Hipertensão arterial pulmonar e doenças da tireoide <span class="so-article-trans-title" dir="auto"> Translated title: Pulmonary arterial hypertension and thyroid disease </span>

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Abstract

Estudos recentes têm sugerido uma associação entre hipertensão arterial pulmonar (HAP) e tireoidopatias (hipotireoidismo e hipertireoidismo). Esta associação tem um bom prognóstico, porque o aumento na pressão da artéria pulmonar geralmente é leve e reversível com o tratamento da tireoidopatia. O mecanismo exato envolvido na patogênese desta associação não está estabelecido, e a influência direta dos hormônios da tireoide e a autoimunidade são consideradas como hipóteses. Devido à alta prevalência de doenças da tireoide em pacientes com HAP, testes de função tireoidiana devem ser considerados na investigação de todo paciente com HAP. Neste artigo de revisão, descrevemos a prevalência de HAP em pacientes com doenças da tireoide e a prevalência de tireoidopatias em pacientes com HAP, assim como destacamos os principais efeitos das doenças da tireoide no sistema respiratório. A seguir, relatamos os efeitos do tratamento destas patologias.

Translated abstract

Recent studies have suggested an association between pulmonary arterial hypertension (PAH) and thyroid diseases (hypothyroidism and hyperthyroidism). This combination has a good prognosis, because the increase in the pulmonary artery pressure is usually slight and reverses after the treatment of the thyroid disease. Although the exact mechanism involved in the pathogenesis of this combination has not yet been established, it has been hypothesized that thyroid hormones and autoimmunity have a direct influence. Due to the high prevalence of thyroid disease in patients with PAH, thyroid function tests should be considered in the investigation of every patient with PAH. In this review, we describe the prevalence of PAH in patients with thyroid diseases and the prevalence of thyroid disease in patients with PAH, as well as addressing the principal effects that thyroid diseases have on the respiratory system. In addition, we report the treatment effects in patients with these diseases.

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Most cited references 36

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Expression of endothelin-1 in the lungs of patients with pulmonary hypertension.

A Giaid, M Yanagisawa, D. Langleben … (1993)

Pulmonary hypertension is characterized by an increase in vascular tone or an abnormal proliferation of muscle cells in the walls of small pulmonary arteries. Endothelin-1 is a potent endothelium-derived vasoconstrictor peptide with important mitogenic properties. It has therefore been suggested that endothelin-1 may contribute to increases in pulmonary arterial tone or smooth-muscle proliferation in patients with pulmonary hypertension. We studied the sites and magnitude of endothelin-1 production in the lungs of patients with various causes of pulmonary hypertension. We studied the distribution of endothelin-1-like immunoreactivity (by immunocytochemical analysis) and endothelin-1 messenger RNA (by in situ hybridization) in lung specimens from 15 control subjects, 11 patients with plexogenic pulmonary arteriopathy (grades 4 through 6), and 17 patients with secondary pulmonary hypertension and pulmonary arteriopathy of grades 1 through 3. In the controls, endothelin-1-like immunoreactivity was rarely seen in vascular endothelial cells. In the patients with pulmonary hypertension, endothelin-1-like immunoreactivity was abundant, predominantly in endothelial cells of pulmonary arteries with medial thickening and intimal fibrosis. Likewise, endothelin-1 messenger RNA was increased in the patients with pulmonary hypertension and was expressed primarily at sites of endothelin-1-like immunoreactivity. There was a strong correlation between the intensity of endothelin-1-like immunoreactivity and pulmonary vascular resistance in the patients with plexogenic pulmonary arteriopathy, but not in those with secondary pulmonary hypertension. Pulmonary hypertension is associated with the increased expression of endothelin-1 in vascular endothelial cells, suggesting that the local production of endothelin-1 may contribute to the vascular abnormalities associated with this disorder.

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Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension.

A Giaid, D. Saleh (1995)

