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)

Africa, the "dark continent" and the source of such wonderful tales as King Solomon's Mines and Jock of the Bushveld, has an equally enthralling story to tell about malignant disease in general and the lymphomas in particular as they occur among its varied people. It is uncertain how far back in history contact existed with the rest of the world, primarily in the form of slave trading and colonization by, among others, the Portuguese and the British. Until recent times, however, Africa's secrets have remained largely undisturbed. Fragments of medical information are recorded in the diaries of those early, intrepid explorers, such as Albert Cook, Henry Stanley, David Livingstone, and Albert Schweitzer. However, it is only in recent years that the great natural experiments that have for so long been underestimated, and very much less understood, belatedly started to attract attention. Examples are the systematic studies by Denis Burkitt, who through perseverance unraveled the lymphoma that now bears his name, and the thought-provoking description of the immunoproliferative small intestinal disease carried out by the Cape Town group, with both illustrating the axiom that "the study of man is man." Despite such occasional outstanding achievements, there is still considerable paucity of data pertaining to the various lymphoreticular malignancies, so that only limited conclusions are possible. Certainly, lymphoma in Africa differs from that elsewhere in the world. In part, this may reflect a background of immunologic disturbance attributable to parasitic infestation, viral infection, rampant malnutrition, and the impact of a wide variety of vectors, such as mosquitoes, in disease transmission. Striking differences exist in the distribution of these tumors as the incidence and pattern are followed from the equator to the milder climates in the south. This confirmed phenomenon gives rise to the tantalizing suggestion that, to some significant extent, the changes reflect the influence of geography. Thus, there may be associated alterations in the fauna and flora that determine the presence of intermediary hosts that have an impact on the eventual expression of the malignant clone. Many questions remain unanswered. For example, how can the lower incidence of Hodgkin's disease and the predominance of high-grade malignancies in the tropics and subtropics be explained? To what extent does the lymphocytic and plasmacytic hyperplasia, ascribed to intense antigenic stimulus in Burkitt's lymphoma and myeloma--perhaps even other lymphomas, such as IPSID--predispose the host to a mutational event that leads to the emergence of each distinctive neoplasm?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The malignant lymphomas in Africa. 193 63

Of a series of 300 patients with histologically verified Hodgkin's lymphoma, six cases of familial occurrence of the disease involving three families were reported from two clinical centers. In two families the affected patients were next of kin (daughter and father in the first family and two brothers in the third one). The interval between the onset of the disease was 6 years in the first and 4 months in the third family. In the second family an aunt and her niece were affected with an 18 year interval in the onset of the disease. The histological type was identical within the families involved (1 x LP and 2 x NS). Deficiency of cellular immunity was established in all the members of the two Prague families and the expression of HLA-A and B antigens of the MHC was determined in the first family. The involvement of environmental and genetic factors in familial Hodgkin's disease was analyzed also in the light of findings reported in the literature.
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PMID:[Familial occurrence of Hodgkin's disease]. 225 44

Antilymphocytic monoclonal antibodies of HKO and OKT series were used to study surface antigens of peripheral blood and lymph node lymphocytes in 13 untreated patients with Hodgkin's disease. The purpose of the study was to identify the pathogenetic mechanism underlying the development of immunodeficiency in the early disease stages. The data obtained have demonstrated that the deficiency of T lymphocytes in the peripheral blood was connected with that of mature T cells in the lymph nodes revealed with the use of differential antigens complex. Deficiency of immunologically differentiated T lymphocytes in the lymph nodes combined with high counts of the cells whose membranes carry Ia-like antigen point to the immunologically unfavourable course of the disease.
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PMID:[Pathogenesis of immunologic deficiency in the initial stage of lymphogranulomatosis in children]. 278 85

