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)

Sixty-day bioassays of iodinated glycerol, trichlorfon, and acetaminophen were conducted using a leukemia transplant model in 6- to 8-week-old F344 rats to investigate the potential of these chemicals to affect tumor progression. The chemicals were administered in the drinking water at doses that approximated those used in previously conducted 2-year carcinogenesis studies. Simultaneous with dose administration, half of a group of young, healthy, syngeneic rats were given subcutaneous transplants of mononuclear cells derived from spleens of leukemic donors. Variables used to quantitate tumor progression included body weight, spleen weight, white blood cell (WBC) and red blood cell (RBC) counts, packed cell volume, hemoglobin concentration, and platelet counts. Iodinated glycerol at 1.25 or 2.5 mg/ml caused a greater increase in leukocytosis in dosed transplant recipients in comparison to that experienced by undosed recipients: trichlorfon at 2.5 or 5.0 mg/ml enhanced splenomegaly and induced greater reductions in RBC parameters in dosed recipients in comparison to that experienced by undosed recipients. Acetaminophen at 3.0 and 6.0 mg/ml resulted in insignificant but dose-related increases in spleen weight and leukocytosis only in the female rat transplant recipients, as was observed in 2-year studies. Based on results from the short-term leukemia transplant model, data from 2-year carcinogenicity studies, and structure-activity considerations, exposure to iodinated glycerol and trichlorfon was more strongly associated with the expression of leukemia than exposure to acetaminophen. The potential carcinogenicity of each of these chemicals should be taken into consideration when calculating estimates of risk and decisions for their use.
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PMID:The effects of iodinated glycerol, trichlorfon, and acetaminophen on tumor progression in a Fischer rat leukemia transplant model. 145 7

A 44-year-old man had several episodes of tingling sensation in his lower extremities, head and face over 1 year and presented mental disturbance 2 months prior to admission. He additionally suffered from dysuria and acute onset of gait disturbance 18 days before admission. Physical and neurological examination revealed marked splenomegaly, stupor, abnormal behavior, spastic tetraparesis and sphincter disturbances, and meningoencephalitis was suspected. There was lymphocytosis in peripheral blood, some of which showed atypical morphology. CSF examination revealed increased protein content and mononuclear pleocytosis. The titers of antibodies against E-B virus were elevated as follows; VCA IgM (X320), VCA IgG (X20,480), EA (X10,240) and EBNA (X10) in serum, and VCA IgM (X4), VCA IgG (X160), EA (X40) and EBNA (less than 1) in CSF. CT and MRI examination revealed ring enhanced lesion adjacent to left lateral ventricle with surrounding diffuse edema. Administration of intravenous glycerol and oral prednisolone induced substantial improvement in sensory, mental and sphincter disturbances and brain CT findings but not in splenomegaly and pyramidal tract signs. Antibody titer against VCA IgM also decreased. After withdrawal of prednisolone, CSF and CT findings worsened, and the antibody titer became elevated again, and CSF and CT findings improved by readministration of prednisolone. From the above signs and laboratory data, especially continuous elevation of antibody titer against E-B VCA IgM for as long as 1 year, this case was considered to be a meningoencephalitis caused by persistent E-B virus infection.
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PMID:[A case of meningoencephalitis caused by persistent Epstein-Barr (E-B) virus infection]. 254 1

A case of liver glycogen storage disease with amylo 1,6-glucosidase deficiency is reported. Enlarged liver was found at birth, and it is now accompanied by splenomegaly, low fasting blood glucose with ketonuria, elevation of transaminase values and glycogen accumulation with connective periportal tissue in liver histological study. In this glucogenosis results of functional tests on carbohidrate metabolism and glycogen enzymatic assay showed a direct relationship between functional and biochemical behaviour of liver cells. Amylo 1,6-glucosidase deficiency is accompanied by absence of glucogenolysis when glucagon is administrated after a long fast, and an increase of blood glucose when glucagon is administrated after food ingestion. Glycolisis tests show blood lactate elevation when some hexose or alanine are administrated; glyconeogenesis tests show blood glucose elevation when hexose, alanine or glycerol are administrated.
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PMID:[Glycogen storage disease by amylo 1,6-glucosidase deficiency (author's transl)]. 693 53

