Publications

OBJECTIVE

In randomized trials, the most common way to measure the effect of treatment on the frequency and severity of menopausal hot flashes is a 7-day self-reported diary. However, adherence with completing the hot flash diary in real time may be poor, and completing a diary is cumbersome for study participants. Our objective was to determine if a shorter diary for recording self-reported hot flashes is as accurate and precise as the traditional 7-day diary.

METHODS

Using cross-sectional data from a multicenter randomized clinical trial of an herbal preparation (MF101, an estrogen receptor beta-selective agonist for treatment of menopausal hot flashes), we compared findings based on shorter diaries with findings based on a 7-day diary.

RESULTS

With 3 days of diary keeping, the mean number of hot flashes per day and mean severity were almost identical to the means based on the 7-day diary, the SDs of the means were almost identical, and the intraclass correlations were almost perfect. The difference in the mean number of hot flashes per day compared with the 7-day diary was only 12% of one hot flash. Data from a different clinical trial revealed similar correspondence between the findings of a 3- and 7-day diary.

CONCLUSIONS

In our study, the optimal duration of diary keeping to record menopausal hot flashes seems to be 3 days. In addition to being as good as a 7-day diary, a 3-day diary would be less burden on study participants and research staff and less expensive.

Although Cl- transport in fetal lung is important for fluid secretion and normal lung development, the role of Cl- transport in adult lung is not well understood. In physiological studies, the cystic fibrosis transmembrane regulator (CFTR) plays a role in fluid absorption in the distal air spaces of adult lung, and alveolar type II cells cultured for 5 days have the capacity to transport Cl-. Although both alveolar type I and type II cells express CFTR, it has previously not been known whether type I cells transport Cl-. We studied Cl- uptake in isolated type I cells directly, using either radioisotopic tracers or halide-sensitive fluorescent indicators. By both methods, type I cells take up Cl-. In the presence of beta-adrenergic agonist stimulation, Cl- uptake can be inhibited by CFTR antagonists. Type I cells express both the Cl-/HCO3- anion exchanger AE2 and the voltage-gated Cl- channels CLC5 and CLC2. Inhibitors of AE2 also block Cl- uptake in type I cells. Together, these results demonstrate that type I cells are capable of Cl- uptake and suggest that the effects seen in whole lung studies establishing the importance of Cl- movement in alveolar fluid clearance may be, in part, the result of Cl- transport across type I cells.