A conexão hipotireoidismo-hipertensão

O hipotireoidismo pode estar por trás de certos casos de hipertensão

[Imagem: azertag.az ru]

[Este artigo já foi publicado no nosso antigo blog do substack ao qual, recentemente,  me foi vetado o acesso para postar novas publicações. Dessa forma e para que possa ser conhecido pelos leitores deste novo blog -  intitulado outramedicina2024.substack.com - , faço aqui a republicação do artigo]

No quadro de hipotireoidismo, se instala uma tendência à perda de sal na urina. Sal plasmático é mais frequentemente eliminado pelos rins em portador de hipotireoidismo.

A inibição relativa da respiração celular produzida pela menor oferta celular do hormônio tireoidiano [T3] induz uma maior permeabilidade capilar e perda de sal [e de albumina, portanto, albuminato de sódio] para o tecido extravascular. O sangue fica alterado, mais espesso, enquanto líquido extravasa do vascular para o extracelular [Ver nota a respeito no blog].

Ao mesmo tempo, a diminuição de sal vascular [hiponatremia] faz com que o organismo, reativamente, aumente a adrenalina, também a aldosterona. Adrenalina e aldosterona são vasoconstrictores.  Está em marcha um mecanismo que, em determinado prazo, tende a construir um quadro de hipertensão. Que teria começado no hipotireoidismo [e que pode ser incrementado pelo doutor quando recomenda, àquele paciente, uma dieta hipossódica, restrita em sal; ou quando veta açúcar, outro antagonista da adrenalina].

Hipotireoidismo, portanto,  é uma causa fundamental de hipertensão.

Também por outras razões.

O hipotireoidismo, pela insuficiência do T3, tende a diminuir a força de contração do coração [ver nota a respeito no blog] o que contribui para processos, mais adiante, de insuficiência cardíaco-congestiva. E, no argumento de R. Peat, “a hipoosmolaridade produzida pelo hipotireoidismo no sangue, aumentando a excitabilidade do endotélio vascular e da musculatura lisa, provavelmente é um mecanismo contributivo para a hipertensão no hipotireoidismo”. Também pode levar, circunstancialmente, na direção oposta, à hipotensão ortostática, por conta da redução do volume sanguíneo.

Já foram feitas pesquisas nas quais o tratamento do hipotireoidismo, por si só, baixou a pressão arterial de pacientes hipertensos [A]; havia resistência periférica elevada ao fluxo do sangue, menor debito cardíaco, o que tinha a ver, no primeiro caso, com  aumento do tônus simpático [adrenalina].

Dados de outra pesquisa também demonstraram que o hormônio tireoidiano participa no controle da homeostase da pressão arterial em pessoas normotensas [C]; também observaram que existe ativação simpática e adrenal no hipotireoidismo.

Pesquisa também já mostrou que hipotireoidismo, mesmo subclínico, apareceu associado a hipertensão e colesterol total elevado [B]. E “hipotireoidismo aberto pode resultar em aterosclerose acelerada e doença coronariana” [B].

Outras pesquisas evidenciaram também risco mais alto de arteriosclerose acelerada em pacientes com hipotireoidismo subclínico [D]. Pacientes “com hipotireoidismo, mesmo em caso de hipotireoidismo subclínico, mostraram comprometimento da função endotelial, função sistólica deprimida, disfunção diastólica ventricular esquerda em repouso e disfunção sistólica e diastólica de esforço [...] e também uma tendência a pressão arterial diastólica aumentada, como resultado de resistência vascular sistêmica aumentada” [E].

Mais experiências existem, todas apontando aquela conexão hipotireoidismo-hipertensão.

A título de conclusão essa pode ser uma conversa a ser levada com seu doutor quando ele for tratar sua hipertensão da forma convencional. Quando usar drogas – todas tóxicas – para atacar os efeitos hipertensivos sem [medicina dos sintomas] ir à eventual raiz do problema. Abra um diálogo com ele. Quem sabe, ele será aberto, humano e paciente.

De toda forma, será muito importante, portanto, pesquisar – da forma adequada – a presença de um hipotireoidismo crônico construindo aquela hipertensão; uma hipertensão que o doutor vai, eventualmente e pateticamente, chamar de “idiopática”.

G Dantas    [Publicado originalmente em 22-5-24]

As informações aqui presentes não pretendem servir para uso diagnóstico, prescrição médica, tratamento, prevenção ou mitigação de qualquer doença humana.  Não pretendem substituir a consulta ao profissional médico ou servir como recomendação para qualquer plano de tratamento. Trata-se de informações com  fins estritamente educativos. Nenhuma das notas aqui presentes, neste blog, conseguirá atingir o contexto específico do paciente singular, nem doses, modo de usar etc. Este trabalho compete ao paciente com seu médico. Isso significa que nenhuma dessas notas - necessariamente parciais - substitui essa relação.

