Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular invasion is not a prominent feature of cholangiocarcinoma (CCC), in contrast to hepatocellular carcinoma (HCC), which frequently shows extensive vascular tumor thrombi. We report an autopsy case of CCC with extensive portal tumor thrombi and portal hypertension. A 57-yr-old man presented with abdominal pain. Liver imaging revealed no tumors, but showed intrahepatic portal venous obstruction. HCC with portal tumor thrombi was suspected clinically. His clinical course was rapid; he died of hepatic failure 50 days after admission. At autopsy, the liver (2,700 g) was studded with diffuse whitish yellow granular areas with flecks of coalescent granules. Intrahepatic portal veins were diffusely occluded by tumor thrombi. Microscopically, the tumor was poorly differentiated adenocarcinoma with mucin; tumor cells were immunohistochemically positive for carcinoembryonic antigen, CA 19-9, DU-PAN-2, and biliary type cytokeratins, but negative for alpha-fetoprotein. Tumor cells were diffuse in the liver, and there were numerous tumor thrombi in the small portal veins. Hepatic veins and small arteries were occasionally occluded by tumor thrombi. There was ascites, splenomegaly and tumor thrombi in the gastric and esophageal veins, suggesting that portal hypertension had been present. This tumor seemed to have marked affinity to invade portal veins. It must be stressed that there are CCCs with extensive portal tumor thrombi and resultant portal hypertension.
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PMID:Extensive portal tumor thrombi with portal hypertension in an autopsy case of intrahepatic cholangiocarcinoma. 132 98

Thirty patients suffering from active intestinal S. mansoni infection, were classified into 3 groups. The first group: 13 cases with early active intestinal schistosomiasis without hepatosplenomegaly. The second group: 11 cases with hepatosplenomegaly and the third group: 6 cases with splenomegaly and ascites. Also 10 normal individuals were included as a normal control group. Histopathological examination of rectal mucosa showed hyperaemia with extravasation of blood in early cases and granulomatous lesions in the second group with hepatosplenomegaly. The structural changes were severe in the late ascitic group. In this group the rectal mucosal glands showed distorted irregular tubular branching in addition to the granulomatous and the fibrous reactions. Histochemical studies including periodic acid schiff, alkaline phosphatase and acetyl cholinestrase reactions were done. Using the periodic acid shiff stain, the goblet cells showed strong reaction for neutral mucin in cases of group I (early cases) and group II (late hepatosplenomegalic cases). In group III (late ascitic cases) the goblet cells were faintly stained. A notable difference was observed between the lightly and heavily infected patients of this group. No alkaline phosphatase reactivity could be identified in rectal crypts of patients and controls. Alkaline phosphatase reactivity was sharply localised in S. mansoni egg shell. There was obvious decrease in the acetyl cholinesterase stained nerve fibres in the rectal mucosa of all studied patients. The decrease was more in chronic and heavily infected cases rather than in the acute and lightly infected ones.
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PMID:Histochemical studies on rectal mucosa in active intestinal schistosomiasis. 190 99

Albino mice (8-10 wks) weighing between 14 and 25 g were divided into 2 groups and dosed orally once per week with 2 doses (7 mg/kg and 21 mg/kg) of the gut-stimulating principle in Croton penduliflorus seeds (CP crystals) for 12 weeks. Some mice (3-4) from each group were killed at 10 days intervals for the first 6 wks of the experiment and at 20 days intervals for the last 6 weeks. Gross and histopathological changes in the brain, heart, liver, kidney, adrenal, spleen, testis, lung and various segments of the gastrointestinal tract including the stomach, duodenum, ileum and colon were observed. The relative weights of the visceral organs were also recorded. Significant weight change in the spleen was evident. The congestion of the lung was the most common gross pathological observation made. Other observations were splenomegaly, enlarged heart, swollen uterine horns, etc. Histopathological changes observed included haemorrhages in the lungs, myocardium, liver, kidney, testis, brain etc. Goblet cell hyperplasia with mucin present in the lumen were observed in the jejunum, ileum and colon. In conclusion, CP crystals produced severe lesions in the visceral organs and the brain after chronic oral administration at low and high dosage levels which should indicate caution in administering the extract to humans.
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PMID:The toxic effects of a chronic administration of the gut-stimulating principle in Croton penduliflorus hutch. seeds in mice. 271 10

