Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolism of thyroid hormones is accelerated during acute infection in man and in experimental animals. The pathogenetic mechanisms mediating this phenomenon are uncertain, but activated leukocytes of the infected host have been implicated as potentially important sites of hormone degradation. The present studies were conducted in an attempt to assess the in vivo contribution of leukocytes and peripheral leukocytosis to the enhancement of L-thyroxine (T4) clearance seen during infection, and to evaluate further the possible roles of fever and of changes in the extracellular binding of T4. In 10 rhesus monkeys inoculated with virulent yellow fever (YF) virus, peripheral disposal of T4 was significantly accelerated (2-fold) during the febrile phase of the illness. This experimental viral infection was not accompanied by neutrophilic leukocytosis nor by detectable changes in serum free T4 levels, suggesting that neither an increased circulating neutrophil mass nor diminished extracellular binding of T4 contributed appreciably to the increase in metabolism of T4. A pathogenetic role for fever in the enhancement of T4 degradation was not specifically excluded in these infected monkeys. However, the failure of T4 turnover to increase during other febrile infections, such as that which followed inoculation of monkeys with Venezuelan equine encephalitis virus, indicates that the acceleration of peripheral disposal of T4 seen in infection is not a simple concomitant of fever. In monkeys with bacterial sepsis and in those inoculated iv with zymosan particles, T4 turnover was similarly accelerated in the absence of detectable changes in serum free T4 levels, suggesting a pathogenetic role for enhances cellular uptake and metabolism of hormone. However, in these monkeys deiodination of T4 by leukocytes did not appear to account for the increase in T4 disposal. During sepsis and following zymosan administration, T4 turnover was markedly increased in both intact monkeys with a neutrophilic leukocytosis and in those with irradiation-induced neutropenia. Therefore, the cellular sites of increased T4 degradation during infection remain uncertain. Fixed tissue macrophages serve as the major site of clearance of YF virus, circulating bacteria and zymosan particles. Accordingly, a relationship between activation of these phagocytic cells and the acceleration of T4 metabolism seemed possible but was not established by our studies.
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PMID:Accelerated host metabolism of L-thyroxine during acute infection: role of the leukocyte and peripheral leukocytosis. 23 22

A male infant and a three year old girl, both with acute febrile illness, were admitted to our hospital for suspected meningitis/sepsis and gastroenteritis/severe viral infection, respectively. Both showed all six principal features of Kawasaki syndrome and revealed several other symptoms and laboratory findings commonly associated with the disease. The infant had multiple coronary aneurysms. The girl developed ascites, pancreatitis and iritis, all of which are seldomly recognized symptoms of the Kawasaki syndrome. The prompt and satisfactory therapeutic responses of both patients to the combined therapy consisting of oral acetylsalicylic acid (50-100 mg/kg b.w./d) and intravenous gamma-globuline (400 mg/kg b.w./d) at the eight and even eleventh day of illness support the use of gamma-globuline therapy beyond the first week of the disease. Prior to their illnesses both children had been exposed to carpet shampoo, an agent which has been repeatedly associated with an increased risk of Kawasaki syndrome.
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PMID:[Kawasaki syndrome. Association with exposure to carpet shampoo and successful therapy with immunoglobulins in the second week of the illness]. 161 54

Serum and/or cerebrospinal fluid (CSF) alpha interferon (aIFN) levels were determined in 31 neonates hospitalized for suspected sepsis. Final diagnosis was bacterial sepsis in 15, viral infection in 13 and no infection in 3. Among the 13 neonates with viral infection, enterovirus was isolated 5 times and coxsackievirus 4 times. No aIFN was found in cerebro-spinal fluid and/or serum among the neonates with bacterial sepsis or without infection. By contrast, in neonates with viral infection, CSF and/or serum aIFN levels were always elevated except in one case in which serum aIFN determination was not available. We conclude that in neonates, elevated levels of CSF and serum aIFN appear to be specific of viral infection, and that this might be helpful in the differential diagnosis of suspected sepsis.
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PMID:[Viral infection in the neonatal period: diagnostic difficulties, the role of interferon alpha levels]. 166 55