Pulmonary hypertension is characterized by abnormal thickening of the pulmonary arteries and increased pulmonary vascular resistance. Nitric oxide is a potent endothelium-derived vasorelaxant substance and an inhibitor of smooth-muscle-cell growth. Nitric oxide is produced in various cell types by the action of an enzyme, nitric oxide synthase. We compared the expression of endothelial nitric oxide synthase in the lungs of control subjects with that in the lungs of patients with pulmonary hypertension. We investigated the expression of endothelial nitric oxide synthase by histochemical and immunohistochemical analysis, in situ hybridization, and Northern blot analysis in the lungs of 22 patients with plexogenic pulmonary arteriopathy (arteriopathy of grades 4 through 6), 24 patients with secondary pulmonary hypertension (arteriopathy of grades 1 through 3), and 23 control subjects. In the lungs of the control subjects, nitric oxide synthase was expressed at a high level in the vascular endothelium of all types of vessels and in the pulmonary epithelium. In contrast, little or no expression of the enzyme was found in the vascular endothelium of pulmonary arteries with severe histologic abnormalities (i.e., plexiform lesions) in patients with pulmonary hypertension. The intensity of the enzyme immunoreactivity correlated inversely with the severity of histologic changes. There was an inverse correlation between the arterial expression of the enzyme and total pulmonary resistance in patients with plexogenic pulmonary arteriopathy (r = -0.766, P = 0.004). Pulmonary hypertension is associated with diminished expression of endothelial nitric oxide synthase. It is possible that decreased expression of nitric oxide synthase may contribute to pulmonary vasoconstriction and to the excessive growth of the tunica media observed in this disease.

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An imbalance between the excretion of thromboxane and prostacyclin metabolites in pulmonary hypertension.

B Christman, C D McPherson, J. Newman … (1992)

Constriction of small pulmonary arteries and arterioles and focal vascular injury are features of pulmonary hypertension. Because thromboxane A2 is both a vasoconstrictor and a potent stimulus for platelet aggregation, it may be an important mediator of pulmonary hypertension. Its effects are antagonized by prostacyclin, which is released by vascular endothelial cells. We tested the hypothesis that there may be an imbalance between the release of thromboxane A2 and prostacyclin in pulmonary hypertension, reflecting platelet activation and an abnormal response of the pulmonary vascular endothelium. We used radioimmunoassays to measure the 24-hour urinary excretion of two stable metabolites of thromboxane A2 and a metabolite of prostacyclin in 20 patients with primary pulmonary hypertension, 14 with secondary pulmonary hypertension, 9 with severe chronic obstructive pulmonary disease (COPD) but no clinical evidence of pulmonary hypertension, and 23 normal controls. The 24-hour excretion of 11-dehydro-thromboxane B2 (a stable metabolite of thromboxane A2) was increased in patients with primary pulmonary hypertension and patients with secondary pulmonary hypertension, as compared with normal controls (3224 +/- 482, 5392 +/- 1640, and 1145 +/- 221 pg per milligram of creatinine, respectively; P less than 0.05), whereas the 24-hour excretion of 2,3-dinor-6-keto-prostaglandin F1 alpha (a stable metabolite of prostacyclin) was decreased (369 +/- 106, 304 +/- 76, and 644 +/- 124 pg per milligram of creatinine, respectively; P less than 0.05). The rate of excretion of all metabolites in the patients with COPD but no clinical evidence of pulmonary hypertension was similar to that in the normal controls. An increase in the release of the vasoconstrictor thromboxane A2, suggesting the activation of platelets, occurs in both the primary and secondary forms of pulmonary hypertension. By contrast, the release of prostacyclin is depressed in these patients. Whether the imbalance in the release of these mediators is a cause or a result of pulmonary hypertension is unknown, but it may play a part in the development and maintenance of both forms of the disorder.

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Journal

Journal ID (publisher-id): jbpneu

Title: Jornal Brasileiro de Pneumologia

Abbreviated Title: J. bras. pneumol.

Publisher: Sociedade Brasileira de Pneumologia e Tisiologia (São Paulo, SP, Brazil )

ISSN (Electronic): 1806-3756

Publication date (Print and electronic): February 2009

Volume: 35

Issue: 2

Pages: 179-185

Affiliations

[01] Porto Alegre RS orgnameHospital de Clínicas de Porto Alegre orgdiv1Serviço de Pneumologia Brasil

[02] Porto Alegre RS orgnameUniversidade Federal do Rio Grande do Sul orgdiv1Faculdade de Medicina orgdiv2Departamento de Medicina Interna Brasil

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Publisher ID: S1806-37132009000200012 Publisher ID: S1806-3713(09)03500212

SO-VID: c1182bcf-1ca2-4da6-a843-1be4c23cca5c

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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

History

Date accepted : 29 September 2008

Date received : 03 June 2008

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Figures: 0, Tables: 0, Equations: 0, References: 36, Pages: 7

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Hipertensão arterial pulmonar e doenças da tireoide Translated title: Pulmonary arterial hypertension and thyroid disease

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Most cited references 36

Expression of endothelin-1 in the lungs of patients with pulmonary hypertension.

Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension.

An imbalance between the excretion of thromboxane and prostacyclin metabolites in pulmonary hypertension.

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