Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the clinical records between 1980-1989, there are 3,386 diagnosis of diseases, 34 percent of them were infections, the first great cause of diseases in ten years; the second cause was cardiovascular 16.3%. Infectious disease were localized in urinary tract 19%, Typhoid Fever 15%, pneumonia 11%, tuberculosis 8.5%, cellulitis 8.5%, Viral Hepatitis 8%, Brucellosis 5%, gastrointestinal Tract infections 5% and others 20%. It is necessary improve the epidemiological criteria in the practice of internal medicine, because the elevated numbers of infectious diseases that we are seeing in the Internal Medicina Section.
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PMID:[Incidence of infective diseases at an internal medicine service]. 184 Aug 47

Eighty-six patients received orthotopic cardiac transplants at the Royal Victoria Hospital in Montreal between 1985 and 1989. Of these, 16 mortally ill, being sustained in hospital by the intravenous administration of inotropic agents (15 patients [94%]) or intra-aortic balloon counterpulsation (6 [38%]). There was one early death (at 7 days), for a death rate of 6.3% (versus 8.6% for the 70 "elective" transplants). Two others died of delayed infection: one of viral hepatitis at 6 weeks, and one of pneumonia due to Pneumocystis 4 months after transplantation. The other 13 patients are alive and well 12 to 66 months postoperatively. Nine have returned to their preoperative work, three have decreased activity levels but are functioning well, and one is retired.
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PMID:Cardiac transplantation: treatment for cardiogenic shock. 186 88

This report described seventeen patients suffering from fulminant hepatitis and had a rapid fatal course. They were all residents of Southern Thailand. Fourteen cases were recognized between April and August which is the beginning of the rainy season in this part of the country. All age groups were found with males slightly predominant. Clinical manifestation presented with fever and later developed jaundice, convulsion and other central nervous system symptoms, liver failure and acute renal failure. Four cases had pneumonia and another three cases had pleural effusion. Laboratory investigations revealed hyperbilirubinemia, marked increase in serum transaminases, a variable alkaline phosphatase level and electrolytes derangement. HBsAg was positive in only two of fourteen cases. Blood cultures and serological examination for infections were unfruitful. Histopathological changes of the liver were classified into three types; type 1 massive hepatocellular coagulation necrosis; type 2 massive scattered hepatocellular necrosis and type 3 massive bridging hepatocellular necrosis. Electron microscopy of five cases revealed spherical viral-like particles ranging in size 70 to 90 nm in diameter, in the cytoplasm of liver cells. This is believed to be a unique type of fulminant hepatitis, possibly viral in origin, and were clinically and pathologically different from the previously described fulminant viral hepatitis.
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PMID:Fulminant hepatitis, possible virus origin: a report of seventeen cases in southern Thailand. 208 15

A quantitative histopathological method has been developed for the evaluation of the effects of hexachlorobenzene (HCB) on the pathogenesis of three virus infections in the mouse. Hexachlorobenzene was selected because a substantial amount of immunotoxicological data already exists with which we could compare our results. To establish the validity of the method a systemic virus infection (mouse cytomegalovirus, MCMV), a pneumonia causing virus (pneumonia virus of mice, PVM) and a hepatitis virus (mouse hepatitis virus, MHV) were used. We have compared the existing data with the actual pathological effects of hexachlorobenzene on virus disease processes, to gain a more realistic idea of the value of the risk assessment to be derived from extrapolating the in-vitro data in particular, to the in-vivo situation. The results show that the data derived from previous studies on the immunotoxicity of HCB were accurate in predicting the exacerbation of the viral hepatitis, especially in immunodeficient athymic 'nude' mice. It is proposed that this histopathological technique could be a useful technique in the evaluation of host resistance changes following exposure to potentially immunotoxic compounds, but caution will have to be exercised in interpretation in relation to human disease.
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PMID:Immunotoxic effects of hexachlorobenzene on the pathogenesis of systemic, pneumonic and hepatic virus infections in the mouse. 217 97

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41

We describe our experience in the treatment of acute liver failure in 620 patients who developed grade 3 or 4 encephalopathy between 1973 and June 1985. The principal aetiologies were paracetamol-induced hepatic necrosis, viral hepatitis, halothane hepatitis and idiosyncratic drug reactions. Cerebral oedema is a major cause of death in these patients and is most effectively treated with mannitol (20%). Renal failure occurs in between 30% and 75% of cases, depending on aetiology, and is most effectively managed by haemodialysis. Electrolyte and acid-base abnormalities are common. Haemodynamic abnormalities encountered include a high cardiac output, low peripheral vascular resistance, hypotension and venodilatation. Assisted mechanical ventilation is frequently required to treat hypoxia caused by pneumonia, atelectasis, haemorrhage and oedema. A coagulopathy is always present but coagulation factors and platelets are given only when the patient is clinically bleeding. These patients are prone to sepsis and this is a significant cause of death. Hypoglycaemia is common and must be actively and frequently sought. The use of charcoal haemoperfusion has been associated with improved survival, especially when it is started during the grade 3 phase of encephalopathy. Recently survival figures of between 47% and 60% have been achieved for patients with paracetamol-induced liver failure and hepatitis A and B. However the figure for non A non B hepatitis and halothane- and drug-induced liver failure are disappointing at around 15% and liver transplantation is being explored as a treatment option in these patients.
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PMID:Management of acute liver failure. 308 71

