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)

A 37-year-old man suddenly fell ill with high fever (up to 39.6 degrees C), headache and lumbar pain. There was marked thrombocytopenia (minimal level of 48,000/microliters), moderate anaemia and a slow rise in serum lipase concentration to maximally 1352 U/l. Marked sinus bradycardia (to as low as 34 beats/min) occurred in the further course of the disease, as well as upper abdominal pain (endoscopically diagnosed as antral gastritis), subileus and splenomegaly. Two haemodialysis treatments were needed because of acute renal failure. An IgG antibody titre of 1:512 and an IgM titre of 1:80 against hantavirus antigen confirmed that this virus was responsible for the haemorrhagic fever with renal syndrome. This infection, transmitted by wild rodents and frequently observed in Asian countries, has a rising incidence in Central Europe. It should be included in the differential diagnosis of acute renal failure of uncertain cause.
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PMID:[Acute kidney failure caused by hantavirus infection]. 168 52

Fibreoptic endoscopy was carried out on 100 Malawian adults consecutively admitted to the department of medicine, Kamuzu Central Hospital, Lilongwe, with acute upper gastrointestinal bleeding. The principal causes of haemorrhage were oesophageal varices (45%), duodenal ulcer (16%), gastritis/erosions (9%) and gastric ulcer (7%). 69% of 29 patients with oesophageal varices who were investigated had S. mansoni infection. A palpable spleen positively predicted oesophageal varices in 91% of cases, while no palpable spleen predicted a source of haemorrhage other than varices in 97% of cases. In Malawi oesophageal varices are the major cause of upper gastrointestinal bleeding in adults, and the presence or absence of splenomegaly is a useful clinical pointer respectively to the presence or absence of oesophageal varices.
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PMID:Upper gastrointestinal bleeding in Malawian adults and value of splenomegaly in predicting source of haemorrhage. 278 73

A 12-year-old Thoroughbred mare, with a history of anorexia, dramatic weight loss, fluctuating pyrexia and intermittent diarrhoea after an episode of colic, was presented for examination with depression, emaciation and ataxia. Thoracic and abdominal paracenteses yielded copious quantities of inflammatory exudate. Palpation per rectum revealed an enlarged spleen. The primary alterations in haematology included a severe leucocytosis with a left shift, and a hyperproteinaemia characterised by hypoalbuminaemia and hypergammaglobulinaemia. Post-mortem examination revealed a low grade pleurisy and peritonitis with fluid accumulation in both cavities. A suppurative gastritis with full thickness perforations of the stomach wall associated with Gasterophilus intestinalis larvae had extended to the juxtaposed organ initiating an extensive suppurative splenitis. Streptococcus zooepidemicus was cultured.
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PMID:Suppurative splenitis and peritonitis in a horse after gastric ulceration caused by larvae of Gasterophilus intestinalis. 363 94

Histoplasmosis naturally occurring in laboratory guinea pigs is described in its clinical, necropsy, histological and mycological aspects.The animals if adult show a chronic disease with progressive emaciation and lameness of the hind legs. The young below three months of age died in 2 to 4 weeks presenting ruffled fur, great dorsal curvature and sometimes closed eyelids and catarrhal conjunctivitis. At necropsy the principal lesions were ulcerative gastritis, hemorrhagic and catarrhal enteritis, enlarged spleen and mesenteric lymph nodes. Sometimes the liver, lungs, mediastinal lymph nodes and other organs showed lesions. Histological and mycological demonstration of the fungus completed the diagnosis and the surviving animals were burned and sanitation measures instituted. Histological evidence of histoplasmosis in a cow's lung from the area from which the grass was obtained for the feeding of the guinea pigs suggests an epidemiological link. Efforts will be made to isolate and demonstrate H. capsulatum in wild animals on the same area.
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PMID:Naturally occuring histoplasmosis in guinea pigs. 422 13

