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 case report is presented of a patient who had liver fibrosis, splenomegaly and ascites, associated with the habit of nibbling tea leaves. The splenomegaly and the ascites remitted when she ceased eating tea, but liver fibrosis is still present 15 years later. No other cause for the liver disorder was found.
Med J Aust 1975 Sep 13
PMID:Liver dysfunction and tea eating. 118 51

A feline erythropoietic porphyria was studied in an affected female Siamese cat and 2 male offspring. The principal elevated porphyrins were Type I isomers of uroporphyrin and coproporphyrin; the porphyrin precursors, porphobilinogen and sigma-aminolevulinic acid, were also detected. Porphyrins were present in the blood and in all the viscera, teeth, bones, and excreta. There was severe macrocytic hypochromic anemia, hepatomegaly, splenomegaly, and uremia associated with a renal disease characterized by mesangial hypercellularity and proliferation (resulting in narrowing of glomerular capillaries) and ischemic tubular injury. There was thickening of tubular basement membranes and tubular epithelial lipidosis, degeneration, and necrosis. Electron microscopic studies of bone marrow and kidney revealed the presence of membrane-enclosed lamellar bodies 150 to 1000 nm in diameter in cytoplasmic and extracellular locations.
Am J Pathol 1975 Sep
PMID:Feline congenital erythropoietic porphyria associated with severe anemia and renal disease. Clinical, morphologic, and biochemical studies. 123 63

Maternal transmission of a murine leukemia virus (MuLV) mixture named LP-BM5 MuLV, which is knwon to induce murine AIDS (MAIDS), was investigated. Adult female C57BL/10 mice were inoculated intraperitoneally with LP-BM5 MuLV. When the virus-inoculated female mice developed splenomegaly or lymphadenopathy, they were mated with normal C57BL/10 male mice. Of 56 offspring born to MAIDS mothers, 14 appeared to develop MAIDS, as assessed by the occurrence of splenomegaly or lymphadenopathy as well as the mitogen response of spleen cells. The occurrence of MAIDS in offspring was found to be accompanied by the maternal transmission and expansion of a defective virus genome from which almost the entire pol and env regions are deleted. On the other hand, the ecotropic helper virus genome was detected in all offspring regardless of the occurrence of MAIDS. To examine the mode of maternal transmission of LP-BM5 MuLV, foster-nursing experiments were conducted. The ecotropic helper viruses were found in all normal offspring nursed by a MAIDS mother, and some of them developed MAIDS. In contrast, none of offspring born to a MAIDS mother that were nursed by an uninfected foster mother either carried the LP-BM5 MuLV or developed MAIDS. Finally, both the defective and the ecotropic helper viruses were detected in LP-BM5 MuLV-infected mother's milk. These results indicated that maternal transmission of LP-BM5 MuLV occurs with a high frequency and is mediated by mother's milk.
J Virol 1992 Sep
PMID:High frequency of transmission of murine AIDS virus in C57BL/10 mice via mother's milk. 132 88

The Duplan strain of murine leukemia virus induces murine AIDS in C57BL/6 mice. When spleen cells from C57BL/6 mice infected with the virus were transplanted into nude mice, subcutaneous solid tumors at the transplanted sites were formed and splenomegaly and lymphadenopathy were induced. These transplantable cells were Thy-1- CD4+ alpha-beta T-cell receptor-positive T cells and integrated with the pathogenic defective viral genome. These results indicate that neoplastic cells of T-cell lineage were induced by infecting C57BL/6 mice with murine AIDS virus.
J Virol 1992 Sep
PMID:Presence of transplantable T-lymphoid cells in C57BL/6 mice infected with murine AIDS virus. 132 20

The primary infection of BALB/c mice with murine herpesvirus 68 (MHV-68) was investigated. When the virus was introduced intranasally, the lung was the main tissue infected, the virus being associated with alveolar epithelium and mononuclear cells. A productive infection lasted for 10 days, after which viral DNA could be detected by in situ hybridization up to 30 days after infection. At that time lymphoproliferative accumulations were also observed in the lung, with formation of germinal centres. Virus could also be recovered from the heart, kidney, adrenal gland and spleen during the primary infection. In addition, the spleen appeared to be the major site of virus persistence, with latently infected cells detected up to 90 days post-infection. During the primary infection, there was atrophy of the thymus and spleen of clinically sick animals. In contrast, lymphoproliferative responses, typified by splenomegaly, were frequently seen in asymptomatic animals. The pattern of infection observed in MHV-68-infected mice is similar to that seen in infectious mononucleosis of man following Epstein-Barr virus infection. The model described in this paper may prove to be useful in studying natural gamma-herpesvirus infections of man and domestic animals.
J Gen Virol 1992 Sep
PMID:Virological and pathological features of mice infected with murine gamma-herpesvirus 68. 132 91

