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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human diseases caused by atypical mycobacteria are reviewed. Pulmonary illness and childrens' lymphadenitis are the commonest, but cutaneous, disseminated, bony, articular, renal and meningeal diseases are also produced by atypical mycobacteria. Disseminated infections are often manifested by fever, hepato-splenomegaly and hematologic changes. Most diagnosis are made by sputum and gastric-juice cultures, bonemarrow and liver biopsies. Disseminated diseases are often fatal but may be cured with medical treatment. In general, atypical mycobacterial diseases are quite similar to tuberculous diseases in different organs. A unique isolation of atypical mycobacteria is not diagnostic "by it self", and other conditions are required. Diagnostic criteria and treatment are discussed.
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PMID:[Pathogenicity of atypical mycobacteria]. 16 50

Over a period of 9 years in general practice temporary enlargement of the spleen was found in 29 episodes of pharyngitis or tonsillitis, in 2 episodes of acute upper respiratory tract infection other than pharyngitis and in 6 episodes of acute cervical lymphadenitis. In five patients more than one episode of illness associated with splenomegaly was recorded. In 26 of the 37 episodes a possible aetiology was identified. Evidence only of infection with group A streptococci was found in 14 episodes, adenoviruses or coxsackie B viruses were isolated alone in 4 episodes and in 4 episodes the only finding was the presence in the blood of more than occasional atypical mononuclear cells; in 4 episodes there was evidence of both streptococcal and viral infection. Episodes with evidence of streptococcal infection only tended to be of shorter duration and to be more evenly distributed over the year than were episodes without such evidence. Temporary splenomegaly was noted also in two children with varicella (one of whom also had streptococcal infection) and in an adult with probable rubella.
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PMID:Splenomegaly in acute infections due to group A streptococci and viruses. 139 11

Sjogren's syndrome (SS) is frequently associated with both reactive and neoplastic lymphoproliferative disease. Over a 12-year period beginning in 1970, 21 of 138 patients with SS followed at two tertiary university medical centers had biopsies taken of enlarged lymph nodes (18) or extranodal lymphoid infiltrates (8). Many had immunologic studies performed on fresh tissue and all had paraffin-embedded tissue available for histochemical and immunoperoxidase studies. Eight of our patients had malignant lymphomas which were chiefly B cell neoplasms including two lymphoplasmacytic lymphomas and two follicular center cell lymphomas. The remaining 13 patients had either reactive adenitis (usually with follicular hyperplasia) or atypical lymphoid hyperplasia which failed to meet both histopathologic and immunopathologic criteria for malignancy. None of the nine patients with reactive hyperplasia has yet progressed to lymphoma, while one of four patients with atypical lymphoid hyperplasia progressed to overt lymphoma. Clinical features such as age, duration of disease, extent of lymphadenopathy, splenomegaly, or parotid swelling failed to identify those subsets of patients with lymphadenopathy at increased risk for lymphoma. Recognition of lymphoma in two patients was greatly facilitated by tissue immunologic studies demonstrating focal areas of monotypic B cell proliferation. In one patient in whom the histopathologic diagnosis was immunoblastic sarcoma of B cells, tumor cells were L26-negative and strongly UCHL1-positive suggesting T cell differentiation. In three patients with relatively homogeneous extranodal lymphoid infiltrates, B cell polyclonality on tissue immunoperoxidase studies, and the absence of cytologic atypia, precluded a diagnosis of malignant lymphoma; none of these three patients has progressed to overt lymphoma. Our results indicate that (1) patients with SS develop a variety of B cell lymphomas and other lymphoproliferative disorders, and (2) the nature of the lymphoproliferative disorder is best determined by multiparameter analysis including immunologic phenotyping.
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PMID:Nodal and extranodal lymphoproliferative disorders in Sjogren's syndrome: a clinical and immunopathologic study. 211 Sep 29

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

A 39-year-old woman had an adenitis colli followed by anaemia, splenomegaly, atypical lymphoid cells in blood with increased B-lymphocytes, reduced T-suppressor/cytotoxic cells, increased polyclonal IgM, high titres of EB VCA IgG, EB EA IgD&R +/- and EBNA IgG-. The disease progressed slowly for 2 years, splenectomy was followed by clinical improvement; spleen morphology was compatible with a benign disease of viral origin.
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PMID:Chronic infectious mononucleosis; a case report. 225 27

Various haematological abnormalities commonly occur in active tuberculosis (TB). However, thrombocytopenia is rare and immune thrombocytopenic purpura (ITP) is mentioned only in few case reports. We found that of 846 cases with active TB, 9 (1%) presented with ITP as the only abnormality. Three out of these 9 cases had disseminated miliary TB, 3 an abdominal abscess or lymphadenitis, and 3 pulmonary TB; none had palpable splenomegaly. All patients had purpura and the platelet count varied between 4 and 21 x 10(9)/l, and the bone marrow showed increased megakaryocytes. All tuberculous patients showed initially a poor platelet count response to steroid therapy. The platelet count returned to normal 2-6 weeks after oral prednisone combined with antituberculous drugs.
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PMID:Tuberculosis presenting as immune thrombocytopenic purpura. 892

