Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study two groups of patients with acute Chagas' disease were identified. Group one consisted of five patients with apparent acute Chagas' disease. These patients showed symptoms and signals of an acute illness, such as high fever and enlarged spleen. One of these patients developed severe myocarditis and heart failure. Group two consisted of seven patients with inapparent acute Chagas' disease. This was a nonclinical entity, not perceived by the patient who did not seek medical care. The diagnosis was made by the shift of a serologic test which indicates the presence of immunoglobulin M antibodies to Trypanosoma cruzi. The patients with apparent acute Chagas' disease showed positive delayed-type skin response to T. cruzi antigen. Also, their leukocytes showed significant inhibition of migration in the presence of this antigen. By contrast, the patients with the inapparent acute Chagas' disease did not show positive delayed-type skin response to T. cruzi antigen and no significant inhibition was observed when their cells migrated in the presence of this antigen. Of interest, none of these patients was capable of developing contact sensitivity to 2,4-dinitrochlorobenzene. However, three out of five patients with the apparent acute disease and all the normal control subjects showed positive contact reaction after sensitization to this drug. The results of these experiments would suggest that the thymus-derived (T)-lymphocyte function is depressed in patients with the clinically inapparent acute Chagas' disease. This immunodepression seems to be acquired in the course of the T. cruzi infection because all patients showed positive delayed-type skin response to at least one ubiquitous microbial extract, thus indicating previously normal T-cell function. We hypothesize that T. cruzi antigens may directly stimulate T cells with the concomitant release of factors that might become supressive for T-cell responses. Furthermore, the suppressive effect might interfere with the T-cell response to other antigens, such as to 2,4-dinitrochlorobenzene.
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PMID:Acquired cell-mediated immunodepression in acute Chagas' disease. 10 95

Diplococcous infection was observed in 15 calves aged 3 to 30 days. Diplococcous pneumoniae was isolated from synovial fluid and parenchymal organs in affected joints of dead calves. Clinically and morphologically the disease had an active course in calves aged up to 20 days, while in the older ones a subacute or chronic course of the disease was observed. The morphological changes depended on the type of infection. In acute infections a septic course of the disease, including hemorrhagic diathesis, enlarged spleen, myocarditis, hyperaemia, oedema and isolated hemorrhages of the brain meninges was observed, while in the chronic cases pneumonia, pleutisy, pericarditis, arthritis of the knee, elbow, dorsal and carpal joints and ofien suppurative meningoencephalitis were encountered.
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PMID:[Morphological changes in diplococcosis in calves]. 54 5

A 38-year-old man with AIDS presented with fever of unknown origin, splenomegaly, anemia, and thrombocytopenia. Admission laboratory data revealed a positive toxoplasmosis titer in the blood. The initial chest x-ray showed small bilateral pleural effusions, a normal cardiac silhouette, no infiltrates, and no interstitial edema. Ga-67 imaging revealed markedly abnormal uptake in the myocardium. A diagnosis of toxoplasmosis myocarditis was made based on laboratory and imaging data. The patient was treated for toxoplasmosis. No myocardial uptake of tracer was demonstrated on a follow-up Ga-67 scan, performed after completion of treatment for toxoplasmosis.
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PMID:Ga-67 citrate myocardial uptake in a patient with AIDS, toxoplasmosis, and myocarditis. 205 84

An allergic disease may develop in any organ or system. The respective etiological factors include foreign proteins, infectious agents such as various microbes, viruses, moulds, parasites, chemical compounds often in the form of drugs usually designated as haptens, polysaccharides, benign and malignant neoplasms. Of the factors operating in the causal pathogenesis of such diseases the most important one is an exaggerated formation of antibodies, which appears to be uncontrolled and occurring irrespective of the demands of the organism. The essential morphological features in allergic inflammation are rather variegated, their diagnostic value differing in a wide range but being never absolute. The above features include eosinophilic leucocytes, allergic arteritis and phlebitis, fibrinoid necrotic glomerulonephritis, histiocytic granulomatous inflammation or histiocytic granuloma. Granulomatous capsulitis and trabeculitis affecting the spleen and lymph nodes are believed to be of major diagnostic significance. The immunofluorescent and immunoperoxidase methods and electron microscopy are important diagnostic tools. It has been generally acknowledged that many drugs operate as antigens. They may cause death of the respective patient, but allergic manifestations may subside after withdrawal of such drugs. On occasion they operate as a trigger mechanism with the allergy progressing even after treatment had been interrupted. Therefore they have been receiving extreme attention. Our collection of cases a case of giant-cell myocarditis following sulfamethoxypyridazine, anaphylactic shock has been reported to occur after intravenous administration of novocaine, and generalized cutaneous vasculitis developed in the same patient during the subsequent phase. A similar cutaneous finding was reported to have developed after penicillin injection, granulomatous inflammation developed owing to sulfonamide treatment. Allergic tumour-like lymphadenitis developed after administration of anti-anthracic serum; an anticonvulsive syndrome developed after hydantoinate administration. The latter consisted of generalized exanthema, hepatomegaly, splenomegaly and generalized lymphadenopathy. The lymph nodes showed tumour-like lymphadenitis mimicking lymphogranuloma or reticulosis. Allergic diseases appear as either isolated organ lesions or systemic diseases. Thus, isolated and systemic polyarteritis nodosa, isolated nasal, pulmonary or systemic Wegener's granulomatosis have been recognized. Temporal arteritis has been recognized as a localized form of systemic giant-cell arteritis. The haemolytic-uraemic syndrome appears to be a milder variety of thrombotic thrombocytopenic purpura. Allergic diseases or manifestations occasionally affect two or more organs or systems.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathology of allergic diseases. 248 27

