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)

The dynamics in schoolchildren's health status varies in time, as the incidence of some chronic diseases decreases and that of the others increases. As a result, the health status of schoolchildren has deteriorated due to a reduction in the number of healthy children and an increase in the number of chronic patients in the past 30 years. Nervous, immune (allergic), and blood diseases have become frequent. Chronic ENT diseases have been encountered more infrequently due to the noticeable reduction in the incidence rates of tonsillitis and otitis. The positive trend is that schoolchildren have no rheumatism, infective allergic myocarditis, chronic pneumonia and diffuse glomerulonephritis and that the prevalence of locomotor disorders, renal and metabolic (obesity) diseases is low. During school time, the health status of children slightly improves due to the lower incidence rates of chronic diseases and the higher proportion of healthy children, but it has remained still worse than it was 30 years ago. The formation of chronic diseases has been found to occur in health group II children, who have morphological and functional changes, in 50% of cases from the first to the sixth forms and in 20% of cases from the seventh to the tenth forms. The present-day children are characterized by a combination of abnormalities and functional disturbances. This all require active and timely prophylactic measures to block chronization at the premorbid stage. Lifestyle (to keep the hygienic school regime, to do exercises and to go in for sports), sociohygienic conditions and genetic factors have profound effects on the health status.
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PMID:[The health status dynamics of schoolchildren and the importance of biomedical factors in its development]. 768 98

Anti-neutrophil cytoplasmic antibody (ANCA) determinations appear to be useful in the diagnostic evaluation and therapeutic monitoring of patients with necrotizing vasculitis. The purpose of this study was to determine whether semiquantitative ANCA measurements are useful in distinguishing between increases in primary disease activity and complications of cytotoxic or immunosuppressive therapy. The authors reviewed clinical data from 27 consecutive ANCA-positive patients who had at least three ANCA determinations performed at the University of Michigan Medical Center. Eleven patients had Wegener's granulomatosis (WG), 3 had "limited" WG; 9 had "ANCA-positive" vasculitis; and 4 had "pauciimmune" rapidly progressive glomerulonephritis. During a period of 3 months to 3.8 years, 159 ANCA determinations were performed, primarily for the purposes of diagnosis and monitoring disease activity. Eleven episodes were identified in which a single ANCA assay was used to distinguish between increased primary disease activity and a suspected therapeutic complication. The suspected therapeutic complications included pneumonia (8 of 11), bacterial sinusitis (1 of 11), cyclophosphamide-induced pneumonitis (1 of 11), and cyclophosphamide-induced vestibular toxicity (1 of 11). In 10 of 11 instances in which an ANCA assay was used to distinguish between an exacerbation in vasculitic disease activity and a therapeutic complication, interpretation of the ANCA titer was pivotal in arriving at a therapeutically appropriate decision either to increase or discontinue cytotoxic therapy. This study suggests that ANCA determinations can be used reliably to distinguish between increased primary disease activity and complications of therapy that mimic an increase in disease activity.
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PMID:Use of anti-neutrophil cytoplasmic antibody assay to distinguish between vasculitic disease activity and complications of cytotoxic therapy. 794 22

The present study addressed the causal role of Aleutian mink disease parvovirus (ADV) in acute interstitial pneumonia in mink kits. All the examined isolates of ADV caused interstitial pneumonia in newborn kits, although the severity of disease and the mortality varied. These findings indicate that ADV is the direct causal agent of this disease in mink kits and that cofactors, which could have been present in the original ADV-K isolate, do not play a role. Acute interstitial pneumonia characterized by hypertrophy and hyperplasia of alveolar type II cells, intranuclear viral inclusions, interstitial edema, and hyaline membrane formation was experimentally reproduced in mink kits infected as newborns with five different isolates of ADV. Four hundred forty-nine newborn mink kits were included in the study, of which 247 were necropsied. The lesions caused by the different isolates were indistinguishable by histopathologic examination, but the incidence (50-100%) and severity (mortality of 30-100%, n = 218) of disease among the mink kits varied. Also, the content of ADV antigens in the lungs of infected kits varied among the groups. According to these features, the examined isolates could be placed in groups of high and low virulence. ADV-K, ADV-Utah I, and ADV-DK were in a highly virulent group producing a mortality of 90-100% (n = 110) in mink inoculated as newborns. ADV-GL and ADV-Pullman belonged to a group of low virulence, with an incidence of clinical disease of 50-70% and a mortality of approximately 30-50% (n = 118) in kits inoculated as newborns. The mortality in the control group receiving a mock inoculum was around 12% (n = 34). The period from infection to development of fatal disease varied from approximately 12 days for the highly virulent isolates up to around 20 days for the isolates of low virulence. The 107 mink kits that survived inoculation with ADV as newborns developed lesions typical of classical Aleutian disease irrespective of the ADV isolate used. The lesions consisted of chronic immune complex-mediated glomerulonephritis and infiltrations with mononuclear cells, including plasma cells in lung, liver, spleen, kidney, mesenteric lymph node, and intestine. Surviving kits also had hypertrophy of the bronchus-associated lymphoid tissue and focal subpleural, intraalveolar accumulations of large cells with foamy cytoplasm, so-called lipid pneumonia.
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PMID:Acute interstitial pneumonia in mink kits inoculated with defined isolates of Aleutian mink disease parvovirus. 820 85