In the immunocompromised patient, even mild forms of any combination of headache, meningismus, altered mental status, or focal neurologic signs should initiate an evaluation for possible CNS infection. The limited signs and symptoms of acute CNS infection are not due to specific organisms but to pathologic changes at the neuroanatomic site of infection. The initial clinical history, examination, laboratory, and neuroradiographic data will narrow the problem to one of several groups of agents, although it may not be possible to specify a single causative agent. It should be remembered that several concurrent infections (i.e., CMV and toxoplasmosis, aspergillosis, and bacterial sepsis) may be present. Thus, the clinician should rely on broad antibiotic coverage appropriate to the suspected causative agent or agents at the site of infection. It may be necessary to offer broad-spectrum antibiotic coverage for a CSF presentation that is subsequently found to result from a viral illness or from a noninfectious cause. However, one should avoid undertreating those infections for which specific therapy can be offered, and broad-spectrum treatment usually will not be regretted. Uncertainty in diagnosis following noninvasive procedures should lead to a brain biopsy. Although many of the infections discussed in this article have a poor prognosis, some of the most common pathogens, such as Cryptococcus, Listeria, and Toxoplasma, have effective specific therapies to which the patient should have access as rapidly as possible. The clinician who has successfully treated a patient with CNS infection should remain vigilant for late sequelae or recurrence of infection. Chronic treatment of some infections, such as toxoplasmosis or aspergillosis, may be necessary. The reintroduction of steroids for the treatment of an underlying cancer may reactivate previously treated disease, such as cryptococcosis, and periodic CSF surveillance is appropriate under these circumstances. Recurrence of the symptoms should raise the suspicion of recurrent or new infection, and the patient also should be evaluated with CT or MRI for the development of hydrocephalus or for new metastatic disease. In patients who have had varicella-zoster infection, postherpetic neuralgia and delayed arteritis may develop. Seizures, hearing loss, and neuropsychologic sequelae may follow any meningoencephalitis. The patient should always be reevaluated for the possibility of infection with a different opportunistic organism. CNS infections remain a major cause of morbidity and mortality in immunosuppressed patients with malignancies. In one series, 60% of such patients died as a result of their CNS infection, many at a time when the underlying disease had an otherwise good prognosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system infections in cancer patients. 175 29

Twenty-five pediatric orthotopic liver transplantations (OLTs) performed in 22 patients at Sainte-Justine Hospital were reviewed for infections complications. One patient died within 12 hours posttransplantation and is excluded. The patients had an average age of 6.1 years (range, 1.25 to 19 years) and an average weight of 20.4 kg (range, 11 to 55 kg). Two patients (9%) were cytomegalovirus (CMV) seropositive and 9 of 19 patients (48%) were Epstein-Barr virus (EBV) seropositive preoperatively. Five of the donors (20%) were CMV seropositive. The most common indications for OLT were biliary atresia (8) and tyrosinemia (7). There were 4 deaths, for an overall mortality rate of 19%. In 3 patients, deaths were related to infection (CMV hepatitis and duodenitis with aortoduodenal fistula, adult respiratory distress syndrome [ARDS] with Streptococcus viridans pneumonia, Escherichia coli cholangitis with progressive hepatic failure). Fifteen patients (72%) had 41 major infections, most of them bacterial, during the first month posttransplantation. These include pneumonia (25%), line sepsis (17%), cholangitis (14%), and tracheitis (14%). There was only one major viral infection, a CMV hepatitis that occurred in the first month posttransplantation. Three patients had fungal infections (8%) associated with hepatic artery thrombosis and recurrent cholangitis. All three patients required retransplantation. There was only one protozoal infection (Pneumocystis carinii pneumonia) causing life-threatening respiratory failure, from which patient recovered without sequelae. Infection still remains a serious complication of OLT. Bacterial infection is common and is usually associated with technical complications. The low rate of CMV infection is related to low incidence of CMV in the donor pool and the minimal use of strong immunosuppressants.
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PMID:Infectious complications of pediatric liver transplantation. 191 82

At the height of the United Kingdom influenza A epidemic in December 1989, three children receiving treatment for non-T cell acute leukaemia developed pancytopenia with concomitant influenza A infection. Bone marrow histology showed prominent marrow erythrophagocytosis by morphologically mature histiocytes, consistent with the picture of virus associated haemophagocytic syndrome (VAHS). In two cases there was an initial spontaneous recovery, though recurrence of VAHS developed in one case in association with a different viral infection (cytomegalovirus) following autologous bone marrow transplantation. The third child died from cardiorespiratory failure secondary to infection with influenza A and Klebsiella pneumoniae sepsis. It is suggested that influenza A should be added to the list of infective causative agents.
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PMID:Influenza A and the virus associated haemophagocytic syndrome: cluster of three cases in children with acute leukaemia. 203 Jan 47

