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)

The major components of untreated wood--cellulose, hemicellulose, and lignin--have not been implicated as toxicants, but extractive substances, especially in heartwood, can be toxic. Decay-resistant woods are more likely to contain irritants or sensitizers than nondurable woods. Short-term exposures to certain wood dusts may result in asthma, conjunctivitis, rhinitis, or allergic dermatitis, but long-term effects may include nasal cancer and Hodgkin's disease. Some thermophilic microorganisms found in wood are human pathogens, and septic splinters (chromomycosis) and inhalation of ascomycete spores from stored wood chips have been implicated in human illnesses. Reconstituted wood can contain formaldehyde resins, which pose health risks in enclosed humid areas. Pentachlorophenol (PCP)-treated wood is particularly toxic--short-term exposures to PCP-treating solutions can lead to aplastic anemia and mortality, while diseases such as Hodgkin's disease are associated with long-term exposures. Since much commercial lumber is dipped in PCP, the separation of the chronic effects of wood dust from PCP exposure is difficult. Chromated copper arsenate (CCA)- and ammoniacal copper arsenite (ACA)-treated wood may leach arsenic. CCA-treated wood is potentially safer, since it contains the pentavalent arsenic, which is a common constituent in the environment. ACA contains the trivalent arsenic, which is more toxic.
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PMID:Health hazards of natural and introduced chemical components of boatbuilding woods. 390 39

The biological effect of exposure to wood dust depends on its composition and the content of microorganisms which are an inherent element of the dust. The irritant and allergic effects of wood dust have been recognised for a long time. The allergic effect is caused by the wood dust of subtropical trees, e.g. western red cedar (Thuja plicata), redwood (Sequoia sempervirens), obeche (Triplochiton scleroxylon), cocabolla (Dalbergia retusa) and others. Trees growing in the European climate such as: larch (Larix), walnut (Juglans regia), oak (Quercus), beech (Fagus), pine (Pinus) cause a little less pronounced allergic effect. Occupational exposure to irritative or allergic wood dust may lead to bronchial asthma, rhinitis, alveolitis allergica, DDTS (Organic dust toxic syndrome), bronchitis, allergic dermatitis, conjunctivitis. An increased risk of adenocarcinoma of the sinonasal cavity is an important and serious problem associated with occupational exposure to wood dust. Adenocarcinoma constitutes about half of the total number of cancers induced by wood dust. An increased incidence of the squamous cell cancers can also be observed. The highest risk of cancer applies to workers of the furniture industry, particularly those dealing with machine wood processing, cabinet making and carpentry. The cancer of the upper respiratory tract develops after exposure to many kinds of wood dust. However, the wood dust of oak and beech seems to be most carcinogenic. It is assumed that exposure to wood dust can cause an increased incidence of other cancers, especially lung cancer and Hodgkin's disease. The adverse effects of microorganisms, mainly mould fungi and their metabolic products are manifested by alveolitis allergica and ODTS. These microorganisms can induce aspergillomycosis, bronchial asthma, rhinitis and allergic dermatitis.
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PMID:[Biological effect of wood dust]. 823 99

Type 2 helper T-cell immune responses can be demonstrated in the human atopic disorders atopic dermatitis and allergic asthma/rhinoconjunctivitis. The CD30 (Ki-1) antigen, originally described on Hodgkin and Reed-Sternberg cells, has recently been proposed as a marker of T cells with potent B-cell helper activity producing IL-5 and gamma-IFN, as well as on CD4+ and CD8+ T cells with a Th2 cytokine profile. As a soluble form of CD30 (sCD30) is released by CD30+ cells in vivo, we studied its clinical significance in atopic disorders compared with allergic contact dermatitis and healthy controls. Elevated sCD 30 levels were associated with atopic dermatitis (P < 0.0001), but not with respiratory atopic disorders or allergic contact dermatitis. sCD30 levels in patients with atopic-dermatitis were independent of serum IgE. The particular occurrence of serum sCD30 in patients with atopic dermatitis indicates a special regulatory function of CD30+ cells in this disease.
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PMID:Elevated serum levels of soluble CD30 are associated with atopic dermatitis, but not with respiratory atopic disorders and allergic contact dermatitis. 929 64

Natural killer (NK) cells are large granular lymphocytes that play important roles in immunity against viral infection. NK cell deficiency is associated with recurrent episodes of severe herpes group virus reactivation. Few cases of NK cell deficiency have been reported. Here, we report the case of a Taiwanese girl who had suffered from severe atopic dermatitis since infancy, and recurrent episodes of herpes virus reactivation since the age of 3 years old. NK cell deficiency was diagnosed based on the finding of persistently low NK cell counts in peripheral blood. Hodgkin's lymphoma developed when she was 6 years old. The present case suggests that NK cell deficiency may be an important risk factor in the development of Hodgkin's lymphoma.
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PMID:Natural killer cell deficiency associated with Hodgkin's lymphoma: a case report. 1191 Oct 42