Side effects due to azathioprine (the nitroimidazole derivative of 6-mercaptopurine) can be classified as toxic (myelosuppression, hepatotoxicity) and idiosyncratic (fever, rigors, arthralgias, pneumonitis, and gastrointestinal symptoms). While the toxic effects are due to 6-mercaptopurine, the hypersensitivity reactions are believed to be caused by the nitroimidazole moiety. A 21-year-old male patient developed end-stage renal failure due to antiglomerular basement membrane (AGBM) disease (rapidly progressive glomerulonephritis with linear immunoglobulin G deposits and positive circulating AGBM antibodies). The patient became dependent on continuous ambulatory peritoneal dialysis and, later, hemodialysis, and received two renal allografts at the ages of 23 and 27 years. He received three courses of azathioprine treatment: one course for AGBM glomerulonephritis and two courses for rejection episodes. Each course was followed within 4 to 7 days by symptoms compatible with Goodpasture's syndrome, ie, high fever, rigors, arthralgias, diarrhea, myalgias, and pulmonary infiltrates with hemoptysis. All signs and symptoms always resolved completely on discontinuation of azathioprine. During the treatment for rejections, AGBM antibodies were not elevated, and during one episode AGBM disease in the lung (Goodpasture's syndrome) was excluded by open lung biopsy. Treatment of a subsequent rejection episode with 6-mercaptopurine was well tolerated. We conclude that azathioprine hypersensitivity can mimic the pulmonary manifestations of Goodpasture's syndrome. Hypersensitivity probably is due to the nitroimidazole moiety of azathioprine. Thus, differential diagnosis of Goodpasture's syndrome (and probably of any "pulmonary renal syndrome") should include azathioprine hypersensitivity.
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PMID:Azathioprine hypersensitivity mimicking Goodpasture's syndrome. 820 72

The first symptoms of immunooseous dysplasia were growth retardation and myopia. Nephrotic syndrome was diagnosed at the age of 8 years. Skeletal roentgenograms showed spondyloepiphyseal dysplasia. In the renal biopsy there was nodular accumulations of PAS-positive hyaline material at the base of the granular stalks. There was lymphopenia with decreased CD4 and CD8 subpopulations. The condition of the patient gradually worsened until she died unexpectedly at 10 years with clinical symptoms of encephalitis. Autopsy documented cytomegaloviral pneumonia and advanced mesangioproliferative glomerulonephritis. In the spleen there was PAS-positive hyaline material massively infiltrating the walls of the central arterioles of the splenic follicles. There was marked depletion of lymphocytes in the spleen and in lymph nodes. The differential diagnosis of immunooseous dysplasia in the framework of spondyloepiphyseal dysplasia is discussed.
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PMID:Spondyloepiphyseal dysplasia with nephrotic syndrome (Schimke immunoosseous dysplasia). 820 84

A colony of sphha/sphha mice with congenital hemolytic anemia and an abnormality in erythrocyte spectrin assembly was screened to determine the cause of premature death. Sphha/sphha mice have decreased life span, with 50% of animals dying by 6 months of age. The phenotype of these mutant mice includes moderate anemia (hematocrit: 21 to 28%), reticulocytosis, leukocytosis, lymphocytosis, extensive extramedullary hematopoiesis in spleen and liver, lymph node hyperplasia and membranoproliferative glomerulonephritis. With increased surveillance of this mouse colony, 20 clinically sick anemic mice were evaluated (complete blood counts and cultures of blood), euthanized and necropsied. Compared with anemic mice without clinical signs of disease, sick anemic mice had significantly higher white blood cell counts with only 4 (20%) of 20 animals being severely anemic (hematocrit: 4 to 8%). Blood from 11 (45%) of 20 animals was culture-positive for Pasteurella pneumotropica, Enterococcus, and/or Escherichia coli. In addition to the usual lesions in sphha/sphha mice, sick anemic mice had pneumonitis (95%) with thrombosis and infarction (80%) of one or more organs (spleen, myocardium, pancreas, liver, or bone marrow). The thrombotic tendency that accompanies the chronic hemolytic anemia in sphha/sphha mice, as well as the other clinicopathologic changes in these mutant mice, bears a striking resemblance to some poorly understood sequelae in human patients with sickle cell anemia. This mouse model may be useful in studying the pathophysiology of complications associated with sickle cell anemia in humans.
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PMID:Pathologic features associated with decreased longevity of mutant sphha/sphha mice with chronic hemolytic anemia: similarities to sequelae of sickle cell anemia in humans. 835 80