The preparation, pharmacokinetics, clinical uses, dosage and administration, and adverse effects of intravenous immune globulin (IVIG) are reviewed. IVIG, which consists primarily of immunoglobulin G (IgG), is initially prepared from pooled human plasma by using the Cohn-Oncley fractionation procedure. Secondary treatments render the preparation suitable for i.v. use. The specific antibody content of IVIG depends on the geographic location of the plasma donors, the product, and the product lot. The metabolism of IgG appears to follow a multicompartmental, first-order process. The half-life of IgG is dependent on the half-lives of the IgG subclasses; three of the four subclasses have half-lives in the range of 23-25 days. IVIG is indicated in the treatment of idiopathic thrombocytopenic purpura (ITP) and as replacement therapy in primary humoral immunodeficiencies (PHI). IVIG has also been used for antimicrobial prophylaxis in bone marrow transplant and burn patients and in patients with malignancies. Patients with HIV infection, cystic fibrosis, neonatal sepsis, and respiratory syncytial virus infection may also benefit from prophylaxis or treatment with IVIG. The recommended dosage of IVIG in ITP is 400 mg/kg/day for two to five days. For the treatment of PHI, the usual dosage is 100-400 mg/kg every three or four weeks. Adverse reactions are often mild and are usually related to the infusion rate. Intravenous immune globulin is a valuable therapeutic tool in several immunodeficiency and autoimmune states, but IVIG products are expensive, and conclusive data on their efficacy in the treatment of many disorders remain to be obtained.
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PMID:Clinical uses of intravenous immune globulin. 229 73

For arthritis or arthralgia there is no simple system for diagnostic analysis, but whether it is polyarthritis or monoarthritis, acute or chronic in onset, some general rules apply. Common causes include osteoarthritis (primary and secondary) and viral infection. Drugs should be considered, including those inducing gout. It is still imperative not to miss rheumatic fever, sepsis and tuberculosis in assessment. We may encounter more cases of Lyme disease presenting as arthritis.
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PMID:Arthralgia: a diagnostic strategy. 224 64

Peripartum cardiomyopathy is a syndrome of undetermined etiology whose most common initial symptoms are those of congestive heart failure. The syndrome carries a five-year mortality estimated at 40%. Single noxious factors, such as viral infection, have been proposed as direct precipitants of this syndrome, but none have been conclusively linked to it. The cases of two patients with identifiable cardiac stress factors who developed peripartum cardiomyopathy are presented here: one with sepsis complicated by disseminated intravascular coagulopathy and severe anemia, and a second with an otherwise normal pregnancy who engaged in strenuous aerobic exercise throughout the last trimester. A review of previously published cases reveals the frequent association of multiple nonspecific cardiac stress factors that may predispose women to peripartum cardiomyopathy. Various cardiac stress factors may act synergistically with the stress of pregnancy to precipitate peripartum cardiomyopathy in susceptible women.
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PMID:Peripartum cardiomyopathy. A role for cardiac stress determinants other than pregnancy? 252 36

Cytomegalovirus (CMV) infection involving the skin in three transplant patients is presented. Patient 1, whose infection apparently was localized only to a cutaneous wound induced by extravasated ionotropic solution, survived. Mixed CMV and Candida infections developed in patient 2 in the cutaneous ulcer. He died of disseminated herpes simplex virus infection in two weeks. Patient 3 had CMV pneumonia and purpuric maculopapular eruption. He died of Pseudomonas sepsis 17 weeks later. Eighteen cases with CMV skin lesions are reported in the English literature. The clinical findings and the outcome of the current and the reported cases are analyzed. All patients were immunocompromised. CMV infection, when detected in the skin, appears to be associated with grave prognosis. Seventeen of 20 patients whose final outcome was recorded died within six months after the onset of CMV skin lesions. The outcome of one case is unknown. The mortality was 85%. The fatal cases had either concurrent disseminated CMV infection or mixed cutaneous or systemic infections. When the infection is localized in the skin wounds, the prognosis seems fairly good. All three such patients survived.
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PMID:Cytomegalovirus infection involving the skin in immunocompromised hosts. A clinicopathologic study. 254 21


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