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)

Serum IgE concentrations were determined and IgE turnover studies were performed in control individuals as well as in patients with several disease states. Patients with common variable hypogammaglobulinemia, thymoma and hypogammaglobulinemia, ataxia telangiectasia, and selective IgA deficiency had significantly decreased mean serum IgE concentrations. In turnover studies, this was found to be due to decreased IgE synthesis. In spite of these depressed mean values, some patients with common variable hypogammaglobulinemia had normal serum IgE concentrations and synthetic rates. Patients with the Wiskott-Aldrich syndrome had a significantly elevated mean serum IgE concentration. In one of four patients studied with the turnover technique, a strikingly high IgE concentration was present and was associated with an elevated IgE synthetic rate. Three other patients had both normal serum IgE concentrations and synthetic rates. Patients with chronic lymphocytic leukemia had significantly decreased mean serum concentrations and synthetic rates for IgE. The depressed IgE synthesis was associated with a significantly prolonged IgE half-life. Patients with Hodgkin's disease had significantly increased serum IgE concentrations. One of three patients studied had a high serum IgE concentration and synthetic rate of IgE. The two other patients had normal serum IgE concentrations associated with normal synthetic rates. Finally patients with protein-losing enteropathy or familial hypercatabolic hypoproteinemia had normal IgE concentrations associated with normal IgE metabolic parameters. In these cases, the disorder in the catabolic rate was not severe enough to affect the total amount of circulating IgE because IgE normally has a very high fractional catabolic rate. In general, IgE levels in a variety of disease states were correlated with IgE synthetic rates and abnormalities in the catabolic rate of IgE in disease did not exert an important effect on IgE concentration.
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PMID:The metabolism of IgE in patients with immunodeficiency states and neoplastic conditions. 40 20

An etiologic study was made of 107 cases of granulomatous hepatitis which were observed in a Department of Internal Medicine between January, 1971 and December, 1977 (excluding the hepatobiliary diseases). The most common etiology was tuberculosis (30 cases, 28 percent) followed by sarcoidosis (19 cases, 17.7 percent), Mediterranean exanthematous fever (13 cases, 12.1 percent), brucellosis (8 cases, 7.4 percent) typhoid fever (7 cases, 6.5 percent) and the idiopathic forms (8 cases, 7.4 percent). A lower rate of incidence was among Hodgkin's disease, toxoplasmosis, adenocarcinomas, leprosy, and those of unknown etiology, classified in this way because the study and follow-up of the patients could not be completed. There were, moreover, individual cases caused by mononucleosis, BCG reaction, hypogammaglobulinemia, celiac disease, and temporal arteritis. From a clinical point of view 50 percent of the patients had hepatomegaly and moderate disturbance of the liver enzymes. The most important enzymatic increases were detected in the cases caused by brucellosis; in the cases which were secondary to sarcoidosis the liver enzymes were normal. A comparison is established between the etiologic incidence of the present series and of others published in the literature. The causes and diagnostic problems of this type of lesion are discussed.
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PMID:[Granulomatous hepatitis. Etiologic study of 107 cases (author's transl)]. 45 94

149 patients with non Hodgkin lymphomas (NHL) were observed at the III. Medical Department of the Hanusch Hospital during 1972--1978. 15 out of 106 patients with low malignant NHL had autoimmune hemolytic anemia (AHA). None of the patients with high malignant NHL showed evidence of hemolysis. In 10 cases AHA was diagnosed together with the lymphoproliferative disease. In 4 cases diagnosis of AHA and NHL was established at the same time and in only 1 patient diagnosis of AHA preceded the lymphatic disease. All patients had distinct signs of hemolysis with moderate to severe anemia. 4 patients with immunocytic lymphomas had IgM paraproteins and an elevation of gamma-globulins, all other patients had mild to severe hypogammaglobulinemia. Therapy in all cases consisted of corticosteroids and cytostatics (Chlorambucil, Cyclophosphamide). In none of our cases splenectomy was performed. AHA seems to be a bad prognostic factor in patients with chronic lymphocytic leukemia. Survival time in patients with chronic lymphocytic leukemia and AHA was 18 months shorter than in all other patients suffering from chronic lymphocytic leukemia.
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PMID:[Accompanying hemolysis in lymphoproliferative diseases]. 55 12