Pruritus is a common manifestation of dermatologic diseases, including xerotic eczema, atopic dermatitis, and allergic contact dermatitis. Effective treatment of pruritus can prevent scratch-induced complications such as lichen simplex chronicus and impetigo. Patients, particularly elderly adults, with severe pruritus that does not respond to conservative therapy should be evaluated for an underlying systemic disease. Causes of systemic pruritus include uremia, cholestasis, polycythemia vera, Hodgkin's lymphoma, hyperthyroidism, and human immunodeficiency virus (HIV) infection. Skin scraping, biopsy, or culture may be indicated if skin lesions are present. Diagnostic testing is directed by the clinical evaluation and may include a complete blood count and measurement of thyroid-stimulating hormone, serum bilirubin, alkaline phosphatase, serum creatinine, and blood urea nitrogen levels. Chest radiography and testing for HIV infection may be indicated in some patients. Management of nonspecific pruritus is directed mostly at preventing xerosis. Management of disease-specific pruritus has been established for certain systemic conditions, including uremia and cholestasis.
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PMID:Pruritus. 1452 1

Ultraviolet-based therapy has been used to treat various pruritic conditions including pruritus in chronic renal failure, atopic dermatitis, HIV, aquagenic pruritus and urticaria, solar, chronic, and idiopathic urticaria, urticaria pigmentosa, polycythemia vera, pruritic folliculitis of pregnancy, breast carcinoma skin infiltration, Hodgkin's lymphoma, chronic liver disease, and acquired perforating dermatosis, among others. Various mechanisms of action for phototherapy have been posited. Treatment limitations, side effects, and common dosing protocols are reviewed.
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PMID:Ultraviolet phototherapy for pruritus. 1629 8

The authors report a case of Hodgkin lymphoma developing in a 4.5-year-old female child with hyper-IgE syndrome. This is one of the few cases of malignancy reported in this syndrome. The patient had severe atopic dermatitis, asthma, recurrent pneumonia, recurrent skin infections, and growth retardation. Immunologic evaluation revealed a high level of immunoglobulin E (7000 IU/mL) and peripheral eosinophilia. She was found to have normal values for serum IgG, IgM, IgA, WBC chemotaxis, serum complement function and normal sweat chloride test. The development of fatal Hodgkin lymphoma in this patient with hyper-IgE syndrome may suggest an increased risk for developing premature malignancies in hyper-IgE syndrome, although the precise immunologic defect is still unknown.
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PMID:Hodgkin lymphoma developing in a 4.5-year-old girl with hyper-IgE syndrome. 1632 14

Mast cells are involved in many disorders where the triggering mechanism that leads to degranulation and/or cytokine secretion has not been defined. Several chronic inflammatory diseases are associated with increased mast cell numbers and upregulation of the TNF receptor family member CD30, but the role of elevated CD30 expression is poorly understood. Here we report what we believe to be a novel way to activate mast cells with CD30 that leads to degranulation-independent secretion of chemokines. CD30 induced a de novo synthesis and secretion of the chemokines IL-8, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta, a process involving the MAPK/ERK pathway. Mast cells were found to be the predominant CD30 ligand-positive (CD30L-positive) cell in the chronic inflammatory skin diseases psoriasis and atopic dermatitis, and both CD30 and CD30L expression were upregulated in lesional skin in these conditions. Furthermore, the number of IL-8-positive mast cells was elevated both in psoriatic and atopic dermatitis lesional skin as well as in ex vivo CD30-treated healthy skin organ cultures. In summary, characterization of CD30 activation of mast cells has uncovered an IgE-independent pathway that is of importance in understanding the entirety of the role of mast cells in diseases associated with mast cells and CD30 expression. These diseases include Hodgkin lymphoma, atopic dermatitis, and psoriasis.
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PMID:Mast cell CD30 ligand is upregulated in cutaneous inflammation and mediates degranulation-independent chemokine secretion. 1696 9

Celiac disease is an autoimmune disease associated with increased risk of several diseases including a variety of malignancies. This is the first report of the concomitance of atopic dermatitis and Hodgkin's lymphoma in a child with celiac disease. Here, we report an 11-year-old boy with chronic diarrhea, glossitis, chronic dermatitis, and megaloblastic anemia who later developed Hodgkin's lymphoma.
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PMID:Concomitant Hodgkin's lymphoma and atopic dermatitis in a child with Celiac disease. 1940 Jun 14

The transmembrane receptor CD30 (TNFRSF8) and its ligand CD30L (CD153, TNFSF8) are members of the tumor necrosis factor (TNF) superfamily and display restricted expression in subpopulations of activated T-and B-cells in nonpathologic conditions. CD30 expression is upregulated in various hematological malignancies, including Reed-Sternberg cells in Hodgkin's disease (HD), anaplastic large cell lymphoma (ALCL) and subsets of Non-Hodgkin's lymphomas (NHLs). Increased CD30L expression was found on mast cells within HD tumors and preclinical and clinical studies with compounds targeting the CD30/ CD30L system in HD and ALCL demonstrated therapeutic benefit. Upregulation of CD30 and CD30L is also linked to leukocytes in patients with chronic inflammatory diseases, including lupus erythematosus, asthma, rheumatoid arthritis and atopic dermatitis (AD). Preclinical studies conducted with transgenic mice or biologic compounds suggested important regulatory functions of the CD30-CD30L system in various aspects of the immune system. Such key regulatory roles and their low expression in normal conditions combined with increased expression in malignant tissues provided a strong rationale to investigate CD30 and CD30L as therapeutic targets in hematologic malignancies, autoimmune and inflammatory diseases. In this report, we review the pharmacodynamic effects of specific therapeutic compounds targeting the CD30/CD30L system in preclinical- and clinical studies.
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PMID:Targeting CD30/CD30L in oncology and autoimmune and inflammatory diseases. 1976 74


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