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Article: Thyroid functions in patients treated with interleukin-2 and lymphokine-activated killer cells

TitleThyroid functions in patients treated with interleukin-2 and lymphokine-activated killer cells
Authors
Issue Date1992
Citation
Quarterly Journal Of Medicine, 1992, v. 82 n. 297, p. 33-42 How to Cite?
AbstractTreatment of malignant disease with interleukin-2 and lymphokine-activated killer cells activates autoreactive T lymphocytes, stimulates release of cytokines and induces expression of HLA-class II antigens by tumour cells. We studied eight patients with hepatocellular carcinoma treated with a total of 16 courses of recombinant human interleukin-2 and lymphokine-activated killer cells and observed them for features of autoimmune thyroid disease. During the course of treatment there were significant decreases in total serum T4 and T3 and free thyroxine levels, but no change in TSH levels when all patients were analysed as a group. This was due to a number of factors including suppression of thyroid hormone release, haemodilution during interleukin-2 infusion and actual removal of thyroid hormones from the circulation during leukapheresis. Thyroid hormones returned to normal levels during resting period. One patient subsequently developed compensated hypothyroidism (normal total T4, total T3 and free T4 but elevated TSH) and four patients had features of 'sick euthyroid syndrome' (low total T4, total T3 or free T4 but normal TSH). None of the patients studied developed antibodies to thyroglobulin or microsomes. In contrast, no abnormality of thyroid function was seen in any of the nine subjects who received no active treatment. In conclusion, thyroid dysfunction was associated with immunotherapy of malignant disease with interleukin-2 and lymphokine-activated killer cells. This may arise from direct hormonal effects of the cytokines on thyroid hormone production.
Persistent Identifierhttp://hdl.handle.net/10722/161925
ISSN
1998 Impact Factor: 2.244
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKung, AWCen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorWong, KLen_US
dc.contributor.authorTam, CFen_US
dc.date.accessioned2012-09-05T05:16:05Z-
dc.date.available2012-09-05T05:16:05Z-
dc.date.issued1992en_US
dc.identifier.citationQuarterly Journal Of Medicine, 1992, v. 82 n. 297, p. 33-42en_US
dc.identifier.issn0033-5622en_US
dc.identifier.urihttp://hdl.handle.net/10722/161925-
dc.description.abstractTreatment of malignant disease with interleukin-2 and lymphokine-activated killer cells activates autoreactive T lymphocytes, stimulates release of cytokines and induces expression of HLA-class II antigens by tumour cells. We studied eight patients with hepatocellular carcinoma treated with a total of 16 courses of recombinant human interleukin-2 and lymphokine-activated killer cells and observed them for features of autoimmune thyroid disease. During the course of treatment there were significant decreases in total serum T4 and T3 and free thyroxine levels, but no change in TSH levels when all patients were analysed as a group. This was due to a number of factors including suppression of thyroid hormone release, haemodilution during interleukin-2 infusion and actual removal of thyroid hormones from the circulation during leukapheresis. Thyroid hormones returned to normal levels during resting period. One patient subsequently developed compensated hypothyroidism (normal total T4, total T3 and free T4 but elevated TSH) and four patients had features of 'sick euthyroid syndrome' (low total T4, total T3 or free T4 but normal TSH). None of the patients studied developed antibodies to thyroglobulin or microsomes. In contrast, no abnormality of thyroid function was seen in any of the nine subjects who received no active treatment. In conclusion, thyroid dysfunction was associated with immunotherapy of malignant disease with interleukin-2 and lymphokine-activated killer cells. This may arise from direct hormonal effects of the cytokines on thyroid hormone production.en_US
dc.languageengen_US
dc.relation.ispartofQuarterly Journal of Medicineen_US
dc.subject.meshAdulten_US
dc.subject.meshAutoantibodies - Analysisen_US
dc.subject.meshCarcinoma, Hepatocellular - Therapyen_US
dc.subject.meshHumansen_US
dc.subject.meshHypothyroidism - Etiologyen_US
dc.subject.meshInterleukin-2 - Adverse Effects - Therapeutic Useen_US
dc.subject.meshKiller Cells, Lymphokine-Activated - Transplantationen_US
dc.subject.meshLiver Neoplasms - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshRecombinant Proteins - Adverse Effectsen_US
dc.subject.meshThyroid Diseases - Etiology - Physiopathologyen_US
dc.subject.meshThyroid Gland - Immunology - Physiopathologyen_US
dc.titleThyroid functions in patients treated with interleukin-2 and lymphokine-activated killer cellsen_US
dc.typeArticleen_US
dc.identifier.emailKung, AWC:awckung@hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityKung, AWC=rp00368en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1332102en_US
dc.identifier.scopuseid_2-s2.0-0026534211en_US
dc.identifier.volume82en_US
dc.identifier.issue297en_US
dc.identifier.spage33en_US
dc.identifier.epage42en_US
dc.identifier.isiWOS:A1992HM43100004-
dc.identifier.scopusauthoridKung, AWC=7102322339en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridWong, KL=55223354400en_US
dc.identifier.scopusauthoridTam, CF=7201442994en_US

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