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)

A factor inhibitory to PHA-induced lymphocyte blastogenesis was found to be present in the serum of a patient with advanced Hodgkin's disease and nephrotic syndrome. The inhibitory activity for both syngeneic and allogeneic lymphocytes was dependent on the presence of peripheral blood monocytes. The Raji-cell serum assay, as well as immunofluorescence and light and electron microscopy of the renal biopsy, showed no evidence of immune complexes. Nevertheless, a high serum IgE level as well as the finding that ultracentrifugation and heating at 56 degrees C significantly reduced the inhibitory activity (P less than 0.01) suggested the possibility that an immune complex might have mediated the suppressive activity. Treatment of the Hodgkin's disease with combined chemotherapy caused a marked reduction in the monocyte-dependent serum inhibitory activity which in turn coincided with a prompt remission of the nephrotic syndrome and marked regression of disease.
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PMID:Monocyte-dependent serum suppression of lymphocyte blastogenesis in Hodgkin's disease: an association with nephrotic syndrome. 621 62

A number of drugs used in cancer chemotherapy have produced hypersensitivity reactions. Generalized urticaria to cyclophosphamide has been reported previously in 5 cases. We have recently observed a 25-year-old patient with M. Hodgkin who developed an anaphylactic shock immediately following an intravenous infusion of cyclophosphamide. Total serum IgE was significantly elevated (1280 U/ml). Using the epicutan skin testing highly positive papulo-vesicular reaction to cyclophosphamide was observed.
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PMID:[Anaphylactic reaction in cyclophosphamide infusion]. 634 94

This paper describes a fluorescent pattern of human antibodies circulating in the serum of a 57 year old patient with lymphogranulomatosis. Following incubation with different FITC-labeled anti-human IgG sera including F(ab)2-fragments and with antibodies to human IgA, IgM, IgD, IgE as well as guinea pig serum and FITC-labeled anti-guinea pig serum (for proof the complement binding), it can be assumed that this is a non complement binding IgG antibody directed first of all against the rat gastric mucosal lamina propria (in the cardia and corpus and weaker in the pylorus region). The titre was 1:640. 1:80 diluted serum did not react with duodenum, jejunum, colon, tongue, oesophagus, parotid gland, trachea, lung, heart, diaphragm, liver, spleen, or kidneys. Among others, the species specificity and the antigen binding sides remain to establish.
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PMID:Immunohistochemical demonstration of human circulating antibodies against lamina propria of gastric mucosa. 641 Jun 63

One hundred and forty-eight patients with Hodgkin's disease (HD) were stratified into 4 groups according to atopic status. Group 1 had a personal history of atopy and Group 2 a family history of atopy. In Groups 3 and 4 there was no history of atopy but high serum IgE levels (Group 3) and normal IgE levels (Group 4). Comparison of the survival of these groups by the logrank method showed a significant trend (P = less than 0.0001) where survival was ranked Group 1 greater than 2 greater than 3 greater than 4. Known prognostic factors in HD--age, sex, stage, symptoms and histology--had to be taken into account, since their distribution differed between the atopic groups. In Group I there was more stage IA and IIA disease and less "B" symptoms, in Group 3 more nodular sclerosis histology and more "B" symptoms and in Group 4 more lymphocyte-depleted histology and a higher mean age than expected from their distribution in the combined groups. Adjustment to allow for the variation in each of the other prognostic factors and for a combination of age, symptoms and histology still showed a significant trend of survival on the basis of atopic status. The increased survival of atopic patients suggests that atopic mechanisms or the genetic basis to atopy has a protective effect in HD either directly or by interaction with treatment.
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PMID:Atopy--a favourable prognostic factor for survival in Hodgkin's disease. 688 61

Serum IgE levels were evaluated in 119 untreated and 112 treated patients with Hodgkin's disease (HD). 38 of the nonatopic untreated patients showed significantly increased (> 300 IU/ml) IgE concentrations. No relationship could be found between increased IgE levels and depressed lymphocyte response to phytohemagglutinin (PHA) or the imbalance of TM and TG lymphocyte subsets. On the other hand, the mean level of suppressor activity elicitable from cells of untreated HD patients by concanavalin A preincubation did not differ significantly from that of healthy control subjects. In contrast, in treated patients, where there was a significant reduction in the number of circulating T lymphocytes, a further depression of the lymphocyte response to PHA, a more marked disproportion of TM and TG cell subsets and a noticeable fall in IgE concentration was found. These data suggest that increased IgE concentrations seen in untreated patients with HD are unrelated to the T-cell defects. They also suggest that hyperproduction of IgE is probably not invariably a consequence of a suppressor cell deficiency.
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PMID:Hyperproduction of IgE and T-cell dysfunction in Hodgkin's disease. 696 58

161 children followed up postoperatively following splenectomy, 29% had spherocytosis, 14% Hodgkin's disease, 12% traumatic rupture of the spleen, 11% portal hypertension and 7% idiopathic thrombocytopenia. Postoperatively a slight wound infection occurred in 5% of the children, while complications were seen in 2% which could be interpreted as directly caused by the operation; in 23 patients, however, (i.e. 15%), severely infections occurred such as pneumonia, meningitis and sepsis. The lethality rate of the infected children was 31.8%. Postoperatively we determined the leucocyte count, thrombocytes and erythrocyte count, the immunoglobulins IgG, IgA, IgM and IgE, the serum concentrations of the complement components C3, C4 and the serum proteins alpha 1-antitrypsin and transferrin. The data obtained were compared with the corresponding data reported in the literature.
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PMID:[Complications of splenectomy in childhood (author's transl)]. 704 92

