Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and histological findings in a 54-year-old patient with enteropathy-associated T-cell lymphoma (EATL) occurring 18 years after renal transplantation are presented. Ten years after adult-onset coeliac disease the patient developed medium to large T-cell non-Hodgkin's lymphoma of the small intestine. Epstein-Barr virus (EBV) genome was detected by polymerase chain reaction in the lymphoma tissue and localized via Epstein-Barr virus RNAs in situ hybridization to some of the tumour cells. This is the first case report of EBV-positive EATL occurring in the setting of immunosuppression.
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PMID:Enteropathy-associated T-cell lymphoma in a renal transplant patient with evidence of Epstein-Barr virus involvement. 133 79

Placental ferritin is a tumour associated antigen present in the serum of patients with active Hodgkin's and non-Hodgkin's lymphoma, and the serum values fall during remission of the disease. There is no correlation between placental and total blood ferritin values. Because of the strong association between coeliac disease and lymphoma, 19 children with active and 25 with inactive coeliac disease were screened for the presence of placental ferritin. Thirty two children with other intestinal disorders served as controls. Placental ferritin was identified by using a monoclonal antibody in an ELISA procedure. The mean (SEM) placental ferritin value in the control serum was 12.6 (2.4) while the values in serum of patients with active and inactive coeliac disease were 117 (22.8) and 43.8 (10.2) U/ml respectively. Patients with active coeliac disease differed significantly from both control subjects (p = 0.0004) and those with inactive disease (p = 0.03). Peripheral blood lymphocytes contained no placental ferritin. It was present, however, in lamina propria lymphocytes of intestinal biopsy specimens from active coeliacs. Placental ferritin was also found in some of the better differentiated malignant cells in two patients with adult onset enteropathy associated lymphoma. Placental ferritin is known to have an immunosuppressive effect, and this may be one of the necessary steps in the development of malignancy associated with coeliac disease. Gluten free diet, by reversing this state, may have a role in the prevention of lymphoma.
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PMID:Placental ferritin in coeliac disease: relation to clinical stage, origin, and possible role in the pathogenesis of malignancy. 191 5

Gastrointestinal disease in AIDS is common and is due to opportunistic infections, aggressive malignancy and possible direct HIV enteropathy. Disabling gastrointestinal symptoms are prominent both in patients with established AIDS and in patients with earlier stages of HIV infection. We report the cases of 160 patients with AIDS who underwent gastroenterological investigations at St Vincent's Hospital, Sydney, between November 1983 to October 1987. Of these, 127 had the diagnosis of AIDS established prior to referral and 33 patients had the diagnosis of AIDS established as a result of gastroenterological investigations. Diarrhoea and weight loss (88%) were the most frequent reasons for undertaking gastroenterological investigations. Swallowing disorders (47%), abdominal pain (20%), oral and perianal disease (74%) and evidence of hepatobiliary disease were the other major indications for investigation. In 90% of cases there was evidence of concurrent and active gastrointestinal disease at two or more sites within the alimentary tract. Results from this series reveal a wide range of infectious pathogens: viral (Cytomegalovirus, Herpes simplex), bacterial (Mycobacterium avium intracellulare) and parasitic (Cryptosporidium, Isospora belli). Kaposi's sarcoma and non-Hodgkin's lymphoma were the only malignancies detected in this series. Gastrointestinal disease associated with HIV infection is common, and contributes significantly to its overall morbidity and mortality. Moreover, chronic diarrhoea, weight loss and malnutrition may also contribute to the overall immunodeficiency.
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PMID:The gastrointestinal manifestations of AIDS. 234 18

In a hamster model of non-Hodgkin's lymphoma which closely parallels the disease in man, and which is induced by an unusual agent(s), a diarrheal bowel disease was a major cause of mortality. This study was initiated to characterize this bowel disease and its relation to lymphoma induction and to natural diseases seen in the hamster. The studies showed that the bowel disease was an ulcerative process and was distinct from natural diseases. The incidence of the bowel disease correlated directly with that of the lymphoma in repeated epizootics, in titration studies, and in agent inactivation tests. The ulcerative bowel lesions were seen at the same stage of the disease as acute and chronic inflammatory infiltrates with necrosis in the thymus and mesenteric lymph nodes. Since necrosis in the gut-associated lymphoid tissue can lead to perforation and sepsis, these bowel lesions were lethal, whereas similar necrosis in other lymphoid tissues (thymus and lymph nodes) could be clinically undetectable. Similar lesions have been reported in man. The ulcerative bowel disease was a reliable early clinical marker for exposure of hamsters to this lymphomagenic agent(s).
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PMID:Lymphoma-associated ulcerative bowel disease in the hamster (Mesocricetus auratus) induced by an unusual agent. 637 5

