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)

Ten cases of acute febrile neutrophilic dermatosis or Sweet's disease have been studied clinically and histologically. Seventy percent of the patients were females with mean age of 43.1 +/-9 years. All of them presented the typical skin lesions consisting of papules and painful erythematous--edematous plaques in face, neck and upper chest. Fever was observed in seven patients and painful joints in four cases. One case presented polyarthritis of the big joints and there was one other case of conjuntivitis. The analytical data revealed a constant increase in sedimentation rate observed in 90% of patients. Leukocytosis was observed in 30% of patients and neutrophilia in 40%. Histologically, the lesions showed a neutrophilic infiltration of the skin without signs of vasculitis. Eight patients received treatment with Prednisone per os, one of whom, because of his relapses, was later given Potassium Iodine. Another patient was treated with Indomethacin, and one patient did not received any treatment. The evolution was favorable in all cases with sustained remissions. Sweet's Syndrome has been described associated mainly with acute myeloid leukemia in 10-20% of patients and in isolated instances with other systemic and neoplasic diseases. The concomitant conditions in 50% of our cases were: Ulcerative colitis, nodular sclerotic Hodgkin disease, infiltrative ductal carcinoma of the breast, carcinoma of the uterus neck and Crohn's disease; these last two associations had not been previously described in the literature.
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PMID:[Sweet's syndrome. A study of 10 cases and review of the literature]. 220 15

The candidacidal activity and the production of oxygen radicals by monocytes were investigated in untreated and long-term remission patients with Hodgkin's disease (HD). Both groups showed a decreased candidacidal function of monocytes with a chemiluminescence (CL) response significantly lower and delayed with respect to normal controls. Indomethacin at 1 microgram/ml corrected the monocyte deficiency increasing the CL response to normal values and normalizing the kinetics in the untreated patients. However, in patients in remission, the peak was delayed and followed by a significant increase in the production of oxygen radicals compared with untreated patients. A direct linear correlation was found between the percentages of lysed Candida and maximum CL peak of stimulated monocytes. When prostaglandin E2 (PGE-2) levels, measured in supernatants of cultured mononuclear cells, were plotted against the percentages of killed Candida, an inverse linear correlation was found. Therefore, monocytes from HD patients have a dysfunction in the generation of oxygen radicals and a decreased candidacidal activity associated with excessive production of PGE-2. Indomethacin can correct the oxidative metabolism in the untreated patients while in apparently "cured" patients the disorder persists.
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PMID:Dysfunction of monocytes in Hodgkin's disease by excessive production of PGE-2 in long-term remission patients. 317 26

In the present study we investigated the role of monocytes and of their soluble products (prostaglandins and hydrogen peroxide) in the modulation of the immune response in 50 untreated patients with Hodgkin's disease (HD) compared with a group of healthy donors. The primary response in vitro has been studied with the method of haemolytic colonies in soft agar. A defective in vitro antibody production has been observed in HD patients. Both Indomethacin addition (10(-6) M, final concentration) and depletion of plastic adherent cells, slightly increased the number of haemolytic areas in cultures from HD patients as compared with healthy donors. Similarly, the addition of catalase (8000 U/ml) which destroys H2O2, that is the main mediator of monocytes suppressor activity in normal subjects, did not restore the response of peripheral blood mononuclear cells (PBMC) from HD patients. These results suggest that monocytic cells play a minor role, if any, in the depression of the immune response in HD patients.
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PMID:[Antibody response in cultures of lymphocytes from patients with Hodgkin's lymphoma: role of monocytes]. 332 76

Peripheral blood lymphocytes (PBL) of patients with Hodgkin's disease were studied for their capacity to produce interleukin 2 upon in vitro phytohemaglutinin stimulation in the presence or absence of either interleukin 1 or indomethacin (2 micrograms/ml); eight patients were studied at the discovery of their disease before receiving any therapy (onset HD; OHD). Seventeen patients were tested in long-term (greater than 3 yr) remission (remission HD; RHD); most RHD were treated with both chemotherapy and irradiation. Fourteen healthy individuals served as controls. PBL from OHD have a significant (P less than 0.01) defect in the production of PHA-induced IL-2. Indomethacin and IL-1 had no effect on IL-2 yield. PBL from RHD yield intermediate levels of IL-2, which are nevertheless significantly lower (P less than 0.02) than control values. RHD recover the capacity of normal PBL to increase their production of IL-2 in indomethacin-supplemented culture medium. Interestingly, PHA responsiveness was significantly decreased only in RHD, thus not explaining the low IL-2 yield obtained in supernatants. In addition, 4-day PHA-blasts from both HD patients and control individuals increase their thymidine incorporation in the presence of purified lectin-free IL-2 to a similar degree, suggesting that their IL-2 receptors are unimpaired. Finally, OHD sera significantly inhibit PHA-induced IL-2 yield of normal PBL, suggesting that a seric component(s) may play a role in some cases. We conclude that defective IL-2 production may play a role in the well-documented deficient cellular immunity seen in Hodgkin's disease.
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PMID:Defect in lectin-induced interleukin 2 (IL-2) production by peripheral blood lymphocytes of patients with Hodgkin's disease. 387 20

