adrenal crisis is a life - threatening emergency , however , the relation between adrenal crisis and life - threatening arrhythmia is not known . a 63-year - old woman was re - admitted to our hospital because of fever , diarrhea and disturbance of consciousness with polymorphic vt . she had been first admitted to our hospital five years ago because of polymorphic vt ( fig .  1 ) . serum concentrations of cortisol , luteinizing hormone , follicle stimulating hormone , and prolactin had been very low with relatively low concentrations of corticotropin , while those of thyroid hormone and serum electrolytes levels had been almost normal . she had had a history of large bleeding by extrauterine pregnancy and her brain mri had shown atrophy of pituitary , suggesting that her hypopituitarism was due to sheehan s syndrome . on admission of this time , she had fever ( 38.0   ) with slightly lower blood pressure ( 92/60  mmhg ) . her ecg showed prolongation of the qt interval ( qtc 567  ms ) ( fig . 2a ) and ecg monitor recorded various arrhythmias such as sinus bradycardia , atrial flutter , paroxysmal atrial fibrillation , and polymorphic vt . routine blood examination revealed normal levels of sodium ( 137  meq / l ) , potassium ( 3.8  meq / l ) , and calcium ( 9.9  mg / dl ) , and slightly high levels of magnesium ( 2.75  mg / dl ) . c - reactive protein and white blood cell counts were elevated 6.9  mg / dl and 11    10l , respectively . ultrasound echocardiography ( ucg ) showed normal cardiac size and function of the left ventricle . we intravenously administered hydrocortisone with large volume of physiological saline and started rapid ventricular pacing at the rate of 120  bpm . in the second day of the treatments , arrhythmias were not observed and the qt interval was normalized ( qtc 394  ms ) ( fig . 1polymorphic ventricular tachycardia recorded in 2009 . a short  long  short pattern of r qtc was measured at lead v5 polymorphic ventricular tachycardia recorded in 2009 . a short  long  short pattern of r qtc was measured at lead v5 although she has been treated with hydrocortisone for secondary adrenal insufficiency due to hypopituitarism , adrenal crisis might be induced by infection of influenza . when she arrived at our hospital , the qt interval was remarkably prolonged , however , it became normal within 12  h with replacement of glucocorticoids . it is well known that hypothyroidism causes qt prolongation , but her serum concentrations of thyroid hormone had been almost normal from the first visit . on the other hand , her serum concentration of cortisol was very low ( 0.4  g / dl ) just before hospitalization and replacement of glucocorticoids promptly normalized the qt interval , suggesting that prolongation of the qt interval is due to lack of glucocorticoid hormone . there have been several reports showing the cases of prolonged qt interval with adrenal insufficiency . previous reports described cases of torsade de pointes associated with hypopituitarism which were treated with steroid and thyroid hormone [ 68 ] . other reports described cases of torsade de pointes associated with hypopituitarism and electrolytes imbalance [ 7 , 8 ] . a case of adrenal insufficiency with severe hypokinesis of left ventricle and t wave inversion at ecg there are few reports of isolated adrenocorticotropic hormone deficiency without any electrolytes imbalance that showed polymorphic vt associated with qt prolongation . in our case , the abnormality was only concentrations of cortisol and there were no electrolytes imbalance , hypothyroidism , or hypokinesis of the left ventricle . although precise mechanisms of qt prolongation by glucocorticoid insufficiency are not known , there are some possibilities . glucocorticoid has been reported to be important for the maintenance of membrane calcium transport function in the cardiac sarcoplasmic reticulum . it has been also reported that glucocorticoid up - regulates expression levels of various ion channels , including iks ( mink , kvlqt1 ) , and ikr ( herg , mirp1 ) by inducing expressions of the serum- and glucocorticoid - inducible kinase ( sgk1 ) . since these ik channels induce outward potassium currents , lack of glucocorticoid may extend duration of action potentials by reducing expressions of sgk1 and these ion channels . in fact , there is a report showing that mutations in the herg gene cause congenital long - qt syndrome . long - qt syndrome causes life - threatening ventricular arrhythmias such as torsades de pointes . since lack of glucocorticoid hormone might induce prolongation of the qt interval , patients with adrenal insufficiency should be paid attention as candidates of lethal arrhythmias particularly when exposed to excessive stresses . this study has been performed in accordance with the ethical standards laid down in the 1964 declaration of helsinki and its later amendments .
a 63-year - old woman who had hypopituitarism was re - admitted to our hospital because of fever , diarrhea and disturbance of consciousness with life - threatening arrhythmia due to prolongation of the qt interval . 
 she has been treated with hydrocortisone consequently , and has shown few ventricular arrhythmias with normalization of the qt interval . 
 there have been several reports showing the case of prolonged qt interval with adrenal insufficiency , but there are few reports of isolated adrenocorticotropic hormone deficiency without any electrolytes imbalance that showed polymorphic ventricular tachycardia associated with qt prolongation . 
 we discuss some possible mechanisms of how adrenal insufficiency causes life - threatening arrhythmia . 
 since lack of glucocorticoid hormone might induce prolongation of the qt interval , patients with adrenal insufficiency should be paid attention as candidates of lethal arrhythmias particularly when exposed to excessive stresses .