Twelve patients with anemias and their close relatives were examined: 8 adults (3 men and 5 women) and 4 children (3 boys and 1 girl). Six of them were Armenians, 1 woman was Russian, and the rest were of mixed origin: 3 Russian-Azerbaijan-Ukrainian, 1 child Russian-Ukrainian-African, and 1 woman Russian-Ukrainian. Hemoglobinopathies were detected in 10 subjects from 4 families (3 families from Donetsk and 1 from Moscow). Homozygotic beta-thalassemia major (Hb F 98.9%) was diagnosed in a 2-year-old Armenian girl from Donetsk. The girl lags behind in development and suffers from anemia with hepatosplenomegaly and jaundice. Heterozygotic beta-thalassemia minor with increased levels of Hb A2 and Hb F was diagnosed in her parents (Armenians from Azerbaijan). A 15-year-old Russian-Azerbaijan-Ukrainian boy from another family in Donetsk had beta-thalassemia with HbD (94%). The boy suffers from anemia with hepatosplenomegaly, jaundice, and chronic hepatitis. Heterozygotic beta-thalassemia with increased levels of Hb A2 and Hb F was revealed in proband's mother and brother; the father was not examined. alpha-Thalassemia is suspected in a 3-year-old boy from a Russian-Ukrainian-African family in Donetsk; he presented with a very small "fast" abnormal hemoglobin fraction. The boy suffers from anemia with splenomegaly and systolic murmur. Blurred form of thalassemia minor is diagnosed in the mother. The father, an African from Zaire, was not examined. Heterozygotic beta-thalassemia with increased Hb A2 level was revealed in a 20-year-old Armenian boy from Moscow. He presented with manifest splenomegaly, chronic gastritis, and mitral valve prolapse. His mother suffers from thalassemia minor, was anemic during pregnancy, and there are cases of anemia in the family. No hematologic disorders were found in the father. No hemoglobinopathies were detected in a 59-year-old Russian women from the town of Tver with very grave anemia; apparently, her condition was acquired, but not hereditary. Data on patients in the city of Donetsk are of special interest, for there are virtually no reports about hemoglobinopathies in the Ukraine.
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PMID:[Beta-thalassemia and Hb D in patients with anemia]. 957 28

In this article, we report the case of a 16-month-old German boy who was admitted to the Children's Hospital of Stuttgart with a 4-week history of intermittent fever, decreased appetite, weakness, fatigue, and difficulty sleeping. He was healthy at birth and remained so for the first 15 months of his life. On admission, physical examination showed enlarged cervical, axillary, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory data revealed pancytopenia, elevated liver function tests, and hypergammaglobulinemia. Blood, stool, and urine culture results were negative. Viral infections and rheumatologic and autoimmune disorders were ruled out, but a positive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral leishmaniasis was made by combining the cultures of both the liver and the bone marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degrees C for 5 days. The parasite was identified by Southern blot analysis as Leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the patient became afebrile. The side effects of treatment, including erosive gastritis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzymes, pancreatitis, and electrocardiogram abnormalities, necessitated the discontinuation of treatment after 17 days. On discharge 4 weeks later, the patient was stabilized and afebrile with a normal spleen, normal complete blood count, normal gammaglobulins, and decreasing antibody titers to Leishmania. During the next 24 months, the patient experienced intermittent episodes of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia. But at his last examination in January 1998, he was well; all symptoms mentioned above had disappeared. Because the child had never left Germany, nonvector transmission was suspected and household contacts were examined. His mother was the only one who had a positive antibody titer against Leishmania donovani complex. She had traveled several times to endemic Mediterranean areas (Portugal, Malta, and Corse) before giving birth to the boy. But she had never been symptomatic for visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy results were within normal limits. Culture results and polymerase chain reaction of this material were negative. A Montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis showed specific recognition by maternal antibodies of antigens of Leishmania cultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical countries, but also to the Mediterranean region. It is transmitted by the sand fly (Phlebotomus, Lutzomyia). Occasional nonvector transmissions also have been reported through blood transfusions, sexual intercourse, organ transplants, excrements of dogs, and sporadically outside endemic areas. Only 8 cases of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother must have had a subclinical infection with Leishmania that was reactivated by pregnancy, and then congenitally transmitted to the child. Visceral leishmaniasis has to be considered in children with fever, pancytopenia, and splenomegaly, even if the child has not been to an endemic area and even if there is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.
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PMID:Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child. 1054 91

Low-risk essential thrombocythemia patients include patients aged 18 to < 80 years with no vascular risk factor or previous thrombosis, no associated disease, a normal life expectancy, and a platelet count between 400 and 1,000 x 10(9)/L up to 1,500 x 10(9)/L. Asymptomatic essential thrombocythemia patients may be at risk for microvascular circulation disturbances. The indication for low-dose aspirin in asymptomatic essential thrombocythemia patients is uncertain, therefore randomization for aspirin 50 mg versus placebo is recommended. Symptomatic essential thrombocythemia patients with erythromelalgia and its ischemic complications, atypical transient ischemic attacks, minor stroke, visual disturbances and "superficial thrombophlebitis" in the absence of bleeding, vascular risk factors, or vascular disease have a clear indication for aspirin in a regular dose. To determine whether 50 mg/day is as effective as 100 mg/day for the prophylaxis of microvascular circulation disturbances in essential thrombocythemia, a randomized trial comparing low-dose aspirin 50 mg versus 100 mg at platelet counts between 400 and 1,000 up to 1,500 x 10(9)/L is recommended. To address the question whether reduction of the platelet count to normal (< 350 x 10(9)/L) is as effective as low-dose aspirin for the long-term relief of microvascular circulation disturbances, a randomized study comparing low-dose aspirin with the correction of platelet count to normal by anagrelide is recommended. High-risk essential thrombocythemia patients have a clear indication for platelet reductive therapy, including: (a) platelets > 1,500 x 10(9)/L, history of major thrombosis (myocardial infarction, stroke, peripheral occlusive vascular disease), or presence of vascular disease (e.g., arteriosclerosis); (b) history or presence of spontaneous or major bleedings, bleedings elicited by low-dose aspirin for the secondary prevention of vascular complications in essential thrombocythemia at platelet counts < 1500 x 10(9)/L, and side effects of long-term aspirin treatment such as gastritis; and progression from low- to high-risk essential thrombocythemia patients during follow-up or progressive myeloproliferative disease such as significant splenomegaly, myelofibrosis, leukocytosis, etc. To address the question of optimal treatment of high-risk essential thrombocythemia patients, randomization for anagrelide versus interferon at < 65 years of age and anagrelide versus hydroxyurea at an age > 65 years is recommended.
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PMID:Aspirin and platelet-lowering agents for the prevention of vascular complications in essential thrombocythemia. 1072 22