Mycobacteria have the ability to enhance or depress immune responses. This paper describes experiments designed to investigate the parameters determining the direction of modulation. It has been shown previously that 10(8) liver Mycobacterium bovis BCG depress the ability of mouse spleen cells to produce a primary antibody response in vitro to SRBC 2-3 weeks after i.v. injection, whereas the same number of dead organisms enhance this response. Using the same growth medium for the BCG (Glaxo glycerol-free medium), we now find that decreasing the BCG dose to mice from 10(8) to 10 (6) liver organisms results in enhanced responses and increasing the dose to more than 10(8) dead organisms results in depressed responses. It thus appears that bacterial load is the important factor determining whether depression or enhancement of the primary antibody response will occur, rather than the viability of the organisms per se. However, when the BCG was grown in Middlebrook 7H9 broth, doses as high as 4 X 10(9) dead BCG/mouse failed to depress although depressed responses were found if sufficient live organisms (7 X 10(8)) were injected. In view of the known growth characteristics of BCG in these 2 bacteriological media, it is suggested that the degree of aggregation of the injected suspension may also be of importance in determining whether or not depression will occur. A comparison of the effects of BCG injected untreated or after dispersion of bacterial aggregates supports this idea. Some degree of splenomegaly was always found in mice with depressed splenic responses but a large spleen did not necessarily yield cell suspensions with depressed responses.
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PMID:Mycobacterium bovis, BCG, modulation of murine antibody responses: influence of dose and degree of aggregation of live or dead organisms. 704 44

Phosphatidylcholine (PC) and licensed formulations containing PC were tested for their influence on the proliferation and viability of cells permanently infected with HIV-1 (human immunodeficiency virus type 1). PC alone, as well as pharmaceutical formulations containing PC, selectively inhibited the growth of productively infected lymphoid cells. The strongest growth inhibition was observed with formulations containing PC, glycerol and triglyceride together. The growth inhibition was dose-dependent for HIV-1-infected cells. Additionally, PC-containing formulations dramatically reduced antigen production from peripheral blood mononuclear cells (PBMCs) infected in vitro with HIV-1. In vivo experiments with Rauscher-MuLV-infected mice showed that PC administered either intraperitoneally or orally was able to inhibit Rauscher-virus-induced splenomegaly. PC-containing formulations are currently used in man for supportive therapy at doses, which in vitro induced 50% growth inhibition of HIV-1-infected cells in vitro. Such doses have been used in man without side effects for many years. Thus, PC-containing formulations may be valuable for the treatment of HIV-1-infected individuals.
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PMID:Reduction of HIV-1 antigen production by phosphatidylcholine containing formulations via growth inhibition of HIV-1-infected cells. 851 63

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

We describe a 6-year-old girl and her mother with dominant beta-thalassemia due to hemoglobin Hradec Kralove (Hb HK). Both patients presented microcytic anemia, jaundice, splenomegaly, cholelithiasis, and recurrent hemolytic bouts. Osmotic resistance tests using saline and coiled planet centrifugation revealed the increased fragility of the red cell membrane. On the other hand, the glycerol lysing time was prolonged, and results of the isopropanol test were weakly positive. Despite mimicking the features of hereditary spherocytosis, the results of the genetic analyses verified the second reported family with Hb HK (codon 115, GCC [Ala] --> GAC [Asp]). Splenectomy was effective for the amelioration of hemolysis. Of 7 reported patients with Hb variants at beta-globin codon 115 (Hb Madrid and Hb HK), 5 underwent splenectomy. Because of the variable augmentation of extramedullary hemolysis in dominant beta-thalassemias, genotyping is necessary for determining the clinical indication of splenectomy.
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PMID:Dominant beta-thalassemia with hemoglobin Hradec Kralove: enhanced hemolysis in the spleen. 1468 90

Growing evidence highlights the endocannabinoid (EC) system involvement in cancer progression. Lipid mediators of this system are secreted by hematopoietic cells, including the ECs 2-arachidonoyl-glycerol (2AG) and arachidonoyl-ethanolamide (AEA), the 2AG metabolite 1AG, and members of N-acylethanolamine (NAE) family-palmitoyl-ethanolamide (PEA) and oleoyl-ethanolamide (OEA). However, the relevance of the EC system in myeloproliferative neoplasms (MPN) was never investigated. We explored the EC plasma profile in 55 MPN patients, including myelofibrosis (MF; n = 41), polycythemia vera (PV; n = 9), and essential thrombocythemia (ET; n = 5) subclasses and in 10 healthy controls (HC). AEA, PEA, OEA, 2AG, and 1AG plasma levels were measured by LC-MS/MS. Overall considered, MPN patients displayed similar EC and NAE levels compared to HC. Nonetheless, AEA levels in MPN were directly associated with the platelet count. MF patients showed higher levels of the sum of 2AG and 1AG compared to ET and PV patients, higher OEA/AEA ratios compared to HC and ET patients, and higher OEA/PEA ratios compared to HC. Furthermore, the sum of 2AG and 1AG positively correlated with JAK2V617F variant allele frequency and splenomegaly in MF and was elevated in high-risk PV patients compared to in low-risk PV patients. In conclusion, our work revealed specific alterations of ECs and NAE plasma profile in MPN subclasses and potentially relevant associations with disease severity.
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PMID:Disease-Specific Derangement of Circulating Endocannabinoids and N-Acylethanolamines in Myeloproliferative Neoplasms. 3240 7