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. 2009 Sep 28;14(10):433-42.
doi: 10.1186/2047-783x-14-10-433.

Estrogen exposure, obesity and thyroid disease in women with severe pulmonary hypertension

Affiliations

Estrogen exposure, obesity and thyroid disease in women with severe pulmonary hypertension

Lori Sweeney et al. Eur J Med Res. .

Abstract

Severe pulmonary hypertension is a lethal group of disorders which preferentially afflicts women. It appears that in recent years the patient profile has shifted towards older, obese, and postmenopausal women, suggesting that endocrine factors may be important. Several studies have revealed an increased prevalence of thyroid disease in these patients, but no studies have evaluated for a coexistence of endocrine factors. In particular, no studies have attempted to evaluate for concurrent thyroid disease, obesity and long-term estrogen exposure in patients. 88 patients attending the Pulmonary Hypertension Association 8th International meeting completed a questionnaire and were interviewed. Information was collected regarding reproductive history, height, weight, and previous diagnosis of thyroid disease. 46% met criteria for obesity. 41% reported a diagnosis of thyroid disease. 81% of women reported prior use of hormone therapy. 70% reported greater than 10 years of exogenous hormone use. 74% of female patients reported two or more of potentially disease modifying endocrine factors (obesity, thyroid disease or estrogen therapy). The coexistent high prevalence in our cohort of exogenous estrogen exposure, thyroid disease and obesity suggests that an interaction of multiple endocrine factors might contribute to the pathogenesis of pulmonary hypertension and may represent epigenetic modifiers in genetically-susceptible individuals.

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Figures

Figure 1
Figure 1
Reproductive risk factor point distribution for the cohort is shown according to menopause status.
Figure 2
Figure 2
Distribution of these risk factors and the combination of risk factors.
Figure 3
Figure 3
Schematic illustrating the potential interactions of pathobiologically relevant risk factos which may contribute to severe angioproliferative pulmonary arterial hypertension. Hypothetically, autoimmunity and chronic inflammation interact via thyroid disease, estrogen and obesity. VEGF = vascular endothelial growth factor, Bcl-2 = antiapoptotic B-cell lymphoma protein.

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