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

Acute hepatitis with severe hepatic failure is an uncommon manifestation of herpes simplex virus (HSV) infection. It has been described in both immunocompromised and immunocompetent patients and is usually fatal. Due to the better survival after acyclovir treatment in a few reported cases, physicians need to be aware of the characteristic clinical abnormalities so that early diagnosis and treatment can be implemented. The authors describe an adolescent diagnosed with Hodgkin disease who developed fatal hepatic failure secondary to acute HSV. Typical signs and symptoms in patients at risk, when there is no other obvious cause of fulminant hepatitis, should lead to early empirical treatment with acyclovir.
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PMID:Fatal hepatic failure secondary to acute herpes simplex virus infection. 1545 44

There is insufficient information on the effects of chemotherapy protocols for Hodgkin's disease (HD) and the course of coexisting hepatitis C virus (HCV) infection. A single literature case reported a patient with HD who developed fulminant hepatitis and hepatic coma after receiving chemotherapy. The case described here is of a female patient previously exposed to prolonged war stress, complicated by intravenous drug abuse and chronic hepatitis C. One year after diagnosis of HCV infection she was diagnosed with HD (nodular sclerosis type II, clinical stage IIIB). The patient received six cycles of ABVD chemotherapy (doxorubicin, bleomycin, vinblastine and dacarbazine) resulting in complete remission of HD. There was no hepatitis flare either during or after chemotherapy. In conclusion, there were no adverse effects of the ABVD regimen on the course of HCV infection in this patient who was successfully treated for HD. Because concurrent HCV infection and HD is extremely rare, we discuss here the possibility of the synergistic contribution of chronic war stress and hepatitis C infection in the pathogenesis of HD.
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PMID:No adverse effect of ABVD chemotherapy in a patient with chronic hepatitis C and Hodgkin's disease. 1594 Oct 81

Cholestasis in a patient with Hodgkin's disease is uncommon, and the causes of cholestasis are mainly direct tumor involvement of the liver, hepatotoxic effects of drugs, viral hepatitis, sepsis and opportunistic infections. Vanishing bile duct syndrome (VBDS) represents a very rare cause for cholestasis in this disease. We report here on a case of a 45-year-old man who developed VBDS during the complete remission stage of Hodgkin's lymphoma. There was no history of hepatitis or intravenous drug abuse, and the patient had negative results for hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. The serological studies for antinuclear antibodies, anti-mitochondrial antibodies and anti-smooth muscle antibodies were also negative. Liver biopsy disclosed the absence of interlobular bile ducts in 9 of 10 portal tracts without any active lymphocyte infiltration and there were no Reed-Sternberg cell in the liver. The patient's cholestasis was in remission and the serum bililrubin level was normalized after two months without treatment, but tumor recurrence was noted at multiple sites of the abdominal lymph nodes on follow-up abdomino-pelvic computed tomogram.
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PMID:[Spontaneous resolution of vanishing bile duct syndrome in Hodgkin's lymphoma]. 1598 Jun 75

Lymphoma is a common hematological malignancy. Hepatitis viruses, especially hepatitis B and hepatitis C, are known risk factors for development of non-Hodgkin lymphomas. However, there are a number of patients with hepatitis in whom no virus can be identified and it was therefore postulated that there may be other agents which may be causing hepatitis. Many new hepatitis viruses have indeed been identified and proposed to have possible roles in pathogenesis of many disorders. Hepatitis G virus (HGV) is an example of a newly detected hepatitis virus. Whethere there is a correlation between infection and development of non-Hodgkin's lymphoma is of interest. Therefore an appraisal of the prevalence of HGV RNA among patients with B cell non-Hodgkin's lymphoma comparing with healthy control subjects was performed. According to the literature review, three reports covering 247 cases of non Hodgkin's lymphoma were recruited. The overall prevalence of HGV RNA positivity was found to be 7.2 % (18/247). Of the three reports, only two had complete data on the prevalence in both patients with B cell non-Hodgkin's lymphoma and healthy control subjects andwere used for further metanalysis study, covering 178 cases and 355 healthy subjects. The overall antibody positive rate in the patients and healthy subjects were 8.4 % (15/178) and 0.8 % (3/355), respectively, with an odds ratio is 10.8. According to this study, it can be seen that individuals who are HGV RNA positive may be at very high risk of B cell non-Hodgkin's lymphoma development.
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PMID:Individuals with HGV-RNA are at high risk of B cell non-Hodgkin's lymphoma development. 1610 37

