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)

Splenomegaly is usually the result of systemic disease. The differential diagnosis can logically be subdivided into infectious, hematologic, metabolic, vascular, and neoplastic diseases which result in abnormalities of the lymphoid, reticuloendothelial, or vascular components of the spleen. Splenic enlargement increases the risk of traumatic rupture of the spleen. Splenectomy, although indicated in some conditions, does not always relieve the hypersplenic state, and its benefit must be weighed against the hazard of life-threatening episodes of sepsis.
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PMID:Splenomegaly in children. Identifying the cause. 42 50

A 39-year-old man is described who presented with the unspecific signs of systemic disease (elevated erythrocyte sedimentation rate, increased gamma-globulins, positive rheumatoid factor; clubbing, splenomegaly) and with fever whose origin remained undiagnosed for 8 years despite numerous investigations. Later in the course of the disease, the signs of mitral stenosis appeared, suggesting left atrial myxoma even in the absence of arterial embolization. This diagnosis was established by echocardiography and confirmed by angiocardiography as well as at operation, after which all the systemic signs and symptoms disappeared.
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PMID:[Fever of long standing in atrial myxoma]. 65 38

Between 1969 and 1988, 146 children with immune thrombocytopaenic purpura (ITP) were seen in the outpatient clinic. The diagnosis was based upon an isolated thrombocytopaenia, without disseminated intravascular coagulation, splenomegaly or systemic disease and a normal bone marrow. Patients who required treatment (116/146) received either steroids (105/116) or IV gammaglobulins (IV-Ig) (11/116) as initial therapy. The long term outcome was similar in both groups. IV-Ig had the advantage to give a rapid increase in the platelet count without major side effects and to be very useful in chronic ITP either as maintenance therapy or as preparation for splenectomy.
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PMID:Treatment of immune thrombocytopaenic purpura in childhood. A review of 146 patients. 169 54

We have attempted to investigate the relative roles of specific cytotoxic T lymphocytes (CTL) and allospecific suppressor T cells (Ts) in the systemic and intestinal manifestations of acute graft-versus-host reaction (GvHR) in mice. Treatment of adult (C57B1/10 x DBA/2)F1 (BDF1) mice with the suppressor cell-specific toxin 2'-deoxyguanosine (dGuo) inhibited the weight loss and mortality which normally occur after induction of GvHR and C57Bl donor cells. dGuo also delayed the development of a destructive enteropathy as typified by jejunal villus atrophy. Paradoxically, dGuo completely prevented villus atrophy during an acute GvHR in neonatal (CBA x BALB/c)F1 hosts, despite having only a slight ability to inhibit the systemic disease. In both models, dGuo had no effect on the generation of splenomegaly or anti-host CTL, and dGuo-treated mice with GvHR actually had increased proliferative alterations in the intestine, as assessed by crypt hyperplasia. In parallel, dGuo prevented the loss of NK cells which normally occurs in acute GvHR. Thus dGuo inhibits many of the destructive features of systemic and intestinal GvHR without affecting the development of CTL. We conclude that a dGuo-sensitive mechanism causes the transition from a proliferative to a destructive GvHR.
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PMID:Experimental studies of immunologically mediated enteropathy. VI. Inhibition of acute intestinal graft-versus-host reaction in mice by 2'-deoxyguanosine. 214 36

Splenomegaly confirmed by surgery or necropsy in 100 dogs was diagnosed histologically as benign neoplasia (n = 1), primary splenic malignancy (n = 59), neoplastic metastases (n = 6), and nonneoplastic disease (n = 34). Dogs with known systemic disease, such as lymphoma and mast cell tumor, that caused splenomegaly were not included in the study. Hemangiosarcoma was the most common splenic disease (43 cases). Overall mean age of the dogs was 10.7 years, the most common breed was German Shepherd dog, and 72 of the dogs weighed more than 21 kg. Dogs with anemia, nucleated red blood cells, abnormal red blood cell morphology, or splenic rupture had a significantly greater chance of having splenic neoplasia (P less than 0.002). A multivariable logistic regression analysis found that the presence of anemia and splenic rupture in dogs with splenomegaly was up to 69% accurate in predicting presence of splenic neoplasia. After splenectomy, the median survival time of dogs with splenic neoplasia was 13 weeks. For dogs with nonneoplastic splenomegaly it was at least 36 weeks.
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PMID:Splenomegaly in dogs. Predictors of neoplasia and survival after splenectomy. 277 49

Twenty-five patients with rheumatoid arthritis (RA) and neutropenia, of whom 19 had a palpable spleen, were compared with 24 patients with uncomplicated RA, and 16 patients with RA and associated splenomegaly without neutropenia. Clinically patients with neutropenia had evidence of a more systemic disease as assessed by prevalence of rheumatoid nodules, weight loss, and recurrent infections. However, there was less evidence of active synovitis than in the other 2 groups. Marrow neutrophil reserve was studied by means of a hydrocortisone stimulation test and was found to be lower in all 3 groups than in normal persons but with most marked depletion in the neutropenic group. Removal of the spleen in some patients with neutropenia resulted in a significant increase in marrow neutrophil reserve. Circulating immune complexes as detected by anticomplementary activity and platelet aggregation tests were detected in 68% of the RA neutropenia group, 31% of the RA splenomegaly group, and 8% of the uncomplicated RA group. Our results show that, assessed both clinically and by the above tests, patients with neutropenia have a greater prevalence of abnormalities which may be directly related to their neutropenia. Patients with splenomegaly alone closely resemble patients with uncomplicated RA.
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PMID:Neutropenia in rheumatoid arthritis: studies on possible contributing factors. 697 79