The present studies were undertaken to evaluate the histologic effects of graft-versus-host disease on the host colon after small bowel transplantation. Graft-versus-host disease was produced in six Lewis x Brown Norway F1 rats by performing vascularized, out-of-continuity small bowel transplants from parental Lewis donors. Host proximal and distal colon were sampled 14 days after operation when signs of graft-versus-host disease, including weight loss and splenomegaly, were present. Tissue was assessed histologically by blinded observer and compared to eight sham-operated controls. Three histologic features were noted to be statistically increased in diseased animals: (1) mucin loss; (2) crypt abscesses; and (3) large lymphoid aggregates in the mucosa and submucosa. These features were more commonly noted in the distal rather than the proximal colon. Another group of five grafted animals treated with cyclosporine A (10 mg/kg/day intramuscularly) still lost weight but did not display overt signs of graft-versus-host disease and had normal-sized spleens. There was normal mucin content and no evidence of crypt abscesses in these treated animals, although large lymphoid aggregates were present. It is concluded that mucin loss, crypt abscesses, and large lymphoid aggregates are characteristics of graft-versus-host disease-induced colonic injury in this model and that these changes are most evident in the distal colon. Cyclosporine A therapy does not completely reverse the histological changes of colonic graft-versus-host disease. This model may be useful in studying the mechanisms by which immune mediated colitides preferentially affect the distal colon.
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PMID:Graft-versus-host disease after small bowel transplantation is associated with host colonic injury. 755 45

A case presentation of a patient with SLE associated with papulonodular mucinosis, generalized lymphadenopathy and splenomegaly is reported, along with a review of the literature. This 24 year old woman had biopsy-proven, skin lesions consistent with dermal mucinosis and a non-homogeneous immunofluorescence pattern. Serum anti-nuclear and anti-DNA antibodies were present and a mesangioproliferative glomerulonephritis was documented. The patient responded dramatically to standard therapy with prednisolone. The nature of the mucin deposits and the pattern of immunofluorescence deposition in the skin are discussed based on the findings reported in the literature.
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PMID:[A case of lupus associated with papulo-nodular mucinosis]. 807 67

During chronic viral infection, persistent exposure to viral Ags leads to the overexpression of multiple inhibitory cell-surface receptors that cause CD8(+) T cell exhaustion. The severity of exhaustion correlates directly with the level of infection and the number and intensity of inhibitory receptors expressed, and it correlates inversely with the ability to respond to the blockade of inhibitory pathways. Friend virus (FV) is a murine retrovirus complex that induces acute high-level viremia, followed by persistent infection and leukemia development, when inoculated into immunocompetent adult mice. In this article, we provide conclusive evidence that FV infection results in the generation of virus-specific effector CD8(+) T cells that are terminally exhausted. Acute FV-induced disease is characterized by a rapid increase in the number of virus-infected erythroblasts, leading to massive splenomegaly. Most of the expanded erythroblasts strongly express programmed death ligand-1 and MHC class I, thereby creating a highly tolerogenic environment. Consequently, FV-specific effector CD8(+) T cells uniformly express multiple inhibitory receptors, such as programmed cell death 1 (PD-1), T cell Ig domain and mucin domain 3 (Tim-3), lymphocyte activation gene-3, and CTLA-4, rapidly become nonresponsive to restimulation and are no longer reinvigorated by combined in vivo blockade of PD-1 and Tim-3 during the memory phase. However, combined blockade of PD-1 and Tim-3 during the priming/differentiation phase rescued FV-specific CD8(+) T cells from becoming terminally exhausted, resulting in improved CD8(+) T cell functionality and virus control. These results highlight FV's unique ability to evade virus-specific CD8(+) T cell responses and the importance of an early prophylactic approach for preventing terminal exhaustion of CD8(+) T cells.
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PMID:Premature terminal exhaustion of Friend virus-specific effector CD8+ T cells by rapid induction of multiple inhibitory receptors. 2066 Mar 55