Results of a two-dose (150 vs 500 mg/kg/month) crossover study with intravenous immunoglobulin (Endobulin, Immuno) (IVIG) carried out on 12 children with primary immunodeficiency syndromes over a period of 2 years are reported. Eight children had received human plasma (20 mg/kg/month) during the 2 years prior to the IVIG study. As these children had been thoroughly monitored during plasma treatment, a retrospective analysis of these data allowed for comparison with IVIG treatment. Children on low-dose IVIG therapy had significantly (P less than 0.01) fewer days with clinical illness, e.g., sinusitis, pneumonia, diarrhea, and arthritis, than did those receiving plasma treatment. High-dose IVIG therapy led to further significant clinical improvement. Lung function tests (MEF25) improved significantly as well. The difference between high- and low-dose therapy with respect to the improvement in clinical symptoms (e.g., cold, fever, otitis) was more pronounced in children with severe clinical symptoms at the initiation of the study. Children with fewer symptoms did comparably well on high- and low-dose treatment, except for those with acute febrile illness, which was less frequent in children on high-dose IVIG. Regular monitoring of liver enzymes in the group of patients on IVIG therapy gave no indication of the transmission of viral hepatitis in the course of the 2-year IVIG treatment.
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PMID:Results of a prospective controlled two-dose crossover study with intravenous immunoglobulin and comparison (retrospective) with plasma treatment. 356 57

Dramatic haemolysis may accompany viral hepatitis and pneumococcal pneumonia in G6PD-deficient patients. Since red blood cells (RBCs) are richly endowed with receptors for activated complement, particularly C3b, we hypothesized that bulky, complement-activating immune complexes (IC) consisting of microbes and antibody might attract granulocytes (PMNs), facilitating oxidative 'innocent bystander' RBC damage. Indeed, opsonization with only two type-2 pneumococcus (PN3)/anti-PN3/C3b complexes per RBC caused agglutination of RBC, a phenomenon termed immune adherence. Addition of as few as one PMN per 20 opsonized RBCs caused the glutathione (GSH) levels of co-incubated G6PD-deficient RBCs to fall by 30% (from 3.5 to 1.8 +/- 0.8 mumoles GSH/g Hb) compared to identically incubated, but nonopsonized, G6PD-deficient RBCs. GSH levels remained normal (5.2 +/- 0.4 mumoles/g Hb) in PMN-exposed opsonized normal RBCs. GSH depletion in G6PD-deficient RBC was directly related to disease severity--falling a mean 33% in RBCs from two Black G6PD A- subjects but 59% in two Caucasian G6PD deficient RBCs. Prevention of C3b generation (with 10 mM EDTA) during opsonization abrogated both immune adherence and PMN-mediated GSH decline in oxidant-sensitive cells. Similarly, removal of C3b receptors by brief trypsin incubation of RBCs eliminated immune adherence and GSH decline. Thus, both phenomena are dependent on IC complement activation and subsequent binding of the bacterial IC to the RBC complement receptors. Although clearance of IC by RBCs may be beneficial in protecting other tissues from inflammatory damage, G6PD-deficient RBCs are vulnerable to oxidants generated by juxtaposed phagocytes--cells attracted to, and stimulated by, the immune complex/C3b combination. It is suggested that this 'Good Samaritan' activity of RBCs may lead to haemolysis during periods of exuberant antibody response to microbes.
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PMID:G6PD-deficiency infectious haemolysis: a complement dependent innocent bystander phenomenon. 370 64

Two cases of hypogammaglobulinemia (Bruton's syndrome) in brothers are described. Their sisters had no this disease. Pronounced changes in the lymph nodes, spleen and thymus typical for this condition were combined in both cases with lung and kidney malformations as well as with chronic pneumonia and inanition. The both boys have viral respiratory infections that followed by marked antibody formation and clear-cut structural alterations characteristic of different stages of these diseases. Besides this the older brother was found to have chronic viral hepatitis B with an unusual giant-cell reaction.
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PMID:[Features of the manifestations of bronchopulmonary pathology and hepatitis B in children with hypogammaglobulinemia]. 672 6

Disease secondary to heroin abuse constitutes a rarity in Spain. While there had been no previous cases in earlier years four young heroin addicts were admitted to the Hospital "1st de Octubre" for severe medical complications of their addiction within the last twelve months. Two patients were admitted in deep coma due to drug overdose, being cardiac arrhythmias and pulmonary edema the main associated complications. Cardiac rhythm disturbances are due to a heightened vagal tone, either secondary to inhibition of acetylcholine hydrolysis or to hypoxia, hypercapnia, and acidosis, factors that diminish cholinesterase activity and act synergistically to increase vagal tone. Pulmonary edema secondary to heroin overdose is non-cardiogenic and probably due to hypoxia added to the local action of heroin on the alveolocapillary membrane. The goal of therapy in such cases is to obtain an appropriate alveolar ventilation, the use of continuous positive pressure ventilation being required when there is pulmonary edema. The third patient had staphylococcal pneumonia with multiple abscess formation secondary to venous septic embolization originated peripherally where the drug was injected. Finally, the fourth patient was admitted because of a clinical and biochemical picture of HBsAg negative acute viral hepatitis, having suffered a similar clinical picture three years previously.
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PMID:[Severe medical sequelae in heroin addicts]. 720 89


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