ABSTRACT
Herein we respond to the controversial United States Food and Drug Administration (FDA) recommendation to perform thyroid function testing in children up to 3 years of age within 3 weeks of exposure to iodinated contrast media (ICM). Considering the many effects of thyroid hormone on the cardiovascular system, the increased risk of thyroid disease in patients with congenital heart disease, the hemodynamic consequences of the Fontan circulation on the thyroid gland, and the potential clinical significance of subclinical hypothyroidism, we share our perspective that the cardiovascular effects of thyroid hormone may carry more influence for patients with single ventricle heart disease. In our opinion, the FDA statement prompts us to consider routine thyroid hormone surveillance testing in the long-term management of patients with single ventricle heart disease.
Subject(s)
Heart Defects, Congenital , Hypothyroidism , Univentricular Heart , United States/epidemiology , Child , Humans , Infant, Newborn , Hypothyroidism/epidemiology , Thyroid Hormones , Thyroid Function Tests , Heart Defects, Congenital/surgeryABSTRACT
Subcutaneous phycomycosis becomes a chronic, debilitating condition if left untreated. Treatment includes oral antifungal therapy, though oral potassium iodide has been used in resource-limited settings. Lugol's iodine has been an effective substitute, but little is known about its safety. We report a case of subcutaneous phycomycosis complicated by heart failure during treatment with Lugol's iodine. We review subcutaneous phycomycosis, iodine-mediated cardiotoxicity, as well as social determinants of health relevant to our case, suggesting that Lugol's iodine may only be an effective treatment with proper dosing and long-term monitoring.
ABSTRACT
Misregulation of transcription elongation is proposed to underlie the pathobiology of MLL leukemia. AF4, AF9, and ENL, common MLL fusion partners, are found in complex with positive transcription elongation factor b (P-TEFb). AF9 and its homolog ENL directly interact with AF4 within these complexes. Previously, we designed a peptide that mimics the AF9 binding domain of AF4 and reported that MLL leukemia cell lines are inhibited by it. Extending these studies, we have modified the peptide design in order to avoid recognition by proteases. The peptide is as effective as its predecessor in vitro and enhances survival in mice bearing MLL leukemia cell lines.