The diagnosis of acute rheumatic fever has become difficult. A growing number of diseases that were not recognized in the past could fulfill its diagnostic criteria. We emphasize its changing incidence, current knowledge of its pathogenesis, and lesser known clinical features such as pneumonitis, encephalitis and glomerulonephritis.
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PMID:Acute rheumatic fever. 850 75

Fourteen mares and their foals were attended at parturition. After mare-foal bonding, 8 colostrum-deprived (CD) foals were removed from their dams, deprived of colostrum, and provided with an alternative milk source for the first 24 h of life. The mares were milked out every 2-4 h during this period to remove colostrum, after which the CD foals were returned to their mares and allowed to nurse. Six colostrum-fed (CF) foals were allowed to suck colostrum in the normal manner. Foal serum IgG concentration was determined by single radial immunodiffusion (means, CD = 0 mg/dl; CF = 1,508 mg/dl). Accepted methods were used to minimise infections in the neonatal foals. Of the 8 CD foals, 7 demonstrated clinical signs of sepsis. Septicaemia was confirmed in 5 of the 7 septicaemic CD foals by ante-mortem blood culture or by culture of tissue at necropsy. Organisms isolated included: Actinobacillus equuli, Escherichia coli, undifferentiated coliforms, Pseudomonas spp., and Actinomyces pyogenes. Clinically ill foals were treated with antimicrobial drugs, intravenous fluid therapy, flunixin meglumine, and anti-endotoxin hyperimmune serum. Three septicaemic CD foals survived. Four of 7 septicaemic CD foals died or were destroyed. Post-mortem lesions included bacterial embolic pneumonia, glomerulonephritis/nephritis, lymphoid depletion/atrophy, splenic and lymphoid necrosis, hepatitis, septic arthritis, and systemic bacterial embolism. None of the CF foals became septicaemic. One CF foal had foal heat diarrhoea and 1 CF foal had a serum IgG concentration of 160 mg/dl (i.e. failure of passive transfer), but both foals were otherwise normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective study of septicaemia in colostrum-deprived foals. 822 85

A 86 year-old woman was re-admitted because of purpura of her upper and lower extremities, abdominal pain and blood stools. Seven weeks previously, she underwent a gastrectomy for gastric cancer. After re-admission, proteinuria and hematuria were noted, and the serum creatinine level increased. Two months, after the onset of purpura, she died of pneumonia. On autopsy examination, fibrinoid vasculitis of acute inflammatory stage (II) at small arteries and/or arterioles in the bladder, rectum, lungs, spleen and crescentic glomerulonephritis without immune deposits were observed. A diagnosis of microscopic polyarteritis nodosa (M-PN) was made based on these clinical and histological findings. M-PN refers to systemic vaculitis with segmental necrotizing glomerulonephritis. However, this condition may be difficult to diagnose because vasculitis such as Scholein-Henoch purpura (SHP) and/or hypersensitivity angitis, diseases in which the small arteries and arteroles are mainly affected, occasionally bears a clinical and histological resemblance to M-PN. Because differential diagnosis from SHP was required, this case provided abundant suggestions with regard to the entity of M-PN.
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PMID:[An autopsy case of microscopic polyarteritis nodosa resembling Schoenlein-Henoch purpura]. 872 Feb 67

In this study, Babesia microti (ATCC30222) from mice was adapted to golden hamsters. The parasite was passaged to immunosuppressed and then adapted to normal hamsters. When 30 normal hamsters were inoculated with this strain, parasitaemia increased to 74% of erythrocytes by day 7 and 70% of the hamsters died. By day 12, parasitaemia extended to 90%, with 97% mortality. Hearts and kidneys from infected animals were enlarged. Histopathology revealed acute myocarditis, hepatitis, pneumonitis, glomerulonephritis and splenomegaly. Giemsa, Acridine Orange and Rhodamine staining of the parasite were compared. Scanning electron microscopy of blood from infected hamsters revealed from 1 to 5 intra-erythrocytic parasites.
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PMID:Acute fulminating babesiosis in hamsters infected with Babesia microti. 887 13


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