A failure of immune regulation has been often suspected as the basic condition leading to the development of Hodgkin's disease (HD), but the precise nature of this immune defects has not been defined. It is shown here that most of the epidemiological features fit the hypothesis of an increased risk for HD linked to an immune disbalance between a weak immune suppressor activity (ISA), and an enhanced polyclonal B cell activation (PBA). Few infections in childhood and an "untrained" immune system would lead to a weak ISA as the main risk factor among adolescent and young adults in the developed world, while an enhanced PBA due to chronic parasitic infections and malnutrition could explain a relatively high risk for HD among small children in undeveloped countries. The different histologic types of HD may reflect a variable contribution of a weak ISA, or an enhanced PBA under different conditions.
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PMID:Hodgkin's disease as a failure of immune regulation: a re-interpretation of the epidemiological findings. 308 73

The authors report the case of a young 16 year-old woman from Gabon hospitalized because of edemas. The laboratory tests show a hypoproteinemia of 32 g/l with hypoalbuminemia of 9.4 g/l. After ruling out a renal, cardiac or hepatic etiology as well as malnutrition, the endoscopic exploration of the G.I tract, performed because of abdominal pain, enables to make the diagnosis: malignant, non-Hodgkin gastric lymphoma, confirmed by biopsies during the procedure. Edemas and hypoproteinemia were related to an exudative enteropathy secondary to ulcerations of the gastric mucosa.
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PMID:[A rare etiology of anasarca in Africa: gastric lymphoma]. 320 51

Meningitis should be suspected in a patient who presents with fever, meningism, or severe headache. A careful physical examination should be performed of perimeningeal foci, with emphasis on the sinuses, ears, throat, neck, and lungs. A history of exposure to tuberculosis, viral disease, rodents, or suspicious dairy products or farm animals may give clues to the source of the meningitis. Immunosuppression through the use of corticosteroids or chemotherapy for such conditions as Hodgkin's disease, lymphoma, leukemia, malnutrition, or acquired immunodeficiency syndrome (AIDS) should also be noted and alert the clinician to the possible presence of an unusual pathogen. Meningitis associated with leukemia or most of the non-T-cell lymphomas is likely to be from a common bacterial agent (often Listeria), unless the patient is being treated with a steroid or is receiving other chemotherapy. Patients with Hodgkin's disease or AIDS or who have been treated with a steroid are more likely to have cryptococcal or tuberculous meningitis. Neonates and the very elderly may present with only irritability or lethargy and fever, without any of the other common symptoms. In neonates up to one week of age, group B streptococcal infection should be suspected. Gram-negative organisms should be suspected in elderly patients and those who have had neurosurgery. In patients with CSF shunts, infection with coagulase-negative Staphylococcus should be assumed and these patients are treated empirically until results of cultures are received. Several noninfectious conditions may mimic infectious meningitis, as may some unusual causes of infectious meningitis (eg, syphilis and schistosomiasis), which have not been discussed in this article.
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PMID:The many causes of meningitis. 361 11

Twenty four cases of pure red cell aplasia were reported. No underlying diseases were found in two cases. Of the 22 cases with secondary form, 10 were from infections, mostly gram negative organisms. Three cases had systemic lupus erythematosus, two had autoimmune hemolytic anemia. The following conditions were found in one each: thymoma, thyroid carcinoma, protein calorie malnutrition, rheumatoid arthritis, non-Hodgkin lymphoma and Sheehan's syndrome. Three patients died, two from uncontrolled infection, the other from uncontrolled SLE and subsequently systemic fungal infection. Only one of the 2 primary cases responded to immunosuppressive drugs. The majority of patients with underlying infections, PRCA resolved after the infections were treated. This is the first reported series of PRCA in Thailand.
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PMID:Pure red cell aplasia in Thailand: report of twenty four cases. 393 65

