Osteoporosis in Chronic Obstructive Pulmonary Disease / 결핵

BACKGROUND: Osteoporosis has been reported in patients with chronic obstructive pulmonary disease, but this association is not well established. This study was undertaken to determine whether the prevalence of osteoporosis was increased in patients with chronic obstructive pulmonary disease and we examined the relationship of corticosteroid administration with osteoporosis. METHOD: Subjects were 23 patients with chronic obstructive pulmonary disease and 20 control patients. We reviewed hospital records and measured bone mineral density using dual-energy x-ray absorptiometry(Lunar, USA). RESULTS: Mean bone mineral density(BMD) of spine in COPD group was 0.683+/-.154 g/cm2 and 0.971 +/-.212g/cm2 in controls(p0.05). Ten patients were received corticosteroid in COPD group. Spinal T score in steroid receiving patients were -3.82+/-.94(SD) and -2.82+/-.97(SD) in not having steroid patients(p<0.01). Cumulative dose of corticosteroid was associated with spinal T score(r=-0.424, p<0.05) and duration of corticosteroid administration also associated with spinal T-score(r=-0.457, p<0.05). Spinal BMD of patients not having corticosteroid in COPD group(n=13) were significantly lower than that of controls(0.71+/-.13 g/cm2 and 0.97+/-.21 g/cm2, p<0.01). CONCLUSION: Prevalence of osteoporosis is increased in patients with chronic obstructive pulmonary disease. Especially patients who are receiving corticosteroid have high risk of osteoporosis or osteopenia and need for preventive management.

Association of QT Dispersion with Left Ventricular Hypertrophy in Essential Hypertensives

BACKGROUND: Left ventricular hypertrophy(LVH) is a powerful indepedent risk factor of ventricular tachycardia and sudden death. Even though it is not clear the mechanism of sudden death in patients with LVH, inhomogenous ventricular repolarization is highly suggested. QT dispersion which reflecting regional inhomogeneity of repolarization is defined as interlead variation in QT intervals of 12 leads ECG. The purpose of this study was to assess whether QT dispersion is associated with LVH in hypertensive patients. METHODS: We assessed 23 untreated hypertensives with echocardiographic LVH and normal left ventricular systolic function. The criteria of 5th Joint National Committee stage I-III was used to define hypertension. Thirty four normotensives was assessed as controls. On a standard 12 lead ECG, the intervals between onset of QRS to end of T wave were measured(QT intervals) and corrected by heart rate(QTc). QT dispersion was calculated by the difference of maximal and minimal QTc. Left ventricular mass(LVM) was calculated from Devereux's formula using the parameters measured by the recommendation of American Society of Echocardiography. LVH was defined by LVM indices over 130 g/m2. RESULTS: LVM indices of hypertensive group were significantly greater than those of controls (162.2+/-39.3 g/m2 vs 84.2+/-16.1 g/m2, p<0.001). Maximal QT and QTc of hypertensive group were significantly prolonged than those of controls(maximal QT=401+/-31 ms vs 380+/-35 ms, p<0.05 ; maximal QTc=432+/-19 ms vs 414+/-17 ms, p<0.001). QT dispersions were significantly greater in hypertensive group than in controls(60.2+/-15.7 ms vs 33.2+/-11.7 ms, p<0.001). In hypertensive group, there was significant association between LVM index and QT dispersion(r=0.492, p=0.017). CONCLUSIONS: Hypertensives with LVH have a prolonged QT and QTc and increased QT dispersion in comparision with controls. QT dispersion in these patients correlates with degree of LVH.