services. Medical institutions need to maintain adequate supplies of equipment and supplies. Statistics and research are needed. Contraception for the health of the child was proposed as the appropriate tool for acceptance of FP. Competition for funds was a problem. Problems were also identified as the power imbalance between the sexes. High risk screening was recommended at the local level by the health worker. Workshops were formed and issues were identified, recommendations made, activities described, and the government and nongovernmental responses given.
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PMID:The perils of motherhood. 1228 38

A neonate presenting to the emergency department can present a challenge to even the most experienced clinician. This article has focused on four deceiving and potentially devastating neonatal diseases. 1. Neonatal herpes is a potentially devastating illness without pathognomonic signs or symptoms. Early recognition and therapy can reduce mortality markedly. Although no specific sign or symptom is diagnostic,the diagnosis should be strongly considered in the presence of HSV risk factors, atypical sepsis, unexplained acute hepatitis, or focal seizure activity. Acyclovir therapy should be initiated before viral dissemination or significant CNS replication occurs. 2. Pertussis is a disease in which infants are at greatest risk of death or severe complication. Neonatal pertussis often presents in an atypical manner, lacking the classic signs and symptoms such as the "whoop."More common signs and symptoms include cough, feeding difficulty,low-grade fever, emesis, increasing respiratory distress, apnea, cyanosis,and seizures. Management should include hospitalization, supportive care, and antibiotics. 3. Congenital heart defects, particularly ductal-dependent lesions, may have an initial asymptomatic period that culminates in a rapidly progressive and fatal course. A neonate with CHD presents with shock refractory to volume resuscitation or pressor support. Resuscitative efforts are ineffective unless PGE, is administered. 4. Inborn errors of metabolism often are unsuspected because of their protean and heterogeneous nature. Signs and symptoms are subtle,are nonspecific, and often mimic other, more common diseases.An elevated index of suspicion, along with application and correct interpretation of a select few laboratory tests, is the key to making a diagnosis. Therapy is relatively straightforward and focused on resuscitation followed by prevention of catabolism and correction of specifically identified abnormalities. Although these disorders are relatively uncommon, prompt diagnosis and therapy can lead to a decrease in morbidity and mortality. The key is to maintain a high index of suspicion.
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PMID:Unsuspected neonatal killers in emergency medicine. 1547 77

Liver disease is a well-known cause of early morbidity and mortality affecting 80% of patients receiving allogeneic bone-marrow transplantation (BMT). Drug toxicity, veno-occlusive disease (VOD), acute graft-versus-host disease (GVHD), and fungal, bacterial, and viral infections are the most frequent hepatic complications during this period. The aim of this retrospective study was to determine the prevalence and etiology of liver disease and its impact on mortality as well as to assess the predictive value of pre BMT hepatic biochemical tests on the subsequent occurrence of acute and/or chronic GVHD and patient mortality. Of a total of 236 patients who underwent allogeneic BMT, 82 were analysed. Liver dysfunction was found in 88%. The causes of liver disease were: acute GVHD, 40.2%; chronic GVHD, 15.9%; unknown, 9.8%; sepsis, 7.3%; hepatotoxicity, 6.1%; VOD, 3.7%; acute hepatitis and disease recurrence, 2.4%. The mortality rate was 37%. We found acute liver failure (ALF) in 10% of the deaths (8 patients). The causes of ALF in these cases were acute GVHD progression in 5, herpetic hepatitis in 1, disease recurrence in 1, and VOD in 1. The correlation coefficients indicating positive predictive values of pre BMT hepatic biochemical tests for the subsequent occurrence of acute GVHD, chronic GVHD, and mortality were 0.27, 0.14, and 0.43, respectively. There was no significant difference between patients with abnormal or normal pre BMT liver function tests in the frequency of acute and chronic GVHD or mortality.
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PMID:[Liver dysfunction in recipients of hematopoietic stem cells. Impact on mortality]. 1607 3


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