Research Round Up
Connie M. Rhee, MD |
Dangerous Dye?
Exposure to iodinated contrast media (ICM) during imaging procedures (e.g., CT scan) is associated with changes in thyroid function, and increased risk of developing hyperthyroidism, according to a study by Connie M. Rhee, MD, and Steven Brunelli, MD, both of the BWH Renal Division.
Steven Brunelli, MD |
The researchers examined data from patients treated between January 1990 and June 2010 who did not have pre-existing hyperthyroidism or hypothyroidism. Patients were matched with euthyroid (normal thyroid function) controls, and exposure to iodinated contrast media was assessed using claims data. A total of 178 patients with incident hyperthyroidism and 213 patients with incident hypothyroidism were matched to 655 and 779 euthyroid persons, respectively.
The researchers found that iodinated contrast media exposure was associated with incident hyperthyroidism, but no statistically significant association was found with incident hypothyroidism. The researchers note that further studies are needed to evaluate these findings, to establish causality and to explore mechanisms.
The study was published in the January 23, 2012 issue of Archives of Internal Medicine.
Thomas Kupper, MD |
Mystery Solved: Campath and CTCL
Conventional wisdom may lead one to think that patients with leukemic cutaneous T-cell lymphoma (L-CTCL) treated with alemtuzumab (Campath) would be prone to infections because the drug is thought to kill all lymphocytes (T-cells and B-cells) in the body. Instead, patients experience remissions without increased infections.
A study by Rachael A. Clark, MD, PhD, BWH assistant professor of dermatology and associate dermatologist, and Thomas S. Kupper, MD, BWH Department of Dermatology chairman, explains why.
Rachael Clark, MD, PhD |
Researchers found alemtuzumab only kills T-cells in the bloodstream, but not in tissues such as the skin. Malignant T-cells that recirculate between the blood and skin were depleted by the drug, but normal skin resident T-cells were spared. This work demonstrated that skin, and likely other tissues such as the gastrointestinal tract and lungs, contain non-recirculating tissue resident T-cells that are highly protective. In a companion piece, Mark Davis, PhD, of Stanford University School of Medicine, called the work a "translational tour de force."
The study was electronically published on January 18, 2012, in Science Translational Medicine.
Paul de Bakker, PhD |
Rheumatoid Arthritis: It's All in the Genes
In a collaborative effort, Soumya Raychaudhuri, MD, PhD, and Paul de Bakker, PhD, both assistant professors of medicine at BWH, and other colleagues have pinpointed the specific positions within HLA genes responsible for the association between the major histocompatibility complex (MHC) genomic region and rheumatoid arthritis. The HLA genes code for immune receptors that recognize antigens on immune cell surfaces, and play a critical role in transplantation, infections and autoimmune diseases.
Soumya Raychaudhuri, MD, PhD |
Researchers looked at the genomic data of 5,018 people with rheumatoid arthritis and 14,974 people without disease. They saw that variation in amino acid residues at positions located within the peptide-binding grooves encoding the HLA-DRb1, HLA-B and HLA-DPb1 protein molecules are responsible for the genetic risk of rheumatoid arthritis attributed to the MHC region. The researchers believe that the study results can help guide the scientific community's understanding of how HLA genes can influence a person's susceptibility to diseases.
The study was published in the January 29, 2012 online issue of Nature Genetics.
Largest Gene Linked to Weak Hearts
Christine Seidman, MD |
Mutations that truncate TTN-the largest gene in the human genome-is the most common cause for unexplained dilated cardiomyopathy (DCM), a common cause for heart failure, according to a collaborative study that included Christine Seidman, MD, BWH Cardiovascular Genetics Center director, and a team of dedicated scientists at Harvard Medical School; Imperial College, London; University of Colorado; and physicians at BWH.
Titin proteins function as a scaffold during the assembly of contractile proteins in muscle cells and also regulate force production. Researchers identified mutations in the TTN gene that occurred in 25 percent of patients with familial DCM and 18 percent of patients with sporadic DCM. The study also found that cardiac outcomes were similar regardless of whether or not a person has TTN gene mutations. However, among those with TTN gene mutations, adverse events such as cardiac transplantation, implantation of a ventricular assist device, or death occurred earlier in men than women.
The study was published in the February 16, 2012, issue of The New England Journal of Medicine.