Referências __________________

[A]   SAITO I SARUTA T, 1994. Hypertension in thyroid disorders. Endocrinol Metab Clin North Am. 1994 Jun;23(2):379-86. “Hypertension is more common in hypothyroidic patients than in euthyroid controls in older age groups. Treatment of the thyroid deficiency alone lowers blood pressure in most patients. Hemodynamically, cardiac output is reduced and total peripheral resistance is elevated. The latter probably is secondary to an increase of sympathetic nervous tone and a relative increase in alpha-adrenergic response. In hyperthyroidism, elevation of diastolic blood pressure is uncommon. Systolic hypertension is more common in younger age groups. Treatment of the hyperthyroidism alone lowers systolic blood pressure in most patients. An increase in cardiac output and a decrease in total peripheral resistance accompany the hyperthyroidism. Potentiation of catecholamine action by an excess of thyroid hormone has been invoked as an explanation, because thyroid hormone excess is accompanied by increased beta-adrenergic receptors in some tissue, including heart”.

 [B]   LUBOSHITZKY R AVIV A 2002. Risk factors for cardiovascular disease in women with subclinical hypothyroidism. Thyroid. 2002 May;12(5):421-5. “Overt hypothyroidism may result in accelerated atherosclerosis and coronary heart disease (CHD) presumably because of the associated hypertension, hypercholesterolemia, and hyperhomocysteinemia. As many as 10%-15% of older women have subclinical hypothyroidism (SH) and thyroid autoimmunity. Whether SH is associated with risk for CHD is controversial. We examined 57 women with SH and 34 healthy controls. SH was defined as an elevated thyrotropin (TSH) (>4.5 mU/L) and normal free thyroxine (FT(4)) level (8.7-22.6 nmol/L). None of the patients had been previously treated with thyroxine. In all participants we determined blood pressure, body mass index (BMI), and fasting TSH, FT(4), antibodies to thyroid peroxidase and thyroglobulin, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides, folic acid, vitamin B(12), creatinine, and total plasma homocysteine levels. The SH and control groups did not differ in their total homocysteine values. Mean diastolic blood pressure was increased in SH patients versus controls (82 vs. 75 mm Hg; p < 0.01). Mean values of TC, HDL-C, LDL-C, triglycerides, TC/HDL-C, and LDL-C/HDL-C were not different in patients with SH compared with controls. Individual analysis revealed that the percentage of patients with SH having hypertension (20%), hypertriglyceridemia (26.9%), elevated TC/HDL-C (11.5%), and LDL-C/HDL-C (4%) ratios were higher than the percentages in controls. Hyperhomocysteinemia (> or = 10.98 micromol/L) was observed in 29.4% of SH and was not significantly different from the percentage in controls (21.4%). No significant correlation between TSH and biochemical parameters was detected. We conclude that subclinical hypothyroidism in middle-aged women is associated with hypertension, hypertriglyceridemia, and elevated TC/HDL-C ratio. This may increase the risk of accelerated atherosclerosis and premature coronary artery disease in some patients”.

 [C]   FOMMEI E  IERVASI G, 2002. The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans. The Journal of Clinical Endocrinology & Metabolism May 1, 2002 vol. 87 no. 5 1996-2000  “
Arterial hypertension is known to be frequently associated with thyroid dysfunction, with a particularly high prevalence in chronic hypothyroidism. However, to our knowledge no comprehensive study addressed causal mechanisms possibly involved in this association. We here report the physiological relationships between blood pressure and neuro-humoral modifications induced by acute hypothyroidism in normotensive subjects. Twelve normotensive patients with previous total thyroidectomy were studied. Ambulatory 24-h blood pressure monitoring was performed, and free T3, free T4, TSH, PRA, aldosterone, cortisol, adrenaline, and noradrenaline were assayed 6 wk after oral L-T4 withdrawal (phase 1) and 2 months after resumption of treatment (phase 2). During the hypothyroid state (TSH, 68.1 ± 27.7 μIU/ml; mean ± SD), daytime arterial systolic levels slightly, but significantly, increased (125.5 ± 9.7 vs. 120.4 ± 10.8 mm Hg; P < 0.05), and daytime diastolic levels (84.6 ± 7.9 vs. 76.4 ± 6.8 mm Hg; P < 0.001), noradrenaline (2954 ± 1578 vs. 1574 ± 962 pmol/liter; P < 0.001), and adrenaline (228.4 ± 160 vs. 111.3 ± 46.1 pmol/liter; P < 0.05) also increased. PRA remained unchanged (0.49 ± 0.37 vs. 0.35 ± 0.21 ng/ml·h; P = NS), whereas both aldosterone (310.3 ± 151 vs. 156.9 ± 67.5 pmol/liter; P < 0.005) and cortisol (409.2 ± 239 vs. 250.9 ± 113 pmol/liter; P < 0.02) significantly increased. By using univariate logistic regression daytime arterial diastolic values, noradrenaline and aldosterone were found to be significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively). In conclusion, our data show that thyroid hormones participate in the control of systemic arterial blood pressure homeostasis in normotensive subjects. The observed sympathetic and adrenal activation in hypothyroidism, which is reversible with thyroid hormone treatment, may also contribute to the development of arterial hypertension in human hypothyroidism”.