In this series, the commonest aetiology was tuberculosis (30 cases, 28%), followed by sarcoidosis (18 cases, 17,7%), mediterranean fever (Olmer's disease) (13 cases, 12,1%), brucellosis (8 cases, 7,4%), typhoid fever (7 cases, 6,6%) and idiopathic forms (8 cases, 7,4%). These were followed by Hodgkin's disease, toxoplasmosis, adenosarcoma, and leprosy. Finally, there were single cases due to infectious mononucleosis, B.C.G. reaction, hypogammaglobulinaemia, coeliac disease and temporal arteritis. Half of the patients had hepatomegaly and an increase, in general moderate, in hepatic enzymes (transaminases, alkaline phosphatase). The highest enzyme levels were seen in cases of brucellosis, hepatic enzymes being normal in patients with sarcoidosis.
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PMID:[Granulomatous hepatitis: aetiological study of 107 cases (author's transl)]. 73 1

We describe a woman in whom hypogammaglobulinemia and severe granulomatous cutaneous lesions had developed during childhood; subsequently, Hodgkin's disease and necrobiotic xanthogranuloma were diagnosed. This case illustrates an apparent association with disease activity and raises the question of a direct relationship of necrobiotic xanthogranuloma with lymphoproliferative disease.
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PMID:The evolution of Hodgkin's disease and necrobiotic xanthogranuloma syndrome. 174 90

Two cases of lymphocyte predominant Hodgkin's disease of nodular subtype (HDNP) are reported. In contrast to classic cases of HDNP which often involve only one lymph node region and show no further symptoms, these two patients exhibited lymphoid infiltrates of the lung and hypogammaglobulinaemia. In patient 2 a monotypic immunoglobulin pattern (light chain kappa) was demonstrated in the L & H-, Hodgkin- and Sternberg-Reed cells. Both cases represent an uncommon variant of lymphocyte predominant Hodgkin's disease.
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PMID:Lymphocyte predominant Hodgkin's disease of nodular subtype combined with pulmonary lymphoid infiltration and hypogammaglobulinaemia. 250 7

Extensive extralymphatic Hodgkin disease developed in a young man with common variable immunodeficiency manifested by hypogammaglobulinemia, recurrent sinopulmonary infections, and multiple autoimmune phenomena. Both humoral and cell-mediated immune dysfunction were present prior to treatment. After two cycles of chemotherapy, irreversible shock developed, and death occurred secondary to overwhelming infection in spite of prophylactic gammaglobulin replacement. The unusual features of this patient's case of extralymphatic Hodgkin disease in association with a primary immunodeficiency disorder have not been previously reported.
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PMID:Hodgkin disease in a patient with common variable immunodeficiency. 275 10

Seven patients with autoimmune hemolytic anemia (AIHA) associated with an underlying lymphoproliferative disorder were treated with intravenous immunoglobulin. Five patients with chronic lymphocytic leukemia, a patient with Hodgkin's lymphoma with severe AIHA associated with a "warm" IgG antibody, and a patient with non-Hodgkin's lymphoma with an IgM "cold" antibody were treated with intravenous immunoglobulin G (0.4 g/kg) daily for five doses followed by maintenance therapy every 21 to 28 days if evidence of recurrence was noted. Two additional patients with refractory chronic lymphocytic leukemia and hypogammaglobulinemia were given maintenance therapy with intravenous immunoglobulin G every 21 days for previously recurrent AIHA and infections. Hematocrit levels of patients with AIHA stabilized followed by a gradual improvement at 21 days after intravenous immunoglobulin G infusion without steroids. Treatment with steroids and intravenous immunoglobulin G resulted in faster and higher increments in hematocrit levels in these patients. Other patients who had partial responses to steroids showed further improvement in their hematocrit levels by the addition of intravenous immunoglobulin G. Another patient with a cold agglutinin disease was refractory to intravenous immunoglobulin G therapy. Five patients with chronic lymphocytic leukemia and acute AIHA and two patients with previous recurrences of AIHA required maintenance intravenous immunoglobulin G every 21 days. All seven patients except one did not have any episodes of AIHA from six months to as long as four years while receiving the three-week intravenous immunoglobulin G therapy. These observations indicate a role for intravenous immunoglobulin G in the management of IgG-mediated but not IgM-associated autoimmune hemolysis in immunocompromised patients with lymphoproliferative diseases.
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PMID:Rapid transient reversal of anemia and long-term effects of maintenance intravenous immunoglobulin for autoimmune hemolytic anemia in patients with lymphoproliferative disorders. 340 Jun 63

