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)

Eruptive herpes zoster infection (VZV) and its primary and secondary diseases are reported in 28 patients aged between 25 and 85 years. In 2 cases, malignant primary diseases were found. In 16 patients, a disorder of glucose utilization was diagnosed, 8 of them accompanied by a disorder of fat metabolism and 5 by a hyperuricemia. In one case a severe encephalomyelitis was observed. In 2 patients the activation of the VZV infection was related to the cytostatic or immunosuppressive therapy of a generalized Hodgkin's disease and a multiple sclerosis. Once a liver abscess as a sequel to amebic dysentery was diagnosed and once a megaloplastic anemia with symptoms of a funicular myelopathy following a vitamin B12 deficiency syndrome. In VZV infection the search for basal metabolic disorders is of particular importance.
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PMID:[Significance of diabetes mellitus in the activation of the varicella zoster virus (author's transl)]. 19 45

Pinealectomy leads to increased formation of fibrous tissue in the abdominal cavity, increased skin pigmentation and elevated cholesterol and alkaline phosphatase levels. It also leads to reduced formation and/or action of prostaglandin (PG) E1 and thromboxane (TX) A2. PGE1 plays an important role in enhancing function of T suppressor lymphocytes which control overactive antibody-producing B lymphocytes. In primary biliary cirrhosis there are increased skin pigmentation, hepatic fibrosis, elevated cholesterol and alkaline phosphatase levels, defective T lymphocytes and hyperactive B lymphocytes. Primary biliary cirrhosis may be a pineal deficiency disease. Serotonin is important in the pineal and the serotonin antagonist methysergide may cause retroperitoneal fibrosis by interfering with pineal function. There is a good deal of other evidence which suggests that melatonin PGE1 and TXA2 are important in the regulation of fibrosis in other situations such as "collagen" diseases, lithium-induced fibrosis and cardiomyopathies. This suggests that enhancement of formation of PGE1 and TXA2 may be of value in diseases associated with excess fibrosis and defective T suppressor cell function. PGE1 levels may be raised by zinc, penicillin, penicillamine and essential fatty acids. TXA2 levels may be raised by low dose colchicine. These new approaches to treatment may prove safer and more effective than existing ones. They may be of value in disorders such as cardiomyopathy, Hodgkin's disease and other lymphomas, multiple sclerosis, Crohn's disease, atopy and other diseases in which defective T cell function is suspected.
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PMID:The pineal and regulation of fibrosis: pinealectomy as a model of primary biliary cirrhosis: roles of melatonin and prostaglandins in fibrosis and regulation of T lymphocytes. 31

The significance of cold lymphocytotoxins, observed at 15 degreesC, is not clearly understood at the present time. The frequency of their appearance has been studied in normal subjects (blood donors, aged people, vaccinated subjects, post-traumatic splenectomy) and in patients with a neurologic disease (multiple sclerosis), a neoplasic disease (breast cancer)and hematologic diseases (thrombocytopenia, acute leukemia, chronic lymphatic leukemia, Hodgkin disease and systemic lupus erythematosus). There are no antibodies found in the geriatric group; they are found only in 3,9 % of blood donors and in 18 % of the subjects after vaccinations. A range of 17 to 30 % is found in subjects with breast cancer or multiple sclerosis. More than 50 % of the individuals with Hodgkin disease or lupus erythematosus produce these antibodies (52 % and 73 % respectively). In acute leukemias and chronic lymphatic leukemias, lymphocytotoxic antibodies sometimes appear at 37 degrees, reacting with autologous cells and having no HL-A specificity.
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PMID:[Cold lymphocytotoxins: their relationship with various physiological and pathological conditions]. 108 28