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

Trypanosoma cruzi may be transmitted to a susceptible human through different routes: a superficial lesion in the skin, such as a scraping of the small wound produced by the hematophagous triatomid bug vector, which becomes infected with its contaminated feces; the placenta, from the infected mother to the product of conception; a transfusion from an infected donor, or even by ingestion of diverse foods infected or contaminated with the parasite. Whichever may be the transmission of the protozoon, it is advisable to have in mind that it is able to produce an asymptomatic or a symptomatic infection, being possible in both cases, using appropriated methods, to detect the T. cruzi and/or the antibodies generated. From the clinical stand-point, Chagas' Disease may present itself as acute or as a chronic disease. Habitually, the acute disease is characterized by general involvement, fever, hepato-splenomegaly, polidenopathy, and occasionally myocarditis and/or encephalitis, whereas, the chronic form of the disease is characterized by presenting itself in an isolated way or combined, chronic myocardiopathy, megaesophagous or megacolon. At any rate, the problems center in the possibility of a reasonable diagnostic assurance which permits the adoption of adequate therapeutic measures. Some facts, which may help to confront these problems are: a) The epidemiological antecedents (origin in an endemic area, personal knowledge of the vector or of being bitten by it, whether the mother or other relatives are affected by the disease, etc.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Problems related to the diagnosis of Chagas' disease]. 251 14

A 29-year-old man had a febrile illness accompanied by chest pain and tachycardia. The ECG suggested either myocarditis or acute ischemia. Heart muscle enzymes were normal, the peripheral blood count showed absolute and relative lymphocytosis, and an echocardiogram disclosed a small pericardial effusion. After defervescence, splenomegaly was noted and the SGPT level was elevated to four times normal. There was a greater than fourfold rise in titer of IgM antibodies to cytomegalovirus. This is only the second report in detail of perimyocarditis caused by cytomegalovirus mononucleosis. An interesting aspect of the case was an afebrile prodrome that lasted for more than one week, during which prostration, palpitations, and breathlessness on exertion were present and the sole physical finding was tachycardia.
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PMID:Perimyocarditis. Report on an unusual cause. 253 10

A case of a 16 year old boy with interstitial lymphomatoid pneumonia coexisting with myocarditis, hepatitis, and splenomegaly is presented. The cause of the above mentioned changes despite a thorough and meticulous diagnostic approach which included microscopical examination of the lung, liver biopsies and bone marrow tap could not be made. Corticosteroid therapy did not bring a permanent improvement in the child clinical state. The boy expired quite unexpectedly. The post-mortem examination also did not provide a final diagnosis.
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PMID:[A case of lymphoid interstitial pneumonia]. 263 73

We observed and recorded clinical and laboratory data from 54 children with fever and a maculo-papular rash admitted to Soroka Medical Center, Beersheva, Israel suffering from serologically confirmed rickettsial spotted fever. The rash generally began on the palms and soles and extended centripetally to the torso. Other clinical findings included myalgia, headache, hepatomegaly, and splenomegaly. None had a "tache noire". A left shift in the white cells, leucopenia, thrombocytopenia, hyponatraemia and impaired liver function tests were common laboratory abnormalities. All recovered following oral doxycycline therapy. Serious sequelae such as myocarditis, encephalitis, and disseminated intravascular coagulation, as reported in Rocky Mountain spotted fever, did not occur.
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PMID:Israeli rickettsial spotted fever in children. A review of 54 cases. 288 43

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.
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PMID:[The chronic form of the Budd-Chiari syndrome]. 297 4


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