Hypothyroidism and Primary Pulmonary Hypertension: An Autoimmune Pathogenetic Link?

  1. David B. Badesch, MD;
  2. Kristine M. Wynne, RN, BSN;
  3. Scott Bonvallet, MD;
  4. Norbert F. Voelkel, MD;
  5. Chester Ridgway, MD; and
  6. Bertron M. Groves, MD
  1. University of Colorado Health Sciences Center, Denver, Colorado. Requests for Reprints: David B. Badesch, MD, Division of Pulmonary Sciences and Critical Care Medicine, Box B-133, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262. Acknowledgments: The authors thank Rubin Tudor, MD for help with interpreting the pathologic findings and John T. Reeves, MD for help with the manuscript. Grant Support: By PHS research grant M501RR00051. Dr. Badesch is supported by a Pfizer Scholar's Award in Cardiovascular Medicine, NIH Clinical Investigator Award HL 02408-04, and the American Heart Association of Colorado. Drs. Badesch and Groves are supported by the Burroughs Wellcome Company for the prostacyclin study. Dr. Voelkel is supported by NIH HL 43180-01A3. Dr. Ridgeway is supported by NIH DK 36843, NIH CA 47411, NIH CA 46934, and NIH RR 00051.

    Abstract

    Primary pulmonary hypertension (PPH), an often fatal disease of unknown cause that primarily affects young women, is a diagnosis of exclusion. The relative roles of genetic predisposition, autoimmunity, viral infection, hormonal influences, and environmental and drug exposures are not known. Among seven patients enrolled by our center in a multicenter trial of continuous prostacyclin in severe PPH, four of the five women had hypothyroidism. Although a causal relationship cannot be established based on this small case series, the possibility of an autoimmune pathogenetic link between PPH and hypothyroidism should be investigated further.

    « Previous | Next Article »Table of Contents