There has been a hypothesis that Hodgkin's disease in young adults and multiple sclerosis may have related causes because the age of clinical onset and the geographic distribution of both are similar. This hypothesis was tested for data in Denmark. Detweeen 1943-62, the average annual incidence rate for Hoadgkin's disease in Denmark was 2.25 per 100,000 population (2.68 male and 1.83 female). Between 1951-69, the average annual death rate for Hodgkin's disease was 2.15 per 100,000 (2.66 male and 1.64 female). The average annual incidence rate for multiple sclerosis in Denmark was calculated from age at onset for 2,481 prevalent cases of 1949, the 1940 population, and an average annual incidence of 128.86 cases for 1939-45: the average annual incidence rate per 100,000 was then 3.35 (3.00 male and 3.69 female). Age specific incidence and death rate for Hodgkin's disease in Denmark each showed a bimodal curve, with one peak at age 25-29 and the other at age 70-74; this was found for each sex, with male rates consistently higher than female. The age specific incidence rates for multiple sclerosis were clearly unimodal with a peak at age 25-29 more definite in females than males. Rates for MS were notably higher for young females than males but about equal by sex for those over the age of 30. The geographic distribution of multiple sclerosis within the counties (amter) of Denmark was markedly non-random, with the major concentration of high prevalence areas middle Jutland and on to Fyn. Geographic distribution of Hodgkin's disease, whether for the young or the old, and whether from incident or death cases, showed no significant variation from a homogeneous distribution. In formal testing there was no correlation of any Hodgkin's distribution with that of MS. A review of the Hodgkin's data for distribution in the United States, on which the original hypothesis was based, suggests the variation there may be little more than reporting artifact. Accordingly, we conclude that there is no relation between distributions of these two disorders, and the factors they do appear to have in common are either quite non-specific or of questionable validity. Thus there is no reason to believe that multiple sclerosis and Hodgkin's disease, even in the young, share a common etiology.
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PMID:Multiple sclerosis and Hodgkin's disease in Denmark. 126 75

Although multiple sclerosis and Hodgkin's disease are reported to have similar epidemiologic features, this is only the first case report in which there was concurrence of these diseases. Fourteen years after successful treatment of Hodgkin's disease, this 31-year-old white male developed multiple sclerosis. The diagnosis of multiple sclerosis was made on the basis of clinical and paraclinical findings that were characteristic of multiple sclerosis. In addition, specific tests were performed to rule out a variety of infectious, metabolic, and neoplastic diseases that simulate multiple sclerosis.
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PMID:Concurrence of multiple sclerosis and Hodgkin's disease. 162 85

2102 samples of lumbar cerebrospinal fluid (CSF) were examined by qualitative cytology for atypical plasma cells. Samples from seven patients contained such cells. Retrospective investigation of these patients revealed that four of them had had neuroborreliosis, one had multiple sclerosis, one herpes zoster and one malignant non-Hodgkin lymphoma. It is concluded that in a case of unexplained meningoradiculitis with lymphoplasmocytic reaction in the CSF, morphological analysis of the plasma cells can provide important diagnostic pointers.
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PMID:[Differential diagnosis of atypical plasma cells in the cerebrospinal fluid]. 280 5