Disseminated infection with Mycobacterium avium complex is described in 3 adult Siamese cats. All cats were the result of father-daughter matings. Clinical signs included anorexia, weight loss, and lethargy. Physical examination revealed pale mucous membranes, lymphadenopathy, splenomegaly, and pyrexia. Nonregenerative anemia was detected in all 3 cats, and macrocytosis was observed in 2. An antemortem diagnosis of mycobacterial infection was made on the basis of identification of acid-fast bacilli in tissue aspirates. The cats died or were euthanatized owing to clinical deterioration, despite antibiotic treatment. Necropsy findings included granulomatous lymphadenitis, enterocolitis, pneumonia, cellulitis, myelitis, and hepatitis. Organisms from the Mycobacterium avium complex were identified in bacteriologic cultures of tissue samples.
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PMID:Disseminated Mycobacterium avium complex infection in three Siamese cats. 812 27

A 70-year-old woman was admitted to our hospital in November 1992 for evaluation of anemia. Physical examination revealed anemia, jaundice, swelling of axial and inguinal lymph nodes, and splenomegaly. Abnormal hematological findings were as follows: Hb of 3.9 g/dl, reticulocyte count of 58.2% (61.7 x 10(4)/microliters), hyperplasia of normal erythroblasts in bone marrow, and eosinophilia (21.0%, 2352/microliters) in peripheral blood. Routine laboratory examinations revealed polycolonal hypergammaglobulinemia 3.0 g/dl, a high level of serum LDH (797 IU/I) and a total bilirubin of 2.4 mg/dl (indirect, 1.6 mg/dl). The serum haptoglobin level was very low (< 5 mg/dl). Results of serological examinations were as follows: IgG of 3366 mg/dl, CH50 of 16.0 U/ml, positive Coombs test 2+, and positive tests for antinuclear antibody, rheumatoid factor, and cold agglutinin. CRP was negative. PHA-stimulated lymphocyte blast formation, NK activity, and ADCC activity were found to be suppressed, and the percentage of CD4-positive lymphocytes in peripheral blood was also low. An axillary lymph node biopsy revealed reactive lymphadenitis. No signs or history suggested allergy, collagen disease, or parasitic infection. Autoimmune hemolytic anemia (AIHA) complicated by immunologic abnormalities and eosinophilia was diagnosed. Oral prednisolone markedly reduced the hemolytic anemia, eosinophilia, lymph node swelling, and splenomegaly, but NK activity remained low.
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PMID:[Autoimmune hemolytic anemia with eosinophilia in elderly patient]. 892 99

Flaky skin (fsn) mutant mice were originally described as a mouse model for psoriasis accompanied by hematological abnormalities. However, homozygous (fsn/fsn) mice develop a number of other pathological changes. Systematic evaluation of over 300 fsn/fsn and normal littermate control (+/+ or +/fsn) mice was carried out to characterize these changes. Psoriasiform skin lesions were first evident as focal epidermal hyperplasia and inflammation at 2 weeks of age. These lesions became confluent and diffuse by 3-4 weeks of age and were associated with marked dermal infiltration of lymphocytes and small numbers of neutrophils and macrophages. Mast cell numbers increased significantly in the dermis from 2 weeks of age onward. Diffuse dermal neovascularization accompanied these cutaneous changes. Systemic lesions included progressive and massive papillomatosis of the stratified squamous epithelium of the forestomach, hyperplasia and dysplasia of the glandular stomach, increased apoptosis of cecal enterocytes, renal glomerulopathy associated with immune complex and complement deposition, testicular degeneration, mixed inflammatory cell infiltrates and fibrosis around portal triads in the liver, splenomegaly due to massive erythropoiesis, and granulomatous lymphadenitis. This spontaneous mouse mutation provides a useful model for modulating neovascularization and keratinocyte hyperproliferation, especially since the cutaneous changes resemble some forms of psoriasis in humans.
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PMID:Development and progression of psoriasiform dermatitis and systemic lesions in the flaky skin (fsn) mouse mutant. 945 97

Histiocytic necrotizing lymphadenitis or Kikuchi-Fujimoto disease (KFD) was described in 1972. Painful, palpable lymphadenitis is localized to one or two sites in the head and neck territories in young adults (third decade) and is associated with fever. Other clinical manifestations are infrequent: arthromyalgias, cutaneous rash, sweating, splenomegaly. Leukopenia is present in 50% of the cases with sometimes "atypical" lymphocytes. A spontaneously favorable outcome is noted after a mean 3 months. Histopathology of the lymph node is the key for the diagnosis of KFD showing lymph node necrosis of 25 to 75% of the surface, in the cortex and the medulla of the lymph nodes with histiocytic proliferation and plasma cells. Histochemistry shows positive straining for monocytic markers (CD68+, KiM1P+). Alpha-beta CD8+ T cells are abundant, NK and B cells are scarce. Pathological examination enables to differentiate KFD from other types of necrotizing lymphadenitis (SLE, malignant lymphoma, pyogenic infections). Kikuchi disease can be the result of local hyperimmune stimulation after viral, bacterial or parasitic infection. CD4+ cells would then become apoptotic cells. In some cases KJD is associated with systemic diseases such as systemic lupus erythematosus or adult Still's disease.
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PMID:[Kikuchi disease]. 1044 90


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