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)

Marked increases in phospholipase B activity were measured in spleen homogenates and sera of CD-1 mice given a primary infection of Plasmodium yoelii. The rise in enzyme activity paralleled parasitemia and splenomegaly, all reaching maximum values 14 days after infection. Maximum enzyme activity and splenomegaly were noted 5 days after challenge in mice given a secondary infection indicating an anamnesticlike response following a subsequent contact with the infecting parasite. These observations represent a new finding of this enzyme activity in a protozoan infection.
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PMID:Elevated levels of phospholipase B in mice infected and challenged with Plasmodium yoelii. 713 Nov 82

A 16-year-old Caucasian girl of Albanian origin was admitted to the hospital complaining of intermittent fever (38 degrees C) for a week, nausea, vomiting, and abnormal laboratory findings (elevated serum aminotransferases levels AST/ALT 77/40 U/l and erythrocyte sedimentation rate 80 mm/first hour, as well as leukopenia 2.5 x 10(3)/mm3), which were found in a blood examination. Physical examination revealed slight hepatomegaly and splenomegaly, as well as cervical and axillary lymphadenopathy. A diagnostic open lymph node biopsy was performed and Kikuchi-Fujimoto disease (KFD) was established based on the characteristic histological pattern. Other abnormal laboratory findings were C-reactive protein 6.8 mg/dl and serum lactate dehydrogenase 900 U/l. Her history included a diarrhoea syndrome 2 months before the present admission, during the summer holidays, for which she was treated with metronidazole. At that time, characteristic cysts of giardia lamblia intestinalis were observed in the stools. Herein, we present this case hypothesising that the protozoal infection caused by the giardia lamblia intestinalis was probably triggering an immune response leading to KFD. The patient's age in combination with this firstly reported protozoal pathogen, as a triggering agent leading to KFD, consist a very interesting originality. Additionally, some review data is also given.
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PMID:Giardia lamblia intestinalis: a new pathogen with possible link to Kikuchi-Fujimoto disease. An additional element in the disease jigsaw. 1564 21

As a result of this study it may be stated that primary splenomegaly of the Gaucher type is a distinct disease, related in all probability to the blood diseases. It begins usually at an early age, frequently affects several members of a family, and runs a chronic course. The clinical manifestations are: pronounced hypertrophy of the spleen, subsequent enlargement of the liver, absence of palpable lymph nodes, absence of jaundice and ascites, absence of characteristic blood changes, discoloration or pigmentation of the skin, and a tendency to epistaxis or other hemorrhages. The lesions are found in the spleen, lymph nodes, bone marrow, and liver. These organs show the presence of iron-containing pigment, and large multinuclear cells with a characteristic cytoplasm. In the early cases peculiar large phagocytic cells arising from atypical large lymphocytes are found in the follicles (keimcentra) of the hemapoietic system. After leaving the follicles these cells possess phagocytic qualities for a certain period. As a result of the phagocytosisthe cells enlarge, the nature of the cytoplasm changes, and the cells acquire a characteristic vacuolated and wrinkled appearance. The cells are carried from the spleen through the portal system to the liver, where they are destroyed. The irritation produced by this destructive process gives rise to an increase in the intralobular connective tissue. The disease is eminently a chronic one, without any of the manifestations of malignancy, and always terminating as the result of some intercurrent affection. The etiology is unknown, although a family predisposition to some toxic agent which causes an irritability of the follicles in the hemapoietic system probably exists. The possibility of some protozoan infection as an etiological factor must not be overlooked.
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PMID:A CONTRIBUTION TO THE PATHOLOGY OF PRIMARY SPLENOMEGALY (GAUCHER TYPE), WITH THE REPORT OF AN AUTOPSY ON A MALE CHILD FOUR AND ONE HALF YEARS OF AGE. 1986 14

Five cats were experimentally inoculated with Trypanosoma evansi in order to evaluate the pathological changes induced by this protozoan infection. Clinical signs observed included vomiting, diarrhoea, hyperthermia, weight loss, facial oedema, corneal opacity, lymphadenopathy and hindlimb instability. Reduction in hematocrit was observed from 7 days post-infection (dpi) (P<0.05). One cat died at 40 dpi and the other four cats were humanely destroyed. Necropsy examination was performed in two cats at 56 dpi and two cats at 120 dpi. Gross findings in all cats included generalized muscle atrophy, pale mucosae, icterus of the subcutaneous and serosal tissue and the intima of arteries, lymphadenopathy and splenomegaly. Other findings included corneal opacity, subcutaneous oedema (mainly of the head) and hydropericardium. Trypomastigotes of T. evansi were observed in impression smears prepared from the aqueous humor. Microscopically, there was lymphoid hyperplasia of the spleen and lymph nodes. The animals with corneal opacity had mild corneal oedema and accumulation of fibrin and inflammatory cells (neutrophils and plasma cells) in the anterior chamber. Similar inflammatory cells infiltrated the iris, ciliary body, corneoscleral limbus and conjunctiva.
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PMID:Pathological findings associated with experimental infection by Trypanosoma evansi in cats. 1995 95