Gastrointestinal (GI) disease is frequent in all types of immunocompromised patients but occurs with greatest frequency in patients with acquired immunodeficiency syndrome (AIDS). Thus, much of this review deals with human immunodeficiency virus (HIV)-related GI diseases. Gastrointestinal diseases in other immunocompromised patients are compared with those in patients with AIDS. Conditions unique to transplant recipients, such as graft-versus-host disease (GVHD) and posttransplant lymphoproliferative disorders (PTLDs), are discussed separately. We have divided these GI diseases into four main categories: (1) HIV-related inflammatory conditions other than opportunistic infections (HIV-related enteropathy, proctocolitis, and CD8 lymphocytosis); (2) inflammatory conditions unrelated to HIV or opportunistic infections (neutropenic enterocolitis, regional enteritislike enteropathy, and GVHD); (3) opportunistic infections (illnesses caused by herpesvirus, cytomegalovirus, and miscellaneous other viruses; Mycobacterium, Candida, Histoplasma, Cryptococcus, Cryptosporidium, Microsporida, Isospora, Leishmania, Toxoplasma and Strongyloides organisms as well as Pneumocystitis carinii; and (4) neoplasias (Kaposi's sarcoma [KS], AIDS-related non-Hodgkin's lymphoma [NHL], HIV-related Hodgkin's disease [HD], PTLDs, and miscellaneous neoplasms). The prevalence, pathogenesis, clinical manifestations, gross pathological findings, and microscopic features of each disease entity are discussed.
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PMID:Gastrointestinal disease in the immunocompromised patient. 795 57

A 22-year-old female with protein losing enteropathy due to congenital intestinal lymphangiectasia who developed non-Hodgkin's lymphoma of the bone, is described. Complete remission of the lymphomatous process and disappearance of the gastrointestinal symptoms were achieved following treatment with combination chemotherapy and local irradiation.
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PMID:Remission of malabsorption in congenital intestinal lymphangiectasia following chemotherapy for lymphoma. 822 Jan 48

A previously healthy 6-year-old boy developed symptoms of small intestinal obstruction and was found to have a large intraabdominal mass. At laparotomy the mass involved the jejunum and adjacent mesenteric lymph nodes, requiring resection. Microscopic and immunohistochemical studies demonstrated a T-cell non-Hodgkin's lymphoma, confirmed by finding clonal T-cell receptor-beta and -gamma gene rearrangements by Southern blot analysis. The immunophenotype of this lymphoma-CD3+CD4-CD8-CD56+TIA-1+ beta F1(-)-suggests that the tumor cells are cytotoxic natural killer (NK)-like T cells, probably of CD3+CD4-CD8- intraepithelial cell origin. Examination of the adjacent and distal small intestinal mucosa failed to show any significant pathologic change. This case was unusual because intestinal lymphomas in children are usually of B-cell origin and most commonly have small noncleaved cell morphology. Childhood intestinal T-cell lymphomas have not been the focus of specific study but appear to be rare. In adults, intestinal T-cell lymphomas often arise in the background of gluten-sensitive enteropathy (celiac disease). In contrast, this child had peripheral T-cell lymphoma, with NK-like T-cell features, in the small intestine with no clinical or histologic evidence of enteropathy.
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PMID:Natural killer-like T-cell lymphoma in the small intestine of a child without evidence of enteropathy. 925 61

An association between celiac disease and non-Hodgkin's lymphoma of the small intestine has been recognized for many years. Coeliac disease is characterized by an enteropathy sensitive to gluten, malabsorption of food and partial or total villous atrophy. Also malignant lymphoma may present with malabsorption and mucosal lesion similar to that found in coeliac patients. The diagnosis of lymphoma in coeliac patients can be extremely difficult because the presenting symptoms and histological lesion are similar, but the presence of a cluster of symptoms such as abdominal pain malabsorption, weight loss in patients older than 40 years with a history of poorly responsive coeliac disease should raise a suspicion of malignancy. We present a case of 55 year-old man with malignant lymphoma and coeliac disease surgically treated in our Institute for intestinal obstruction.
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PMID:[Problems of differential diagnosis of lymphoma and celiac disease. A case report]. 941 4

