A high intake of licorice can cause hypermineralocorticoidism with sodium retention and potassium loss, edema, increased blood pressure and depression of renin-angiotensin-aldosterone system. Glycyrrhizic acid, a component of licorice, produces hypermineralocorticoidism through the inhibition of 11beta-hydroxysteroid dehydrogenase. We report a 55-year-old woman with severe muscle weakness with hypokalemia(Serum K+ : 1.7 mEq/ L) due to raw licorice tea. She boiled the licorice 50 g in water and drunk intermittently for 4 months due to her foreign body sensation on her throat. In Korea there is a traditional recipe that licorice works out for the above symptom. Her serum renin activity and aldosterone level were far beyond normal range which was typical to licorice ingestion. She also had metabolic alkalosis with pH 7.55 and hypertension. After quitting the licorice, hypokalemia and muscle weakness gradually improved and her blood pressure returned to normal.
11-beta-Hydroxysteroid Dehydrogenases ; Aldosterone ; Alkalosis ; Blood Pressure ; Depression ; Eating ; Edema ; Female ; Foreign Bodies ; Glycyrrhiza* ; Glycyrrhizic Acid ; Humans ; Hydrogen-Ion Concentration ; Hypertension ; Hypokalemia* ; Korea ; Middle Aged ; Muscle Weakness ; Pharynx ; Potassium ; Reference Values ; Renin ; Renin-Angiotensin System ; Sensation ; Sodium ; Tea ; Water

The maintenance of peripheral immune tolerance and prevention of chronic inflammation and autoimmune disease require CD4+CD25+ T cells (regulatory T cells). The transcription factor Foxp3 is essential for the development of functional, regulatory T cells, which plays a prominent role in self-tolerance. Retroviral vectors can confer high level of gene transfer and transgene expression in a variety of cell types. Here we observed that following retroviral vector-mediated gene transfer of Foxp3, transductional Foxp3 expression was increased in the liver, lung, brain, heart, muscle, spinal cord, kidney and spleen. One day after vector administration, high levels of transgene and gene expression were observed in liver and lung. At 2 days after injection, transductional Foxp3 expression level was increased in brain, heart, muscle and spinal cord, but kidney and spleen exhibited a consistent low level. This finding was inconsistent with the increase in both CD4+CD25+ T cell and CD4+Foxp3+ T cell frequencies observed in peripheral immune cells by fluorescence-activated cell-sorting (FACS) analysis. Retroviral vector-mediated gene transfer of Foxp3 did not lead to increased numbers of CD4+CD25+ T cell and CD4+Foxp3+ T cell. These results demonstrate the level and duration of transductional Foxp3 gene expression in various tissues. A better understanding of Foxp3 regulation can be useful in dissecting the cause of regulatory T cells dysfunction in several autoimmune diseases and raise the possibility of enhancing suppressive functions of regulatory T cells for therapeutic purposes.
Animals ; Autoimmune Diseases ; Brain ; Gene Expression ; Heart ; Immune Tolerance ; Inflammation ; Kidney ; Liver ; Lung ; Mice ; Muscles ; Spinal Cord ; Spleen ; T-Lymphocytes ; T-Lymphocytes, Regulatory ; Transcription Factors ; Transgenes ; Zidovudine