Assessment of the Effects of Low-Level Laser Therapy on the Thyroid Vascularization of Patients with Autoimmune Hypothyroidism by Color Doppler Ultrasound
Background. Chronic autoimmune thyroiditis (CAT) frequently alters thyroid vascularization, likely as a result of the autoimmune process. Objective. To evaluate the effects of low-level laser therapy (LLLT) on the thyroid vascularization of patients with hypothyroidism induced by CAT using color Doppler ultrasound parameters. Methods. In this randomized clinical trial, 43 patients who underwent levothyroxine replacement for CAT-induced hypothyroidism were randomly assigned to receive either 10 sessions of LLLT (L group, ) or 10 sessions of a placebo treatment (P group, ). Color Doppler ultrasounds were performed before and 30 days after interventions. To verify the vascularity of the thyroid parenchyma, power Doppler was performed. The systolic peak velocity (SPV) and resistance index (RI) in the superior (STA) and inferior thyroid arteries (ITAs) were measured by pulsed Doppler. Results. The frequency of normal vascularization of the thyroid lobes observed in the postintervention power Doppler examination was significantly higher in the L than in the P group ( ). The pulsed Doppler examination revealed an increase in the SPV of the ITA in the L group compared with the P group ( ). No significant differences in the SPV of the STA and in the RI were found between the groups. Conclusion. These results suggest that LLLT can ameliorate thyroid parenchyma vascularization and increase the SPV of the ITA of patients with hypothyroidism caused by CAT. 1. Introduction Chronic autoimmune thyroiditis (CAT) is the most common cause of hypothyroidism in populations who have an adequate dietary iodine intake [1]. The combination of genetic and environmental factors may contribute to the aetiology of the CAT [2, 3]. The autoimmune responses mediated by cells, antibodies and cytokines promote thyroid follicular cell injury in CAT patients [3–5]. This disease leads to the progressive destruction of the follicular cells of the thyroid parenchyma, which can result in hypothyroidism. Recent evidences have suggested that low-level laser therapy (LLLT) may improve thyroid function and reduce the levels of thyroid peroxidase antibodies (TPOAb) in patients with hypothyroidism caused by CAT [6, 7]. Color Doppler ultrasound (CDU) provides important additional information beyond that obtained by B-mode ultrasound, allowing the evaluation of various parameters of thyroid vascularization. The presence of increased vascularization in the thyroid parenchyma in most CAT patients has been demonstrated in recent studies [8, 9]. It was also reported that the systolic peak velocity of the
References
[1]
M. A. Boukis, D. A. Koutras, A. Souvatzoglou, et al., “Thyroid hormone and immunological studies in endemic goiter,” Journal of Clinical Endocrinology and Metabolism, vol. 57, no. 4, pp. 859–862, 1983.
[2]
T. H. Brix and L. Hegedus, “Twin studies as a model for exploring the aetiology of autoimmune thyroid disease,” Clinical Endocrinology, vol. 76, pp. 457–464, 2012.
[3]
S. Fountoulakis and A. Tsatsoulis, “On the pathogenesis of autoimmune thyroid disease: a unifying hypothesis,” Clinical Endocrinology, vol. 60, no. 4, pp. 397–409, 2004.
[4]
A. P. Weetman, “Autoimmune thyroid disease,” Autoimmunity, vol. 37, no. 4, pp. 337–340, 2004.
[5]
B. Rapoport and S. M. McLachlan, “Thyroid autoimmunity,” The Journal of Clinical Investigation, vol. 108, no. 9, pp. 1253–1259, 2001.
[6]
D. B. H？fling, M. C. Chavantes, A. G. Juliano et al., “Low-level laser therapy in chronic autoimmune thyroiditis: a pilot study,” Lasers in Surgery and Medicine, vol. 42, no. 6, pp. 589–596, 2010.
[7]
D. B. H？fling, M. C. Chavantes, A. G. Juliano, et al., “Low-level laser in the treatment of patients with hypothyroidism induced by chronic autoimmune thyroiditis: a randomized, placebo-controlled clinical trial,” Lasers in Medical Science. In press.
[8]
G. Corona, C. Biagini, M. Rotondi et al., “Correlation between, clinical, biochemical, color doppler ultrasound thyroid parameters, and CXCL-10 in autoimmune thyroid diseases,” Endocrine Journal, vol. 55, no. 2, pp. 345–350, 2008.
[9]
M. Iitaka, S. Miura, K. Yamanaka et al., “Increased serum vascular endothelial growth factor levels and intrathyroidal vascular area in patients with Graves' disease and Hashimoto's thyroiditis,” Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 11, pp. 3908–3912, 1998.
[10]
S. L. Schulz, U. Seeberger, and J. H. Hengstmann, “Color Doppler sonography in hypothyroidism,” European Journal of Ultrasound, vol. 16, no. 3, pp. 183–189, 2003.
[11]
L. Brosseau, V. Robinson, G. Wells et al., “Low level laser therapy (Classes I, II and III) for treating rheumatoid arthritis,” Cochrane Database of Systematic Reviews, no. 4, Article ID CD002049, 2005.