This study was designed to assess the efficacy and safety of gemcitabine, cisplatin and methylprednisolone (GEM-P) for patients with relapsed or refractory Hodgkin's disease (HD) and non-Hodgkin's lymphoma. Twenty-one patients were treated with gemcitabine (1000 mg/m2 d 1, 8 and 15), cisplatin (100 mg/m2 d 15) and methylprednisolone (1000 mg d 1-5) given every 28 d. Of these, 20 patients were evaluable for response. The median age was 38 years (range 17-64 years). Histological subtypes were: nodular sclerosing HD (n = 10), diffuse large B cell (n = 5), T cell-rich B cell (n = 2), follicular (n = 2), mantle cell (n = 1) and enteropathy-associated T-cell lymphoma (n = 1). The median remission duration prior to receiving GEM-P was only 42 d. The overall objective response rate was 80%[95% confidence interval (CI): 56-94%], including five complete and 11 partial responses. GEM-P induced responses in all histological subtypes, primary progressive disease and patients who had received a previous autograft. The only grade 3-4 toxicity was myelosuppression. However, no cases of febrile neutropenia or haemorrhage with thrombocytopenia were encountered. Median survival has not yet been reached and survival probability at 1 year was 60.8% (95% CI: 31.9-80.5%). In conclusion, GEM-P is a novel combination salvage therapy for poor-prognostic primary progressive or multiply relapsed lymphoma patients. It has clinically significant activity with a favourable toxicity profile.
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PMID:Gemcitabine, cisplatin and methylprednisolone chemotherapy (GEM-P) is an effective regimen in patients with poor prognostic primary progressive or multiply relapsed Hodgkin's and non-Hodgkin's lymphoma. 1264 66

T-cell non-Hodgkin's lymphoma (NHL) represents approximately 10% to 15% of all lymphomas in Western countries. Patients with T-cell NHL are often treated similarly to patients with intermediate grade B-cell NHL, although many reports have demonstrated lower overall survival rates in patients with T-cell NHL compared to patients with B-cell NHL. Updated classifications have recognized specific clinical and pathologic T-cell entities, such as peripheral T-cell lymphoma, not otherwise characterized, angioimmunoblastic lymphoma, systemic anaplastic T-cell lymphoma, adult T-cell leukemia/lymphoma, subcutaneous panniculitis-like T-cell lymphoma, hepatosplenic T-cell lymphoma, extranodal natural killer (NK)/T-cell lymphoma nasal type, and enteropathy-type intestinal T-cell lymphoma. Furthermore, these distinct T-cell NHL subtypes often warrant individualized diagnostic and therapeutic strategies, such as the associated cytophagic histiocytic panniculitis and hemophagocytic syndrome with subcutaneous panniculitis-like T-cell lymphoma, the chromosomal translocation t(2;5), leading to the nucleophosmin anaplastic lymphoma kinase fusion protein, viral pathogenesis of Epstein-Barr virus, human T-cell lymphotropic virus type-1 associated with extranodal NK/T-cell lymphoma nasal type and adult T-cell leukemia/lymphoma, respectively, and the role of radiation therapy in extranodal NK/T-cell lymphoma nasal type. Other active therapeutic agents in T-cell NHL include purine and pyrimidine antimetabolite agents (eg, nucleoside analogues and gemcitabine, respectively), denileukin diftitox, and antinucleoside or retinoic acid with interferon-alpha combination treatment. The exact role of transplantation in patients with T-cell NHL is unknown, but several case series have documented the feasibility of autologous and allogeneic transplant with reported long-term survival rates similar to transplanted B-cell NHL. Identification of relevant proto-oncogenes and tumor suppressor genes involved in the pathogenesis of T-cell NHL, such as the nucleophosmin anaplastic lymphoma kinase fusion protein, p53 and retinoblastoma gene, cyclin-dependent kinase inhibitors, histone deacetylation inhibitors, and infectious etiologies (eg, Epstein-Barr virus and Helicobacter pylori), in addition to their interplay with the various regulatory pathways of cell-cycle progression and apoptosis, represent potential candidates for molecular-based therapy. Prospective multi-institution clinical trials are critically important to determine the most effective treatment regimens that will continue to improve cure rates in these aggressive, yet treatable and often curable, diseases.
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PMID:Treatment of T-cell non-Hodgkin's lymphoma. 1523 6


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