Adenosine deaminase (EC 3.5.4.4. - ADA) deaminates adenosine and deoxyadenosine to inosine and deoxyinosine. The distribution of ADA isoenzymes depends on a binding protein. Purine nucleoside phosphorylase (EC 2.4.2.1. - PNP) catabolizes inosine and guanosine to hypoxanthine and guanine. Patients with severe combined immuno-insufficiency often suffer from a congenital ADA deficiency. The PNP deficiency is associated with severely defective T-cell immunity and normal B-cell immunity. Deficiency of ADA leads to an accumulation of adenosine, deoxyadenosine, adenine nucleotides (cAMP, dATP). In PNP deficiency an increased production of inosine, guanosine, deoxyinosine and deoxyguanosine was found. The pathogenesis of the immuno-insufficiency is to be traced back to disturbances in the purine metabolism interfering with the mitogenically induced lymphocyte transformation and other lymphocyte functions, as determined by in vitro tests. Deoxyadenine inhibits the ribonucleoside diphosphate reductase and synthesis of DNA. The overproduction of S-adenosyl-L-homocysteine inhibits methyltransferase reactions and 2'-deoxyadenosine the S-adenosylhomocysteine hydrolase. A decrease of ADA activities was found in T-lymphocytes of patients with Hodgkin's disease. Measurements of ADA activity in patients with leukemias do not explain the impairment of the cellular immune response in leukemias and may be regarded as indicator of increased purine metabolism. The ADA activities are increased in patients with acute immature and chronic myeloic leukemias depending on the activity of the disease. The ADA activity is low in chronic lymphatic leukemia. ADA inhibitors were used for the treatment of T-cell leukemias.
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PMID:[Immune insufficiency in enzyme defects of purine metabolism]. 630 5

Hypogonadism, infertility, and sexual dysfunction occur in some men with coeliac disease. We have measured plasma testosterone, dihydrotestosterone, sex-hormone binding globulin, oestradiol, and serum luteinising hormone in 41 men with coeliac disease and have related these findings to jejunal morphology, fertility, semen quality, and sexual function. To determine the specificity of these observations in coeliacs we also studied 19 nutritionally-matched men with Crohn's disease, and men with chronic ill-health due to rheumatoid arthritis and Hodgkin's disease. The most striking endocrine findings in untreated coeliacs were increased plasma testosterone and free testosterone index, reduced dihydrotestosterone (testosterone's potent peripheral metabolite), and raised serum luteinising hormone, a pattern of abnormalities indicative of androgen resistance. As jejunal morphology improved hormone levels appeared to return to normal. This specific combination of abnormalities was not present in any of the disease control groups and, to our knowledge, androgen resistance has not been described previously in any other non-endocrine disorder. Plasma oestradiol concentration was modestly raised in 10% of coeliacs and 11% of patients with Crohn's disease. Unlike plasma androgens and serum luteinising hormone in coeliacs, plasma oestradiol was not clearly related to jejunal morphology. Androgen resistance and associated hypothalamic-pituitary dysfunction appear to be relatively specific to coeliac disease and cannot be explained merely in terms of malnutrition or chronic ill-health. In addition, our findings suggest that this endocrine disturbance may be related to sexual dysfunction in coeliac disease but its relationship to disordered spermatogenesis in this condition has not been clearly established.
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PMID:Male gonadal function in coeliac disease: 2. Sex hormones. 668 19

Causes of morbidity and mortality, in children in the developing world, are changing. Cancer is assuming increasing importance. The incidence in such countries is probably substantially underestimated, particularly in relation to brain tumours. However, real differences, from circumstances in industrialized societies, do exist; as in the relative prevalences of leukaemias and lymphomas. Furthermore, some forms of cancer, e.g. Hodgkin's disease and Wilms' tumour, seem to behave more aggressively in children in developing countries. Challenges to be addressed in these areas include inadequate knowledge, resource deficiencies and co-morbidity (especially malnutrition and infection). Solutions lie in approaches to health information and health care delivery systems, health professional education and essential national health research. To these ends, long-term collaboration should be established with colleagues, partner institutions and relevant organizations from more privileged parts of the world.
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PMID:The challenge of childhood cancer in the developing world. 806 67


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