Endocrine Abstracts

Introduction: Rapid progression of atherosclerosis is classicaly described after e.g. percutaneous transluminal coronary angioplasty or it is defined as an diameter reduction of a preexisting stenosis. However, both initiation and perpetuation mechanisms are rarely descibed in patients on supraphysiological dosages of glucocorticoids (GCs).

Case report: We present male patient, 53-year old, after transsphenoidal operation of hypophysis pp. craniopharyngeoma with consequtive total hypopituitarism, when he was 41-years old (2004y.). Pronison substitution therapy started with 5 mg, but soon, because od polyarthralgia and polymyalgia, switched to antiinflammatory dosage of 20 mg. Diabetes mellitus (type 2) developed after 2 years of such a therapy (HbA1c 7.6%, FBG 5.7 and 2 h pp. 10.7 mmol/l). Inferior ST segment elevation myocardial infarction (STEMI) developed after 5 years (2009.y.), as an occlusion of the ramus intermedius artery (RIM). Drug-eluting stent (DES) was placed in the medial segment of ramus interventricularis anterior (RIA) which was with stenosis of 95%. Myocardial perfusion scintigraphy with Tc-99m sestamibi showed reversible anterolateral wall ischaemia. Because HbA1c of 10.2% evening dose od intermediate-acting insulin of 12j. was introduced as add on therapy to gluformin 2500 mg and glimepirid 2 mg. Patient stopped smoking and atorvastation of 20mg was introduced. After 3 years (2012y.) new anteroseptal STEMI developed as a consequence of RIA occlusion. DES was placed in RIM. Right coronary artery (ACD) showed new stenosis of 40%. Scintigraphy did not show viability of apex but the other parts of the left ventricle were viable. HbA1c was 9.9% with charcteristic pattern of BG: fasting 5.9 and 2 h pp. 14.4 mmol/l. We decided to return GCs on subtitution doses of 5 mg prednison and to leave only insulin sensitizing therapy. Latest HbA1c is 7.1% and BG 6.6 and 2 h pp. 8.9 mmol/l. He is in good condition. Left ventricle ejection fraction improved from 38%, after second STEMI, to 50% on latest control in 2018.y.

Conclusion: Hypercortisolism saturating 11 βHSD type 2 abolishes protective convesion of cortisol into inactive cortisone, so though through mineralocorticoid receptors perpetuating atherosclerotic process. In the presence of repetitive glucose spikes during GC therapy the molecules are expressed via protein kinase C and mitochondrial superoxide production. Any dosages of glucocorticoids in Addison’s patient which are above subtitutional should be patiently weighted between antiinflammatory effects on atherosclerosis but also possible negative promotive atherosclerotic effects.