[12]
J. M. Bjordal, C. Couppé, R. T. Chow, J. Tunér, and E. A. Ljunggren, “A systematic review of low level laser therapy with location-specific doses for pain from chronic joint disorders,” Australian Journal of Physiotherapy, vol. 49, no. 2, pp. 107–116, 2003.
[13]
G. C. Duarte, E. K. Tomimori, R. Y. A. Camargo et al., “The prevalence of thyroid dysfunction in elderly cardiology patients with mild excessive iodine intake in the urban area of S？o Paulo,” Clinics, vol. 64, no. 2, pp. 135–142, 2009.
[14]
C. G. P. Roberts and P. W. Ladenson, “Hypothyroidism,” The Lancet, vol. 363, no. 9411, pp. 793–803, 2004.
[15]
C. M. Dayan and G. H. Daniels, “Chronic autoimmune thyroiditis,” The New England Journal of Medicine, vol. 335, no. 2, pp. 99–107, 1996.
[16]
J. P. Nordmeyer, T. A. Shafeh, and C. Heckmann, “Thyroid sonography in autoimmune thyroiditis. A prospective study on 123 patients,” Acta Endocrinologica, vol. 122, no. 3, pp. 391–395, 1990.
[17]
P. W. Ralls, D. S. Mayekawa, K. P. Lee et al., “Color-flow Doppler sonography in Graves disease: ‘thyroid inferno’,” American Journal of Roentgenology, vol. 150, no. 4, pp. 781–784, 1988.
[18]
X. Gao and D. Xing, “Molecular mechanisms of cell proliferation induced by low power laser irradiation,” Journal of Biomedical Science, vol. 16, no. 1, article 4, 2009.
[19]
F. Mafra de Lima, A. B. Villaverde, M. A. Salgado et al., “Low intensity laser therapy (LILT) in vivo acts on the neutrophils recruitment and chemokines/cytokines levels in a model of acute pulmonary inflammation induced by aerosol of lipopolysaccharide from Escherichia coli in rat,” Journal of Photochemistry and Photobiology B, vol. 101, no. 3, pp. 271–278, 2010.
[20]
M. Yamaura, M. Yao, I. Yaroslavsky, R. Cohen, M. Smotrich, and I. E. Kochevar, “Low level light effects on inflammatory cytokine production by rheumatoid arthritis synoviocytes,” Lasers in Surgery and Medicine, vol. 41, no. 4, pp. 282–290, 2009.
[21]
E. S. Boschi, C. E. Leite, V. C. Saciura et al., “Anti-inflammatory effects of low-level laser therapy (660 nm) in the early phase in carrageenan-induced pleurisy in rat,” Lasers in Surgery and Medicine, vol. 40, no. 7, pp. 500–508, 2008.
[22]
D. Drugǎrin, S. Negru, and A. Koreck, “Th1 cytokines in autoimmune thyroiditis,” Roumanian Archives of Microbiology and Immunology, vol. 57, no. 3-4, pp. 309–319, 1998.
[23]
J. J. Díez, A. Hernanz, S. Medina, C. Bayón, and P. Iglesias, “Serum concentrations of tumour necrosis factor-alpha (TNF-α) and soluble TNF-α receptor p55 in patients with hypothyroidism and hyperthyroidism before and after normalization of thyroid function,” Clinical Endocrinology, vol. 57, no. 4, pp. 515–521, 2002.
[24]
B. Akinci, A. Comlekci, S. Yener et al., “Hashimoto's thyroiditis, but not treatment of hypothyroidism, is associated with altered TGF-beta1 levels,” Archives of Medical Research, vol. 39, no. 4, pp. 397–401, 2008.
[25]
A. Ishay, Y. Pollak, L. Chervinsky, I. Lavi, and R. Luboshitzky, “Color-flow doppler sonography in patients with subclinical thyroid dysfunction,” Endocrine Practice, vol. 16, no. 3, pp. 376–381, 2010.
[26]
A. Antonelli, M. Rotondi, P. Fallahi et al., “Increase of interferon-γ inducible α chemokine CXCL10 but not β chemokine CCL2 serum levels in chronic autoimmune thyroiditis,” European Journal of Endocrinology, vol. 152, no. 2, pp. 171–177, 2005.
[27]
M. Rotondi, L. Chiovato, S. Romagnani, M. Serio, and P. Romagnani, “Role of chemokines in endocrine autoimmune diseases,” Endocrine Reviews, vol. 28, no. 5, pp. 492–520, 2007.
[28]
A. Antonelli, P. Fallahi, M. Rotondi et al., “Increased serum CXCL10 in Graves' disease or autoimmune thyroiditis is not associated with hyper- or hypothyroidism per se, but is specifically sustained by the autoimmune, inflammatory process,” European Journal of Endocrinology, vol. 154, no. 5, pp. 651–658, 2006.
[29]
T. A. A. Macedo, M. C. Chammas, P. T. Jorge et al., “Differentiation between the two types of amiodarone-associated thyrotoxicosis using duplex and amplitude doppler sonography,” Acta Radiologica, vol. 48, no. 4, pp. 412–421, 2007.