We describe the case of a young man of Calabrian origin, who came to our observation for the appearance of erythematous pustular, intensely itching, lesions on the arms, trunk and, in a less extent, on the face. The blood count revealed a differential cell count of 16.8% eosinophils. Serum IgE levels were elevated (1000 IU/ml), and T cell subsets showed an increase in CD8+ and a decrease in CD4+ with an inversion of CD4+/CD8+ ratio (= 0.78). The result of the following investigations were either normal or negative: anti-(ds)DNA antibody, anti-nuclear antibody, anti-smooth muscle antibody, anti-striated muscle antibody, serological tests for viral, bacterial, fungal and parasitic diseases and cultural examination of the material from lesion. Histopathological examination of a biopsy specimen from the left arm showed the presence of abundant perivascular inflammatory infiltrate in the dermis and inflammatory infiltrate, with numerous eosinophils, around sebaceous glands. Taken together, all these data suggest the diagnosis of eosinophilic pustular folliculitis, a dermatosis of unknown etiology, with a histopathological picture identical to Ofuji's disease. Eosinophilic pustular folliculitis can be associated with HIV infection or haematological diseases (as non-Hodgkin lymphomas, myeloma, etc.); it was also reported in adult immunocompetent healthy individuals and in children. On the basis of our findings, we propose that this case should be classified as an idiopathic form, as we were not able to demonstrate any associated disease.
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PMID:[Eosinophilic pustular folliculitis and Ofuji disease. A case report]. 750 2

The mechanism by which PG of the E series (PGE) promote murine B lymphocyte IgE production was investigated. We previously reported that PGE, and other agents that increase intracellular cAMP, synergize with IL-4 and LPS to induce IgE and IgG1 production while inhibiting IgM and IgG3 synthesis. These data suggested that PGE may promote IL-4-induced class switching, but the mechanism by which PGE increases IgE synthesis remained obscure. We report here that 1) PGE increases (up to 14-fold) the number of splenic B cells secreting IgE, even though PGE mildly inhibits proliferation. 2) PGE acts on sorted surface IgM positive B cells, consistent with PGE acting on uncommitted B cells to promote class switching to IgE. 3) PGE synergizes with IL-4 to induce germline epsilon transcripts, demonstrating that PGE acts at the level of transcription in cells that have not yet switched to IgE. 4) In the presence of PGE, rearranged mature V(D)J epsilon mRNA transcripts can be detected earlier and at higher levels than with IL-4 and LPS alone. Taken together, these data provide strong evidence that PGE synergizes with IL-4 and LPS to direct isotype switching to the epsilon heavy chain gene in purified B lymphocytes. PGE is a potentially important in vivo immunoregulator, particularly with regard to IgE production and the genesis of allergy. In support of this hypothesis, there are numerous clinical conditions (hyper-IgE, trauma, sepsis, Hodgkin's lymphoma, arthritis) in which overproduction of PGE is coincident with elevated IgE titers.
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PMID:Prostaglandin E2 promotes B lymphocyte Ig isotype switching to IgE. 799 35

Tissues containing Hodgkin's disease tumors of the nodular sclerosis and mixed cellularity subtypes are frequently infiltrated by numerous degranulating eosinophils that release granule proteins such as eosinophil peroxidase and major basic protein. Until recently, the causes of the eosinophil infiltration and degranulation in Hodgkin's disease tumors were unknown. Analysis of Hodgkin's disease tissues by a sensitive and specific immunoperoxidase technique has now demonstrated the extensive presence of IgE in the Reed-Sternberg cells and adjacent cells of Hodgkin's disease tumors. Because eosinophils express a cell-surface receptor (CD23) for IgE and degranulate in the presence of IgE deposits, the extensive eosinophilia that is frequently present in Hodgkin's disease tumors is, at least in part, attributable to the IgE deposits within the tumor. In this review, we discuss the possible mechanisms and biological significance of IgE-related eosinophilia in Hodgkin's disease.
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PMID:IgE, Reed-Sternberg cells, and eosinophilia in Hodgkin's disease. 834 67

In order to clarify the mechanisms of the eosinophilia frequently observed in patients with Hodgkin's disease (HD), 18 patients and 16 age- and sex-matched controls were studied. Increased eosinophil numbers in peripheral blood and serum IgE, as well as decreased cell-mediated immunity were present in HD patients compared with control individuals. Advanced disease was accompanied by lower eosinophil levels, increased IgE, and lower CD4+ T cell counts in peripheral blood. Eosinophilia correlated with CD4+ T cell counts, suggesting that eosinophil production could be under CD4+ T cell control. GM-CSF production in vitro by Phytohemagglutinin-stimulated mononuclear cells was significantly lower in HD patients with eosinophilia. On the other hand, an eosinophil-survival-enhancing activity was found in sera and culture supernatants from controls and HD patients; this activity was stronger for HD patients and was higher for those with eosinophilia. Furthermore, this activity was completely abolished by preincubation with monoclonal antibodies to IL-5, but not with normal mouse serum. Our results suggest that defects of cell-mediated immunity present in patients with HD are accompanied by a predominant type 2 cytokine profile. IL-5 is involved in the increased eosinophil production observed in these patients.
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PMID:Eosinophilia in Hodgkin's disease: a role for interleukin 5. 868 71


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