Patients with active Hodgkin's disease (HD) often demonstrate an impaired T-cell proliferative response to phytohemagglutinin (PHA). The present study examined if interleukin regulation of the PHA response was defective in HD. The Hodgkin's PHA response was impaired at all concentrations of PHA utilized. Indomethacin increased the proliferative response but did not bring it to control levels. Stimulation of the cells with both PHA and irradiated Ia+ B cells normalized proliferation despite identical PGE2 concentrations as in the PHA alone cultures. Hodgkin's monocytes produced normal amounts of interleukin 1 (IL-1). Interleukin 2 (IL-2) production by Hodgkin's T cells was decreased in the PHA stimulated cultures, but was normal in the PHA and Ia+ cell stimulated cultures. In response to PHA stimulation alone, Hodgkin's T cells expressed less IL-2 receptor than control cells. The data suggest the diminished PHA response in HD is due to impaired IL-2 production resulting in diminished IL-2 receptor expression. However, when an Ia+ cell source is added to PHA as an additional stimulator, both TCGF production and proliferation are normalized. Monocytes serve to modulate the magnitude of the PHA response through production of both interleukin 1 and PGE2. However, in the presence of sufficient IL-2 production the influence of monocytes is minimized.
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PMID:Impaired interleukin regulation of the phytohemagglutinin response in Hodgkin's disease. 392 53

Indomethacin significantly enhances the depressed levels of lymphocyte proliferation to the mitogens phytohemagglutinin and concanavalin A in melanoma patients. We postulated that these results were related to an abnormality in prostaglandin E2 (PGE2)-mediated suppression, since this mechanism has previously has previously been demonstrated in patients with Hodgkin's lymphoma and with head and neck carcinoma. However, the results of three experimental approaches did not support this hypothesis. First, in vitro PGE2 production by cultured blood mononuclear cells was the same in 16 melanoma patients as in 45 normal controls (4.9 versus 4.7 ng/ml). Second, lymphocyte sensitivity to PGE2 for melanoma patients was essentially the same as that for normal controls, since exogenous doses of PGE2 inhibited the mitogen responses to the same degree. Third, another prostaglandin synthetase inhibitor (RO-205720), which is structurally unrelated to indomethacin, did not augment the mitogen response in these patients. Thus PGE2 cannot be implicated as a mediator of immunosuppression in melanoma patients. To further examine the immunomodulatory mechanism of indomethacin, we preincubated the drug with purified populations of either lymphocytes or monocytes, which were then recombined and tested for mitogen response. The results suggested that indomethacin had a direct effect on the responding T lymphocytes rather than an indirect effect on monocytes. These are the first studies demonstrating that indomethacin can act directly as a modulator of cellular immune function, independent of PGE2-mediated suppression.
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PMID:Immune modulatory effects of indomethacin in melanoma patients are not related to prostaglandin E2-mediated suppression. 628 58

Indomethacin is a non-steroidal anti-inflammatory agent that inhibits prostaglandin synthesis. Administration of indomethacin, in doses which were non-toxic to normal BALB/c mice, to mice bearing the BCL1 leukemia resulted in increased mortality of these animals. This effect was only observed if the indomethacin was administered to animals with advanced disease (splenomegaly, hepatomegaly and leukemia). If indomethacin treatment was initiated prior to transplantation of the tumor or 2 weeks post-transplantation, and continued throughout the disease process, there was no effect on either the course of the disease or mortality. Injection of similar doses of indomethacin into mice bearing advanced B16 melanoma tumors did not result in increased mortality. Therefore, metabolic changes which occur in the leukemic animals may uniquely alter host sensitivity to this non-steroidal anti-inflammatory agent. The BCL1 leukemia may be a useful animal model to provide insights into the biochemical basis for the adverse reactions experienced by some Hodgkin's disease patients when they are treated with anti-inflammatory agents such as indomethacin.
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PMID:Increased sensitivity to indomethacin of mice bearing the BCL1-leukemia. 674 40