[D]   PESIC M ANTIC S, 2007. [Cardiovascular risk factors in patients with subclinical hypothyroidism].  [Article in Serbian] Vojnosanit Pregl. 2007 Nov;64(11):749-52. “BACKGROUND/AIMS:
Overt hypothyroidism is disease associated with accelerated arteriosclerosis and coronary heart disease. Whether subclinical hypothyroidism (SH) is associated with increased cardiovascular risk is contraversial. As SH is a high prevalence thyroid dysfunction, specially in older women, it is important to evaluate cardiovascular risk factors in these patients and that was the aim of this study.
METHODS:
We examined 30 patients with SH and 20 healthy controls. Subclinical hypothireoidism was defined as an elevated thyrotropin (TSH) (> 4.5 mU/L) and normal free thyroxine (FT4) level. In all the participants we determined body mass index (BMI), blood pressure, TSH, FT4, antibodies to thyroid peroxidase, antibodies to thyroglobulin, total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglicerides, total cholesterol/HDL cholesterol ratio and LDL/HDL cholesterol ratio.
RESULTS:
Mean BMI in patients with SH was significantly higher (p < 0.05), as well as diastolic blood pressure (p < 0.01) compared with the controls. Average levels of total cholesterol (5.40 +/- 0.62 vs 5.06 +/- 0.19 mmol/l, p < 0.01) and triglycerides (2.16 +/- 0.56 vs 1.89 +/- 0.24 mmol/l, p < 0.05) were also significantly higher in the group with SH. Individual analysis revealed that the percentage of patients with SH having borderline elevated total cholesterol (63.33%), hypertrigliceridemia (43.33%) and elevated total cholesterol/HDL cholesterol ratio (26.67%) were significantly higher than the percentage in the controls. No significant correlation between TSH and lipid parameters was detected.
CONCLUSION: Subclinical hypothyroidism was associated with higher BMI, diastolic hypertension, higher total cholesterol and triglicerides levels and higher total cholesterol/HDL cholesterols ratio. This might increase the risk of accelerated arteriosclerosis in patients with SH”.

 [E]   BIONDI B KLEIN I, 2004. Hypothyroidism as a risk factor for cardiovascular disease. Endocrine. 2004 Jun;24(1):1-13. “The cardiovascular risk in patients with hypothyroidism is related to an increased risk of functional cardiovascular abnormalities and to an increased risk of atherosclerosis. The pattern of cardiovascular abnormalities is similar in subclinical and overt hypothyroidism, suggesting that a lesser degree of thyroid hormone deficiency may also affect the cardiovascular system. Hypothyroid patients, even those with subclinical hypothyroidism, have impaired endothelial function, normal/depressed systolic function, left ventricular diastolic dysfunction at rest, and systolic and diastolic dysfunction on effort, which may result in poor physical exercise capacity. There is also a tendency to increase diastolic blood pressure as a result of increased systemic vascular resistance. All these abnormalities regress with L-T4 replacement therapy. An increased risk for atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency. The “traditional” risk factors are hypertension in conjunction with an atherogenic lipid profile; the latter is more often observed in patients with TSH >10 mU/L. More recently, C-reactive protein, homocysteine, increased arterial stiffness, endothelial dysfunction, and altered coagulation parameters have been recognized as risk factors for atherosclerosis in patients with thyroid hormone deficiency. This constellation of reversible cardiovascular abnormalities in patient with TSH levels <10 mU/L indicate that the benefits of treatment of mild thyroid failure with appropriate doses of L-thyroxine outweigh the risk”.

[E]  FPS, 2012. Comments Offon High Blood Pressure and Hypothyroidism   By Team FPS – April 23, 2012. As referências acima constam da página abaixo citada da FPS. Fonte:  https://www.functionalps.com/blog/2012/04/23/high-blood-pressure-and-hypothyroidism/

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