Short stature due to a partial idiopathic deficiency of the growth hormone. The role of the TW2 method in assessing treatment with r-hGH

The purposes of this study were: (1) to determine whether peripheral arterial occlusive disease (PAOD) patients who smoked had more severe claudication pain, reduced peripheral circulation, and poorer cardiopulmonary measurements at peak exercise than non-smoking patients, and (2) to determine whether the differences between the smoking and non-smoking patients persisted after controlling for the resting ankle/brachial systolic pressure index (ABI). Thirty-eight PAOD patients (ABI = 0.59 +/- 0.15, mean +/- SD) who smoked an average of 1.5 packs of cigarettes per day over 42 years and 100 PAOD patients (ABI = 0.74 +/- 26) who had quit smoking for an average of 7 years were recruited. Smokers refrained from smoking on the day of testing. Claudication pain times, oxygen uptake, ventilation, leg oximetry, and ankle systolic pressure responses to peak exercise were recorded. The smoking group had more severe claudication pain, as maximal pain occurred 1:37 min:s sooner during exercise (p < 0.05), and the pain took 2:21 min:s longer to subside (p < 0.01) compared to the non-smoking group. Additionally, at peak exercise the smoking group had a lower oxygen uptake (12.8 +/- 2.6 vs 13.9 +/- 2.4 ml/kg/min, p < 0.01), a higher ventilation (31.7 +/- 9.2 vs 27.9 +/- 7.1 liters/min, p < 0.05), and a higher oximeter electrode power (409 +/- 55 vs 385 +/- 37 mW, p < 0.01) than the non-smoking group. Differences between the groups persisted (p < 0.05) after adjusting for resting ABI. It is concluded that cigarette smokers with PAOD had more severe claudication pain, reduced peripheral circulation, and poorer cardiopulmonary measurements at peak exercise than non-smoking patients. These differences were independent of resting ABI. Thus, cigarette smoking reduces the exercise capacity of claudicants, placing patients who smoke at an even greater risk of living a functionally dependent lifestyle.