Primary hepatic lymphomas represent rare neoplasms, which are partly observed in association with chronic viral hepatitis, immunosuppression and autoimmune diseases. In contrast, secondary hepatic lymphomas are much more frequent and represent disseminated disease. Lymphomas involving the liver include, with decreasing frequency, diffuse large B-cell lymphoma, small lymphocytic lymphoma, Hodgkin's lymphoma, peripheral T-cell lymphoma, follicular lymphoma and extranodal marginal zone B-cell lymphoma. Many B-cell lymphomas in the liver reveal a characteristic infiltration pattern allowing a rapid and cost-effective diagnosis based on focused immunohistochemical analyses. In contrast, most T-cell lymphomas show a more diverse morphology, which is sometimes difficult to differentiate from a reactive condition. Therefore, additional molecular analyses are frequently necessary. The differential diagnosis includes hepatitis and inflammatory bile duct diseases, undifferentiated carcinoma, inflammatory myofibroblastic tumor as well as histiocytic and dendritic cell neoplasms.
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PMID:[Malignant lymphomas of the liver: new diagnostic algorithms]. 1675 66

Rheumatoid arthritis is the commonest form of inflammatory arthritis and affects about 1-3% of the population in the West and even more in the developing world due to the compounded factors of late detection and inadequate treatment in the overall background of poverty, deprivation, and improper macro and micronutrients in the diet in a sizeable segment of the population. Nearly 90% of patients with aggressive disease will become clinically disabled within 20 years. Furthermore, in patients with severe disease or extra-articular symptoms, mortality is equal to that for patients with triple artery coronary artery disease or Stage IV Hodgkin's lymphoma. Anemia is a very common comorbidity of rheumatoid arthritis. Anemia in rheumatoid arthritis is caused by various factors, for instance, cytokine impact of the advanced arthritic process on the host, or lack of proper nutrition and essential micronutrients in the diet, or coexistent helminthiasis, and/or impact of antiarthritic drugs on the host system, i.e., high steroid induced gastritis or ulcerations in gastric mucosa or subclinical or clinical hepatitis due to methotrexate or salazopyrin effects on bone marrow, only to name a few. Other pre-existing or compounding gastrointestinal problems, which alter the available iron stores or cause bone marrow dysfunction, may also help in adding to an anemic condition. If the anemia is 8 g/dl or less, blood transfusion or erythropoietin injection with adequate hematinic reserve is effective in normal situations, but is not that effective in anemia with a chronic disease background like rheumatoid arthritis. Cord blood, because of its rich mix of fetal and adult hemoglobin, high platelet and white blood cell (WBC) counts, and a plasma filled with cytokine and growth factors, as well as its hypo antigenic nature and altered metabolic profile, has all the potential of a real and safe alternative to adult blood transfusion. Seventy-eight units (42 ml -136 ml mean 80.6 ml +/- 3.6 ml SD, median 82.4 ml, mean packed cell volume 48.2 +/- 2.1 SD, mean percent hemoglobin concentration 16.4 g/dl +/- 1.5 g/dl SD) of placental umbilical cord whole blood was transfused (from 1 April 1999 to April 2005) after lower uterine cesarean section (LUCS) from consenting mothers to 28 informed consenting patients with advanced rheumatoid arthritis who had plasma hemoglobin of 8 g/dl or less. After collection, the blood was immediately transfused following the standard adult blood transfusion protocol. Each case was passed through the institutional ethical committee. The patients received two to six units of freshly collected placental umbilical cord blood without encountering any clinical, immunological or non-immunological reactions. Three days after completion of the transfusion of placental umbilical cord blood, the peripheral blood hematopoietic stem cell (CD34) estimation revealed a rise from the pretransfusion base level (.09%), varying from 2.03 to 23%, which returned to base level in most of the cases at the three-month CD34 re-estimation, without provoking any clinical graft vs host reaction in any of the patients.
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PMID:Placental umbilical cord whole blood transfusion to combat anemia in the background of advanced rheumatoid arthritis and emaciation and its potential role as immunoadjuvant therapy. 1676 35

