Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum angiotensin-converting enzyme (SACE) activity was significantly higher in 90 patients with sarcoidosis (55 +/- [S.D.] 23 nmol min-1 ml-1) than in 80 healthy controls (34 +/- 9 nmol min-1 ml-1). Steroid therapy modified SACE activity; 60 sarcoidosis patients who were not being treated with steroids had significantly higher enzyme activities (58 +/- 24 nmol min-1 ml-1) than 30 steroid-treated sarcoidosis patients (40 +/- 19 nmol min-1 ml-1). In 50% of the non-steroid treated sarcoidosis patients SACE activity was more than 2 S.D. above the mean value for the controls. SACE activity was measured in 22 tuberculous patients (38 +/- 14 nmol min-1 ml-1), 20 leprosy patients (34 +/- 9 nmol min-1 ml-1), 31 with primary biliary cirrhosis (44 +/- 20 nmol min-1 ml-1), 26 with inflammatory bowel disease (31 +/- 9 nmol min-1 ml-1), 8 with hepatic granulomatous disease, 5 with Hodgkin's disease, and 2 with schistosomiasis. The combined false-positive rate for these non-sarcoidosis patients was 10%. Serial SACE assays provide useful information on the course of sarcoidosis and response to steroid treatment.
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PMID:Serum angiotensin-converting enzyme (SACE) in sarcoidosis and other granulomatous disorders. 8 38

Serum angiotensin-converting enzyme (SACE) activity was significantly higher in 90 patients with sarcoidosis (55 +/- [S.D.] 23 nmol min-1 ml-1) than in 80 healthy controls (34 +/- 9 nmol min-1 ml-1). Steroid therapy modified SACE activity; 60 sarcoidosis patients who were not being treated with steroids had significantly higher enzyme activities (58 +/- 24 nmol min-1 ml-1) than 30 steroid-treated sarcoidosis patients (40 +/- 19 nmol min-1 ml-1). In 50% of the non-steroid treated sarcoidosis patients SACE activity was more than than 2 S.D. above the mean value for the controls. SACE activity was measured in 22 tuberculous patients (38 +/- 14 nmol min-1 ml-1), 20 leprosy patients (34 +/- 9 nmol min-1 ml-1), 31 with primary biliary cirrhosis (44 +/- 20 nmol min-1 ml-1), 26 with inflammatory bowel disease (31 +/- 9 nmol min-1 ml-1), eight with hepatic granulomatous disease, five with Hodgkin's disease, and two with schistosomiasis. The combined false-positive rate for these non-sarcoidosis patients was 10%. Serial SACE assays provide useful information on the course of sarcoidosis and response to steroid treatment.
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PMID:Serum angiotensin--converting enzyme (SACE) in sarcoidosis and other granulomatous disorders. 23 39

A case of Hodgkin's disease involving an area of Crohn's colitis in a patient with a 20-year history of inflammatory bowel disease is described. The coexistence of Crohn's disease and Hodgkin's lymphoma has not been reported previously. The possible relationship between gastrointestinal lymphoma and Crohn's disease also is discussed.
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PMID:Hodgkin's disease complicating Crohn's colitis. 91 49

The incidence of various cancers, especially non-Hodgkin lymphoma (NHL), is higher among patients who receive azathioprine for immunosuppression after organ transplants than in the general population. We have studied the risk of neoplasia after azathioprine in 755 patients treated for inflammatory bowel disease. The patients received 2 mg/kg daily for a median of 12.5 months (range 2 days to 15 years) between 1962 and 1991; median follow-up was 9 years (range 2 weeks to 29 years). Overall there was no significant excess of cancer: 31 azathioprine-treated patients developed cancer before age 85 compared with 24.3 expected from rates in the general population (observed/expected ratio 1.27, p = 0.186). There was a difference in the frequency of colorectal (13) and anal (2) carcinomas (expected 2.27; ratio 6.7, p = 0.00001); these tumours are recognised complications of chronic inflammatory bowel disease. There were 2 cases of invasive cervical cancer (expected 0.5), but no case of NHL. Among patients with extensive chronic ulcerative colitis there was no difference in cancer frequency between 86 who had received azathioprine and 180 matched patients who had never received it. Thus, azathioprine treatment does not substantially increase the risk of cancer in inflammatory bowel disease.
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PMID:Long-term neoplasia risk after azathioprine treatment in inflammatory bowel disease. 791 Feb 74