We report a retrospective study of 115 hospitalized non-immunocompromised adults with proved or presumed diagnosis of cytomegalovirus infection. Clinical symptoms were fever (95%), constitutive symptoms (80%), joint and muscle pain (41%), shivering (32%), abdominal pain (26%), non-productive cough (20%), cutaneous eruption (20%), and diarrhea (10%). Examination found hepatomegaly (25%), splenomegaly (23%), cutaneous rash (20%), adenopathy (19%), pharyngitis (9%), jaundice (3%) or signs of meningeal irritation (1%). Seventeen patients had a gastrointestinal form (hepatitis, jaundice, colitis, antral gastritis or cholecystitis), eight had a pattern of hemopathy, two interstitial pneumonitis, two pericarditis, two immune thrombocytopenic purpura, two a polymyalgia rheumatica-like pattern, one thrombotic thrombocytopenic purpura, one cutaneous vasculitis and one meningoencephalitis. Sixty-four percent of the patients had atypical lymphocytosis. Hepatocellular injury occurred in 90% of the patients. Nineteen of the patients had biological immune abnormalities. Cytomegalovirus infection should be mainly suspected in any patient with persistent fever, isolated or associated with signs of poor specificity, or in some patients with visceral manifestations of initially unknown origin.
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PMID:Clinical and laboratory findings of cytomegalovirus infection in 115 hospitalized non-immunocompromised adults. 1147 69

Fatal disseminated toxoplasmosis was diagnosed in a Risso's dolphin (Grampus griseus) dam and its fetus on the basis of pathologic findings, immunohistochemistry, and structure of the parasite. The dolphin was stranded alive on the Spanish Mediterranean coast and died a few hours later. At necropsy the dam was in good condition. From the standpoint of pathology, however, it had generalized lymphadenomegaly and splenomegaly, enlargement of and multifocal hemorrhage in the adrenal glands, diffuse mucosal hemorrhage of the glandular and pyloric stomach, ulcerative glossitis and stomatitis, focal erosions and reddening of the laryngeal appendix, and severe paraotic sinusitis with intralesional nematodes Crassicauda grampicola. The dolphin was pregnant, most probably in the first gestational trimester. The most prominent microscopic lesions were multifocal granulomatous encephalomyelitis, diffuse subacute interstitial pneumonia, mild multifocal necrotizing hepatitis and nonsuppurative cholangiohepatitis, gastritis and adrenalitis, mild lymphoid depletion, medullary sinus and follicular histyocitosis, and systemic hemosiderosis. The fetus had foci of coagulative and lytic necrosis in the kidneys, the lung, and the heart. Most lesions were associated with tachyzoites and tissue cysts of Toxoplasma gondii. The diagnosis was confirmed immunohistochemically. This is the first report on toxoplasmosis in a Risso's dolphin (G. griseus) and on transplacental transmission to an early-stage fetus in any cetaceans.
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PMID:Disseminated toxoplasmosis in a Mediterranean pregnant Risso's dolphin (Grampus griseus) with transplacental fetal infection. 1243 53

This report describes a case of non-Hodgkin's lymphoma in a 31-year-old patient in whom HIV infection was subsequently diagnosed. The woman consulted for epigastralgia. Her medical history included gastritis caused by Helicobacter pylori that was given specific treatment. Clinical examination demonstrated type III splenomegaly and blood film examination demonstrated hypochromic microcytic anemia and neutropenia. Outcome was rapidly fatal and the patient died before start up of anti-retroviral therapy. This case suggests that a possible link between HIV and/or Helicobacter pylori and lymphomagenesis.
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PMID:[Primary gastric lymphoma complicating HIV infection]. 1750 76


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