Sixteen dogs with splenic infarction due to causes other than splenic torsion were identified. Dogs with splenic infarction often had multiple concurrent diseases, and surgical management of splenic infarction was associated with high mortality. Splenic infarction occurred in dogs with hypercoagulable conditions associated with liver disease, renal disease, and hyperadrenocorticism, or as a consequence of uniform splenomegaly, neoplasia, or thrombosis associated with cardiovascular disease. Clinical signs and common laboratory findings generally reflected the underlying disease process. A variety of splenic abnormalities were detected by abdominal ultrasound in 15 dogs, with the ventral extremity of the spleen being most often abnormal. Four dogs were euthanized or died because of the presence of severe systemic disease, whereas 12 dogs underwent laparotomy. Complete splenectomy was performed in 9 dogs and partial splenectomy was performed in 2 dogs. Seven dogs died in the immediate postoperative period, 3 required chronic veterinary care, and 2 had uncomplicated long-term recoveries. Splenic infaraction should be regarded as a sign of altered blood flow and coagulation, rather than as a primary disease, and surgical management should be reserved for patients with life-threatening complications such as hemoabdomen or sepsis.
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PMID:Splenic infarction in 16 dogs: a retrospective study. 767 15

Prolymphocytic leukemia (LPL) is a well defined entity with a relatively low incidence in our country. This disease usually is seen in patients over 50 years of age, and there is a very definite male preponderance. This lymphoproliferative disorder is characterized by very high white cells counts, massive splenomegaly, poor response to therapy and short term survival. The neoplastic cell in prolymphocytic leukemia usually is of B-cell origin (80% of cases). In our patient, affected by B-lineage prolymphocytic leukemia, a acute hepatic failure occurred, leading him to death in a short time. Autoptic findings evidenced a massive leukemic infiltration of the liver with parenchymal necrosis that caused fatal hepatic failure. Autoptic findings did not show histological patterns of acute viral infections or of any other infectious or systemic disease which could have induced a so massive liver injury. In literature there are no evidences of such a massive and lethal involvement of the liver during prolymphocytic leukemia or chronic lymphocytic leukemia and patients affected by LPL generally come to death because of other causes.
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PMID:[Prolymphocytic B-cell leukemia with fatal acute liver failure. A case report]. 818 2

Mycoplasma-like organisms (MLO) are non-cultivated intracellular cell-wall deficient pathogenic bacteria with a distinctive ultrastructural appearance. Diagnosis of MLO disease depends on finding the organisms in parasitized cells using a transmission electron microscope. MLO are a well studied cause of transmissible chronic plant disease responsive to antibiotics. MLO have recently been found to cause human chronic uveitis, orbital, and retinal disease with autoimmune features. Ophthalmic leucocytes in these patients display MLO parasitization. Inoculation of human uveitis MLO into mouse eyelids produced chronic uveitis. MLO also disseminated to produce randomly distributed lethal systemic disease including chronic hepatitis. MLO parasitized leucocytes were present in all disease sites. Direct intrahepatic inoculation of human hepatic pathogens is a simple and efficient technique to produce murine hepatitis. This report describes the delayed onset widespread inflammatory liver disease produced by direct intrahepatic inoculation of human chronic uveitis MLO in 12 of 20 mice versus 0 in 40 controls (P < 0.05). The liver disease was accompanied by elevated serum SGOT levels, splenomegaly, and accelerated mortality. All 12 inflamed livers displayed MLO parasitized leucocytes versus 0 of 10 control livers. The resemblance of human chronic active hepatitis, massive hepatic necrosis, and post-necrotic cirrhosis to the MLO induced murine liver disease, the role of molecular biologic techniques in the detection and classification of those bacteria, and in therapy of MLO disease are discussed.
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PMID:Experimental murine chronic hepatitis: results following intrahepatic inoculation of human uveitis mycoplasma-like organisms. 839 4

In a 52-year-old man with general malaise, muscle stiffness and weakness, POEMS-syndrome was diagnosed based on polyneuropathy, splenomegaly, lymphadenopathy, subclinical hypothyroidism and the presence of a monoclonal paraprotein with osteosclerotic lesions and an indurated skin (POEMS is an acronym for Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal protein, Skin changes). This is a rare systemic disease from the clinical spectrum of plasma cell dyscrasias with polyneuropathy. The clinical picture is broader and more pleomorphic than the acronym suggests. The possibility of a POEMS syndrome should be considered in the differential diagnosis of polyneuropathy in association with monoclonal gammopathy. Quite often it is associated with osteosclerotic myeloma or mixed osteoscleroticlytic lesions. The patient described was treated with high dose corticosteroids which were gradually decreased over the next three months, upon which a marked improvement could be seen. The general malaise subsided, as did the splenomegaly, and the skin became supple again.
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PMID:[A man with plasma cell dyscrasia and polyneuropathy due to POEMS syndrome]. 1187 37


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