The relationship between increased risk in relatives over population prevalence (lambda R = KR/K) and probability of sharing zero marker alleles identical by descent (ibd) at a linked locus (such as HLA) by an affected relative pair is examined. For a model assuming a single disease-susceptibility locus or group of loci tightly linked to a marker locus, the relationship is remarkably simple and general. Namely, if phi R is the prior probability for the relative pair to share zero marker alleles identical by descent, then P (sharing 0 markers/both relatives are affected) is just phi R/lambda R. Alternatively, lambda AR, the increased risk over population prevalence to a relative R due to a disease locus tightly linked to marker locus A, equals the prior probability that the relative pair share zero A alleles ibd divided by the posterior probability that they share zero alleles ibd, given that they are both affected. For example, for affected sib pairs, P (sharing 0 markers/both sibs are affected) = .25/lambda S. This formula holds true for any number of alleles at the disease locus and for their frequencies, penetrances, and population prevalence. Similar formulas are derived for sharing one and two markers. Application of these formulas to several well-studied HLA-associated diseases yields the following results: For multiple sclerosis, insulin-dependent diabetes mellitus, and coeliac disease, a single-locus model of disease susceptibility is rejected, implying the existence of additional unlinked familial determinants. For all three diseases, the effect of the HLA-linked locus on familiality is minor: for multiple sclerosis, it accounts for only a 2.5-fold increased risk to sibs over the population prevalence, compared to an observed value of 20; for coeliac disease, it accounts for approximately a 5.25-fold increased risk to sibs, while the observed value is on the order of 60; for insulin-dependent diabetes mellitus, it accounts for a 3.42-fold increased risk in sibs, while the observed value is 15. In all cases, the secondary determinants must be outside the HLA region. For tuberculoid leprosy, an unlinked familial determinant is also implicated (increased risk to sibs due to HLA = 1.49; observed value = 2.38). For hemochromatosis and Hodgkin's disease, there is little evidence for HLA-unlinked familial determinants. With this formula, it is also possible to examine the hypothesis of pleiotropy versus linkage dis-equilibrium by comparing lambda AS with the increased risk to sibs due to the associated allele(s).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessing the role of HLA-linked and unlinked determinants of disease. 346 4

Antibody to herpes simplex virus (HSV) type 1 and Epstein-Barr virus (EBV) capsid antibody were determined in 333 children from the Faroe Islands, aged 4, 8 and 13 years. An analysis of multi-way frequency tables was performed, testing seropositivity for each virus against combinations of the following variables: sibship size, birth order, mother's age at birth, birth weight, actual height and weight, age and sex. HSV-seropositivity was associated to sibship size, height and age, while EBV-seropositivity was related only to age.--It is discussed how the findings fit into epidemiological patterns described for Hodgkin's disease and multiple sclerosis, which are both supposed to be of viral origin. Our results suggest that HSV, but not EBV, may be among the candidates to be considered.
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PMID:Antibodies to herpes simplex and Epstein-Barr viruses in Faroese children: association with sibship size, height and age. 631 12

In 1970 the epidemiologic similarities between Hodgkin's disease and multiple sclerosis were first described, suggesting that a common agent or agents might be involved in their etiology. The hypothesis proposed at that time was that the agents followed the paralytic polio model: widespread infection with an agent of low pathogenicity at an early age, resulting in acquired immunity in later life. Lack of early infection results in the disease appearing in adulthood, with severe repercussions. This article extends the paralytic polio model to include testicular carcinoma, since the epidemiologic similarities between it and Hodgkin's disease are striking. Specifically, the authors compare age at clinical onset, histologic type, time trends, race, socioeconomic status, geographic variation, occupation, and familial aggregation. It is suggested that the possibility of common etiologies involved in the pathogenesis of these two cancers be tested further by epidemiologic, clinical, or laboratory studies.
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PMID:Epidemiologic comparison of cancer of the testis and Hodgkin's disease among young males. 646 39

When normal human peripheral blood mononuclear cells were tissue-cultured in autologous serum under conditions permitting cell contact, spontaneous fluctuations in cytotoxic activity were found. An analysis demonstrated that monocytes have the capacity to suppress initially (days 1-2) natural killer (NK) activity and that, at later time points (days 3-7), cytotoxic activity against the NK-susceptible target cell Molt-4 occurs which increases above initial NK levels. The newly induced killing depended on adequate cell contact for its induction and correlated with spontaneous proliferation in the cultures. The monocyte-induced NK suppression was found to be independent of cell contact and inhibited by the presence of indomethacin, thus most probably mediated by secreted prostaglandins. Suppressed NK cells (at day 1) had a lower number of target-binding cells (TBCs) and a smaller fraction of active NK cells among TBCs as compared with control cells. The fluctuations in cytotoxicity as seen in the present in vitro system are discussed in relation to clinical conditions with decreased NK activity, such as multiple sclerosis and Hodgkin's disease.
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PMID:Monocyte-induced human natural killer cell suppression followed by increased cytotoxic activity during short-term in vitro culture in autologous serum. 733 74


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