Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this paper is to evaluate the possible clinical association of autoimmune thyroid disease and acute leukemia. This study is a retrospective review of all adult patients with acute leukemia treated at our institutions from 1978-1989. Those with both leukemia and thyroid disease were evaluated and are presented. Twenty-seven of eight hundred seventy patients with acute leukemia had evidence of thyroid disease. This is a 3-fold increase in overall incidence. Twenty-one patients had acute myeloid leukemia, five had acute lymphoid leukemia, and one had accelerated chronic myeloid leukemia. Thyroid disease entities included toxic multinodular goiter (four patients), idiopathic hypothyroidism (eight patients), Graves' disease (eight patients), and Hashimoto's thyroiditis (seven patients). Whereas the association may have had a negative effect on elderly patients, those with Graves' disease and Hashimoto's disease appeared to have an improved outcome of the leukemia. There is an increased association of autoimmune thyroid disease and acute leukemia. Since thyroid hormones are important regulators of hematopoiesis and utilize receptors similar to those of differentiating factors such as retinoids, the association may be important for further study of mechanisms of growth regulations in leukemia.
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PMID:Association of thyroid disease with acute leukemia. 155 Jan 1

Hepatitis C viral infection is a global health problem that affects approximately 4 million people in the United States. Combination treatment with pegylated interferon (IFN)-alpha plus ribavirin has been shown to be most effective in treating patients with chronic hepatitis C (CHC). Despite its efficacy, one of the most common side effects of this regimen is depression. Whereas IFN-alpha has been found to induce depression in chronic myelogenous leukemia, melanoma, and renal cell carcinoma, CHC patients may be especially prone to develop IFN-induced depression. This review includes a summary of differences between IFN-alpha and IFN-beta and addresses whether pegylation of IFN (versus nonpegylated IFN) gives rise to a treatment with reduced potential to induce depressive symptoms. Consideration is also given to evidence showing that treatment with ribavirin may contribute to IFN-induced depression. Thyroid disorders and anemia (as well as other medical conditions) have also been associated with IFN exposure and may account for some incidences of depression in CHC patients. Evidence is reviewed indicating that prior psychiatric and mood disorders (especially previous episodes of major depressive disorder), just prior to IFN treatment, contribute to the propensity to develop depression during treatment. In addition, a brief description is provided of potential biological mechanisms of IFN-induced depression (ie, monoamines, hypothalamic-pituitary-adrenocortical [HPA] axis, proinflammatory cytokines, peptidases, intercellular adhesion molecule-1, and nitric oxide). Finally, a discussion is provided on the use of antidepressants as a preventative versus restorative treatment, including a commentary on risks of using antidepressants in this patient population.
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PMID:Interferon-induced depression in chronic hepatitis C: a review of its prevalence, risk factors, biology, and treatment approaches. 1741 17