The histologic features of acute graft-versus-host disease (GVHD) of the colon are well documented, but chronic mucosal changes associated with GVHD are poorly described. We report here the clinicopathologic findings from five patients with a history of bone marrow transplantation in which colonoscopic biopsies showed chronic mucosal changes reminiscent of chronic idiopathic inflammatory bowel disease (IBD). The patients ranged in age from 2.5 to 31 years. Bone marrow transplantations were performed for leukemia (3 patients), Hodgkin's disease (1 patient), and metachromatic leukodystrophy (1 patient). Endoscopy was performed because of complaints of abdominal pain and diarrhea in all of the five patients. The mean time after transplantation in which histologic features of chronicity were identified was 5.8 months (range, 3-16 mo). All of the five patients had prior colonic biopsies showing acute GVHD. One patient had a previous episode of cytomegalovirus infection. Chronicity was characterized by mild-to-moderate architectural distortion, ie., villiform surface with crypt branching and atrophy, similar to that seen in chronic idiopathic IBD. The lamina propria was hypocellular, with prominent small blood vessels. Focal fibrosis of the lamina propria was noted. One patient had active cryptitis. Superimposed changes of acute GVHD were mild to absent. None of the patients had a history of IBD before receiving the bone marrow transplant. Changes associated with chronicity can be observed in mucosal biopsy specimens from patients with GVHD. It is uncertain whether these changes are directly caused by GVHD or are the result of superimposed infections. The association of chronic mucosal change in the setting of GVHD with the clinical diagnosis of chronic GVHD needs additional investigation.
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PMID:Chronic mucosal changes of the colon in graft-versus-host disease. 964 87

Inflammatory bowel disease (IBD) is associated with an increased risk of lymphoma, which is usually extraintestinal but sometimes may involve the diseased bowel itself. Most lymphomas described in this setting are of non-Hodgkin's type, but rare cases of Hodgkin's disease (HD) have been reported. We describe the clinicopathologic and molecular features of four patients with primary gastrointestinal HD. Three patients had preexistent Crohn's disease (CD), for which two of them had received immunosuppressive therapy. The fourth patient had a longstanding history of diverticulitis and myasthenia gravis and was receiving immunosuppressive therapy for the latter. Multifocal involvement of the bowel by HD was noted in all four cases. Disease was staged as IVA in one patient, IIIB in one patient, and IE in one patient, and the fourth patient died in the postoperative period before further workup. Two patients received chemotherapy, one of whom was dead at 9 months, whereas the other has no evidence of disease at 25 months' follow-up. The patient with IE disease did not receive any therapy because only a few microscopic foci of disease were present and is also without any evidence of disease at 17 months. The Reed-Sternberg (RS) cells in all four cases expressed CD30, CD15, EBER-1, and LMP-1; two of four were focally CD20-positive. VJ-polymerase chain reaction for immunoglobulin heavy chain (IgH) rearrangement showed a polyclonal pattern in all four cases. In two cases, laser capture microdissection was used to isolate individual RS and Hodgkin's cells, which contained rearranged immunoglobulin genes, confirming a B-cell genotype. Whereas one case showed a dominant clonal band present in all isolates, cells from the patient with stage IE disease clearly showed a polyclonal population of RS cells. Our findings indicate that HD arising in the setting of IBD or chronic inflammation is the result of an Epstein-Barr virus-driven lymphoproliferation, analogous to that found in other immunodeficient states. Disordered immunoregulation inherent to CD and immunosuppressive therapy for the latter may contribute to its development. The finding of polyclonal RS cells in a patient with early stage disease and apparent cure by surgical resection versus monoclonal RS cells in the patient with disseminated disease suggests that HD in the setting of immunodeficiency also may show molecular progression, in a manner similar to that occurring in conventional B-cell lymphoproliferative disorders arising in the same setting.
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PMID:Epstein-Barr virus-positive primary gastrointestinal Hodgkin's disease: association with inflammatory bowel disease and immunosuppression. 1063 89

Extranodal Hodgkin disease presenting as a primary localized neoplasm is uncommon, with rare case reports describing primary sites other than lymph nodes. The gastrointestinal tract is the most frequent site of involvement by extranodal Hodgkin disease, typically involving the stomach or small bowel. To date, we have been able to find only one fully documented case of Hodgkin disease of the sigmoid colon confirmed by immunohistochemical studies. We report a case of extranodal Hodgkin disease involving the transverse colon, presenting as inflammatory bowel disease and documented by light microscopic, immunohistochemical, cytogenetic, and molecular studies.
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PMID:Primary localized extranodal hodgkin disease of the transverse colon. 1110 66