Male patients with the X-linked lymphoproliferative syndrome (XLP) have an inherited immune deficiency to Epstein-Barr virus (EBV) infection that results in fatal infectious mononucleosis (IM), acquired hypogammaglobulinemia- or agammaglobulinemia, virus-associated hemophagocytic syndrome, and non-Hodgkin's malignant lymphoma (ML). A clinicopathologic analysis of 17 patients with XLP who developed ML was performed. The median age of the patients at the time of diagnosis was 4.0 years (range, 2-19 years). The median overall survival was 12 months (range, 1-216 months). Eight patients had maternally related male relatives with ML. Other phenotypes of XLP were documented in male relatives of the remaining nine patients. Common presenting symptoms were fever, nausea, vomiting, and abdominal pain. Nine patients had "B" symptoms. All ML occurred at extranodal sites. The intestines, most commonly ileocecal, were involved in 76.5% of the cases. Thirteen patients had localized disease (Stages I and II) and four patients had advanced disease (Stages III and IV). A diffuse histologic pattern of growth was observed in all cases. The distribution of histologic subtypes included small noncleaved (41.2%), large noncleaved (17.6%), immunoblastic (17.6%), small cleaved or mixed cell (11.8%), and unclassifiable (5.9%) ML. Surgical resection, radiation therapy, and chemotherapy resulted in disease-free survivals of up to 192 months in eight patients (median 114 months; range, 12-192 months). Eight of 17 patients (47%) are still alive. A median survival of only 6.0 months (range, 1-12 months) was observed in the nine patients who died. No residual ML was found at autopsy. The small noncleaved subtype had an adverse prognosis (seven of nine deaths versus one of eight survivors; P less than 0.05). Bacterial infection was the major cause of death (seven of nine patients). Characteristics that distinguish ML in XLP from other ML include a maternal family history of XLP, early age of onset, acquired hypogammaglobulinemia, post-EBV infection, and ileocecal involvement.
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PMID:Malignant lymphoma in the X-linked lymphoproliferative syndrome. 381 12

Accumulated evidence indicates that there is a circulating monoclonal Ig protein related to the leukemic cell-associated Ig in the majority of patients with B cell chronic lymphocytic leukemia (CLL) despite the failure to demonstrate such a protein by conventional serum electrophoresis. Methodology has been developed to reveal these hidden monoclonal bands and to show that they are related to the leukemia-associated membrane Ig (mIg). Of nine CLL cases with stainable mIgM and without discernable plasma Ig bands, marked hypogammaglobulinemia was evident in six. In the other three, a significant amount of protein was present in the gamma region. IgM was isolated from the plasma of these patients by affinity chromatography with Sepharose-4B, conjugated with affinity purified anti-human IgM antibodies. One to 3 mg were isolated from 20 to 40 ml of plasma. Agarose electrophoresis revealed a monoclonal Ig band in the isolated IgM in all cases. Eight of these IgM proteins were analyzed by high-pressure liquid chromatography. Five were found to be pentameric IgM. In the remaining three, various amounts of monomeric IgM were detected. Attempts to make anti-idiotypic antibodies to the isolated proteins have been successful. Thus far, a rabbit anti-idiotypic antiserum was obtained in one case and two mouse monoclonal anti-idiotypic antibodies in two additional cases. Immunofluorescence analysis revealed that plasma IgM and mIgM shared similar idiotypic determinants. One other monoclonal antibody was shown to be specific for a V region marker of a minor Ig population. These findings indicate that B leukemic lymphocytes do secrete a small amount of IgM and lend further support to the thesis that the maturation defect in CLL is incomplete. It is also feasible to isolate the secreted IgM and to produce anti-idiotypic antibodies to them. In view of the potential therapeutic effect of anti-idiotypic antibodies, this may offer an alternative and efficient approach to generate a large panel of anti-idiotypic antibodies for clinical trials. The possibility also exists that this approach is applicable to other B cell proliferative disorders such as the non-Hodgkin B cell lymphomas.
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PMID:Circulating monoclonal IgM proteins in B cell chronic lymphocytic leukemia: their identification, characterization and relationship to membrane IgM. 633 59


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