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Abstract: Case Reports |

A 48 year-old Female with Self-Induced Hyperthyroidism, Interstitial Lung Disease, and Severe Pulmonary Hypertension FREE TO VIEW

Mark J. Emerick, MD*; Alan D. Betensley, MD; Samer T. Morcos, MD
Author and Funding Information

Henry Ford Hospital, Detroit, MI


Chest


Chest. 2004;126(4_MeetingAbstracts):933S. doi:10.1378/chest.126.4_MeetingAbstracts.933S
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INTRODUCTION:  Desiccated porcine thyroid preparations have been used as an alternative to synthetic thyroxine (1). The perceived benefits of desiccated porcine thyroid (DPT) are mood elevation, improved cognitive performance and increased activity level. “Holistic” physicians have touted DPT for conditions ranging from Major Depression to infertility. Accordingly, the abuse of DPT may be an under-recognized phenomenon.

CASE PRESENTATION:  A 48 year-old female nonsmoker with a history of restrictive lung disease, fibromyalgia, and chronic fatigue syndrome presented with dyspnea,hemoptysis, and massive lower extremity edema. Previous pulmonary function testing revealed total lung capacity of 3.33 liters (78% predicted) and diffusing capacity of 11.8 mL/mmHg/min (56% predicted). For ten years she had been taking prescription DPT for fibromyalgia and chronic fatigue syndrome. Examination revealed tachypnea, tachycardia, and labored breathing. B-type Natriuretic Peptide(BNP) was 508 pg/mL. Lactate was 2.6 mmol/L. Troponin-I assay was <0.02 ng/mL. TSH was consistently <0.04 uIU/mL during DPT treatment, free thyronine was currently 2.9 pg/mL, free thyroxine was 1.29 ng/dL, and antithyroglobulin and antimicrosomal antibodies were undetectable. Spiral CT revealed a segmental right lower lobe filling defect and multiple small basilar nodules [Fig 1]. Subsequent ventilation-perfusion scan demonstrated multiple bilateral moderate-sized unmatched perfusion defects. Echocardiogram showed severe right-side dilation with paradoxical septal motion and left ventricular ejection fraction of 55%. Cardiac catheterization revealed pulmonary arterial pressure of 84/28 mmHg (mean 51 mmHg). Pulmonary capillary occlusion pressure was 6 mmHg, cardiac index 1.3 L/min/m2, and pulmonary vascular resistance 1789 dynes-sec(-1)-cm(-5). Limited angiogram excluded chronic thromboembolic disease. Adenosine challenge demonstrated 15.8% reversibility in Total Pulmonary Resistance. Prior surgical lung biopsy was then reviewed, and it revealed stellate fibrosis and arteriolar thrombosis with recanalization. Eosinsophilic tissue infiltration was not evident, and S-100 stain was negative [Fig 2].

DISCUSSIONS:  Prior reports suggest that Grave’s thyrotoxicosis is associated with isolated pulmonary hypertension (234). It has been hypothesized that antithyroglobulin is a marker of generalized immune activation leading to both pulmonary hypertension and the hyperthyroid state (5,6). Our patient tested negative for antithyrotropin. Therefore if her pulmonary hypertension was due to hyperthyroidism, it cannot be due to the proposed antibody-mediated mechanism. Our patient had some features consistent with pulmonary Langerhans Cell Histiocytosis (LCH), such as nodules on CT and histiologic findings of stellate fibrosis. Pulmonary hypertension has been described in a series of patients with pulmonary Langerhans Cell Histiocytosis (LCH) (7). Our patient’s presentation was not fully consistent with LCH, because the nodules were predominantly basilar and S-100 staining of her biopsy was negative. Her disease may represent a yet unreported variant of LCH with manifestations of pulmonary hypertension and stellate fibrosis.

CONCLUSION:  Abuse of DPT may induce pulmonary hypertension and/or interstitial lung disease. Caution should be used when prescribing this treatment for euthyroid patients with disorders such as fibromyalgia.

DISCLOSURE:  M.J. Emerick, None.

Monday, October 25, 2004

4:15 PM - 5:45 PM

References

Cooper DS. Combined T4 and T3 Therapy—Back to the Drawing Board.JAMA.2003Dec 10;290(22):3002–3004.
 
Marvisi M, et al. Hyperthyroidism and pulmonary hypertension.Respir Med.2002Apr;96(4):215–20.
 
Virani SS, et al.Graves’ disease and pulmonary hypertension: report of 2 cases.Tex Heart Inst J.2003;30(4):314–5.
 
Nakchbandi IA, et al. Pulmonary hypertension caused by Graves’ thyrotoxicosisChest.1999Nov;116(5):1483–5.
 
Yanai-Landau H, et al. Autoimmune aspects of primary pulmonary hypertension.Pathobiology.1995(63);71–75.
 
Chu JW, et al.High prevalence of autoimmune thyroid disease in pulmonary arterial hypertension.Chest.2002Nov;122(5):1668–73.
 
Fartoukh M, et al. Severe pulmonary hypertension in histiocytosis X.Am J Respir Crit Care Med.2000Jan;16(1):216–23.
 

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Tables

References

Cooper DS. Combined T4 and T3 Therapy—Back to the Drawing Board.JAMA.2003Dec 10;290(22):3002–3004.
 
Marvisi M, et al. Hyperthyroidism and pulmonary hypertension.Respir Med.2002Apr;96(4):215–20.
 
Virani SS, et al.Graves’ disease and pulmonary hypertension: report of 2 cases.Tex Heart Inst J.2003;30(4):314–5.
 
Nakchbandi IA, et al. Pulmonary hypertension caused by Graves’ thyrotoxicosisChest.1999Nov;116(5):1483–5.
 
Yanai-Landau H, et al. Autoimmune aspects of primary pulmonary hypertension.Pathobiology.1995(63);71–75.
 
Chu JW, et al.High prevalence of autoimmune thyroid disease in pulmonary arterial hypertension.Chest.2002Nov;122(5):1668–73.
 
Fartoukh M, et al. Severe pulmonary hypertension in histiocytosis X.Am J Respir Crit Care Med.2000Jan;16(1):216–23.
 
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