Splenic lymphoma with villous lymphocytes (SLVL) is a monoclonal B-lymphoproliferative disorder characterised by splenomegaly and distinctive villous lymphocytes in the peripheral blood. It has not previously been reported from Africa, but we describe ten Ghanaian patients with SLVL seen at one hospital during a 4-year period. The clinical presentation is similar in Africa and in temperate regions, though the lymphocyte count is higher in African patients and the disorder predominantly affects middle-aged women rather than elderly men. It is likely that SLVL has previously been classified as splenic chronic lymphocytic leukaemia or hyper-reactive malarial splenomegaly.
Lancet 1992 Sep 05
PMID:Splenic lymphoma with villous lymphocytes in tropical West Africa. 135 4

We describe retrospectively the experience with 44 cases of AIDS from January 1987 to October 1991 at the Instituto Nacional de Pediatria, a tertiary care children hospital in Mexico City. All patients with 2 ELISA and a positive Western Blot test were included. Thirty three patients were infected perinatally (75%) and 11 through blood transfusion (25%). Fourty one patients belonged to the P2 classification of the Centers for Disease Control. Chronic diarrhea (77%), lymphadenopathy (75%), hepatomegaly/splenomegaly (70%) and oral candidiasis (61%) were the most common clinical findings. Twenty patients died (45.4%). No statistical relation were found between survival rate and the way of transmission and age at onset. Autopsy was performed in 14 patients and revealed a sharp decrease of lymphoid tissue at all levels with severe thymic atrophy.
Bol Med Hosp Infant Mex 1992 Sep
PMID:[AIDS in children. Experience at the National Institute of Pediatrics]. 138 80

The authors report a rare case of splenomegaly, caused by recurring splenic torsion in a 31-year-old patient. On the basis of this experience and literature data, pathogenetic, symptomatological, diagnostic and therapeutic aspects are discussed. Analysis of the clinical history and diagnostic procedures confirm the difficulty in ascertaining this condition preoperatively. In any case, splenic torsion should be considered in the differential diagnosis of painful splenomegalies.
Ital J Gastroenterol 1992 Sep
PMID:Splenic torsion: a rare cause of splenomegaly. 139 27

A 69-year-old man with an enlarged spleen, found by computed tomography scan to be multicystic, underwent a splenectomy. Pathological examination revealed a Low-grade mucinous cystadenocarcinoma that was histologically analogous to a mucinous tumor of the ovary. The serum level of tumor markers carcinoembryonic antigen (CEA)and CA19-9 were elevated preoperatively and returned to normal after the operation. In the absence of a primary tumor elsewhere, we considered this tumor to be primary in the spleen, and it was presumed that the tumor arose either from invaginated capsular mesothelium of the spleen or from heterotopic pancreatic or enteric tissue within the spleen.
Am J Surg Pathol 1992 Sep
PMID:Low-grade mucinous cystadenocarcinoma in the spleen. 141 9

A patient is described presenting with an acute lower gastrointestinal haemorrhage as a result of extensive colonic varices. Further investigation revealed that there were no oesophageal varices or splenomegaly. Liver biopsy showed grade II fatty change only, with no other specific or significant pathological features. Transhepatic portography showed a raised portal pressure (20 mm/Hg) but the portal system was patent throughout. There was an abnormal leash of vessels in the caecum thought to represent a variceal plexus. This patient was diagnosed as having idiopathic colonic varices. This case is discussed together with nine other reports of idiopathic colonic varices from the published literature. Four of these reports describe idiopathic colonic varices in more than one member of the same family. Possible modes of inheritance, aetiology of variceal change, natural history, and prognosis are discussed.
Gut 1992 Sep
PMID:Familial and idiopathic colonic varices: an unusual cause of lower gastrointestinal haemorrhage. 142 83


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