A case of a 32-years old man with a long lasting history of inflammatory bowel disease (IBD) is described. He was treated in the past with adequate medical therapy with considerable improvement of the symptoms. However, after the resolution of the last episode of abdominal pain and diarrhoea, because of multiple protruding masses and sub-stenotic regions found during a colonoscopy, the patient underwent a right enlarged hemicolectomy with jejunal resection. During the surgical procedure 16 enlarged lymphnodes were removed. The histological examination of the surgical specimen showed the presence of numerous Reed-Sternberg cells, compatible with a diagnosis of Hodgkin's disease (HD). None of the removed lymphnodes showed the presence of tumor cells, and in addition the systemic staging procedure was negative. After staging, the ABVD regimen was started, achieving a complete clinical and pathological response. This is a rare case of primary extranodal HD localized to the colon, in a patient with a long standing history of IBD, who showed an optimal response to chemotherapy. The case and the differential diagnosis with other pathological entities of the bowel is discussed.
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PMID:Unusual presentation of Hodgkin's disease mimicking inflammatory bowel disease. 1169 19

We report a case of fulminant Crohn's colitis that occurred following non-myeloablative allogeneic stem cell transplantation for Hodgkin's lymphoma. Adoptive transfer of inflammatory bowel disease by haematopoietic cells is recognised in several animal models of inflammatory bowel disease and remission of Crohn's disease has been reported in patients who have received a bone marrow transplant. However, adoptive transfer of Crohn's disease susceptibility leading to phenotypic manifestation of the disease after transplantation has not been previously reported. Having ruled out an infective cause of a colitis in this case, we speculated that adoptive transfer of Crohn's disease may have occurred and performed a genetic analysis of known susceptibility loci for significant donor-recipient mismatches. The donor and recipient had several haplotype mismatches in HLA class III genes at the IBD3 locus. In addition, the donor (but not the recipient) had a polymorphism of the 5' UTR of NOD2/CARD15 that may be associated with Crohn's disease. This case highlights the question of whether adoptive transfer of Crohn's disease can occur between allogeneic stem cell transplant donor and recipient, in a similar fashion to that reported for other autoimmune diseases. This report should also stimulate debate regarding the need for stem cell transplant donor screening for inflammatory bowel disease.
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PMID:Fulminant Crohn's colitis after allogeneic stem cell transplantation. 1530 9

Due to the development of more effective medications, those infected with HIV are living longer. Consequently, more tumors and infections have been added to the AIDS-defining criteria in the last decade. Our aim was to review the occurrence and clinical course of colorectal (CR) malignancies in HIV infected/AIDS patients from a single institution. A retrospective review of HIV/AIDS patients with colorectal malignant tumors was undertaken. We included adult patients, with ELISA and Western blot test positive for HIV, and primary malignant tumors located in the colon or rectum. Malignant neoplasms of the anus were excluded for the purposes of this study. Twelve patients (9 males and 3 females), mean age 41 years, were identified with the following neoplasm: 6 adenocarcinomas (ACA), 5 non-Hodgkin lymphomas (NHL), and 1 small-cell carcinoma. Intravenous drug abuse was the main risk factor for HIV. No patient had identified risk factors for colorectal neoplasm. Five out of six patients with ACA had metastatic disease at the time of diagnosis. One patient with stage II ACA developed early liver metastases after colonic resection. Seven out of 12 patients underwent surgery. Six (85.7%) of these sustained postoperative complications, primarily wound infection. The overall survival in our series was dismal, averaging 20 months. For NHL average survival was 29 months, and 12 months for CR-ACA. This is the largest series of cases of colorectal cancer in the HIV/AIDS patient population published in the English language and the largest number of colorectal ACA reported in this unique population. Early in our experience, tumors frequently found in immunoincompetent patients were detected (NHL). More recently, we have only treated patients with colorectal ACA; none of them had no risk factors for colorectal cancer (family history, IBD, FAP, HNPCC). These patients developed tumors at earlier ages and were diagnosed at an advanced stage. Therefore, these tumors may be associated with the grade of immunosuppression induced during the course of the HIV infection and with a tumorigenic effect of the HIV on the colonic epithelium. Consequently, a high index of suspicion when evaluating chronic abdominal complaints in such patients is warranted. The use of the new antiretroviral therapy regimens should be further evaluated to know its impact in the survival.
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PMID:Colorectal malignancies in HIV-positive patients. 1462 61


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