This prospective study analyzes the clinical features and histopathological findings in liver biopsies of pediatric patients presenting to the hospital with liver disease during a 10 year period. Only those patients in whom liver biopsy was performed for a tissue diagnosis were included. Fifty patients were investigated, all below the age of 12 years, of whom 36 were male and 14 female. Thirty-two were of neonatal-infantile group, 11 had a diagnosis of neonatal giant cell he hepatitis of infections origin and an intact biliary tree. Two had septic shock and one had leishmaniasis. The remaining 18 patients of the neonatal-infantile group constituted five case of glycogen storage disease, six of infantile obstructive cholangiopathy (biliary atreasia), four of fatty change and one each of congenital hepatic fibrosis, neuroblastoma and nonspecific reactive hepatitis. The eighteen older children had the following diagnoses: thalassemia in five, sickle cell disease in four, two each of Reye syndrome and hepatoblastoma. The remaining were one each of glycogen storage disease, Rotor syndrome, cirrhosis, fatty change and non-Hodgkin lymphoma (NHL). These findings are presented and discussed.
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PMID:Pediatric liver disease in the eastern province of Saudi Arabia: A clinicopathological study. 1758 93

Hepatitis B reactivation after chemotherapy is well known when Ag HBs is positive. Recommendation is to give preventive antiviral treatment before starting chemotherapy. The reactivation when there is only an anti-HBc antibody is rare. We report the case of a woman who developed an hepatitis B reactivation two weeks after the end of a chemotherapy for a high grade non Hodgkin lymphoma. Before chemotherapy, hepatitis B virus serology was positive only for anti-HBc antibody and viral load was negative. She had a fulminant hepatitis with fatal issue although a treatment by lamivudine and adefovir was rapidly started. In the literature, only 13 cases of patients with positive anti body anti-HBc alone who developed an hepatitis B reactivation after chemotherapy have been reported.
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PMID:[Fatal liver failure after hepatitis B reactivation following chemotherapy for lymphoma in a patient with only anti-HBc antibody and review of the literature]. 1816 1

Liver involvement in Hodgkin's lymphoma is common and is caused by hepatic infiltration, biliary obstruction by lymphoma, hepatitis, sepsis or complications of chemotherapeutic treatment. Jaundice caused by the vanishing bile duct syndrome related to Hodgkin's lymphoma is very rare. The mechanism is poorly understood but a paraneoplastic effect seems most likely as liver biopsy samples show cholestasis in the absence of lymphoma cells. Despite adequate treatment almost all reported patients died of liver failure or disease progression. Disease progression is explained partly by the difficulties encountered in the administration of potential hepatotoxic chemotherapy in severely cholestatic patients. We describe a 17-year-old man with vanishing bile duct syndrome and Hodgkin's lymphoma who was treated successfully with chemotherapy. The markedly elevated serum bilirubin levels completely normalized. Our case demonstrates that although dosing of chemotherapy in this situation can be very difficult, a good clinical outcome is possible, which makes the attempt at curative treatment worthwhile.
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PMID:Severe jaundice, due to vanishing bile duct syndrome, as presenting symptom of Hodgkin's lymphoma, fully reversible after chemotherapy. 1818 38

109 patients with hemoblastosis (HB) were examined. Average age was 31.8 +/- 1.4 years in group of lymphogranulomatosis patients, and 44 +/- 5.3 years in group of acute leukemia patients. Group of 46 patients with clinical laboratory signs of hepatic lesion was marked out. Since features of portal blood flow (PBF) revealed at dopplerography did not depend on hepatitis aetiology, all patients with chronic hepatitis were analyzed in one group. These patients were examined clinicobiochemically: functional hepatic tests, markers of viral hepatitis B and C, ultrasonic abdominal scanning, PBF dopplerography, puncture biopsy of hepar. All patients had PBF disturbances such as decrease of portal vein blood flow, increase of venous drainage of hepar and spleen. The degree of disturbances intensity increased depending on degree of chronic hepatitis activity (the index of histological activity) and hepatic fibrosis stage. Thus, presence of chronic hepatitis in HB patients regardless of aetiology, is the factor aggravating patients' stage and corrupting PBF. PBF disturbances (decrease of arterial and venous inflow and increase of venous outflow) and development of fibrous changes apparently related with compression of vessels by connective tissue around central veins, inside of lobules and among of hepatic cells. Consequence of it is including anastomosises in blood flow which leads to redistribution of PBF and portal hypertension forming.
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PMID:[The stage of portal blood flow in patients with hemoblastosis combined with chronic hepatitis]. 1849 89


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