J. C. Caillouette, C. F. Sharp, Grenith J. Zimmerman
et al.
OBJECTIVE Our purpose was to confirm the elevation of vaginal pH expected in patients with bacterial pathogens in premenopausal women and to examine the relationship of serum follicle-stimulating hormone and estradiol levels to vaginal pH in menopausal patients without and with hormone replacement therapy. STUDY DESIGN Vaginal pH was determined by phenaphthazine (Nitrazine) pH paper in 253 patients seen in a solo private practice for routine speculum examination. None of the patients were pregnant. Measurements were made of serum levels of follicle-stimulating hormone and estradiol for 172 patients and vaginal cultures were taken from 82 patients. Vaginal pH was correlated with vaginal cultures and serum follicle-stimulating hormone and estradiol levels by use of statistical analysis. RESULTS Vaginal pH was elevated in all premenopausal patients with documented bacterial pathogens. Serum estradiol levels showed an inverse and serum follicle-stimulating hormone levels a direct statistical correlation with vaginal pH in menopausal patients. CONCLUSIONS Measurement of vaginal pH is useful, effective, and inexpensive for screening purposes. A vaginal pH of 4.5 is consistent with a premenopausal serum estradiol level and the absence of bacterial pathogens. An elevated vaginal pH in the 5.0 to 6.5 range suggests a diagnosis of either bacterial pathogens or decreased serum estradiol. In patients with an elevated pH, vaginal culture should establish the diagnosis. In the absence of bacterial pathogens, a vaginal pH of 6.0 to 7.5 is strongly suggestive of menopause. Titration of estradiol level by vaginal pH during estrogen replacement therapy may help menopausal women avoid side effects or cessation of therapy.
The mechanism by which the intra-erythrocytic form of the human malaria parasite, Plasmodium falciparum, extrudes H+ ions and thereby regulates its cytosolic pH (pH i ), was investigated using saponin-permeabilized parasitized erythrocytes. The parasite was able both to maintain its resting pH i and to recover from an imposed intracellular acidification in the absence of extracellular Na+, thus ruling out the involvement of a Na+/H+ exchanger in both processes. Both phenomena were ATP-dependent. Amiloride and the related compound ethylisopropylamiloride caused a substantial reduction in the resting pH i of the parasite, whereas EMD 96785, a potent and allegedly selective inhibitor of Na+/H+ exchange, had relatively little effect. The resting pH i of the parasite was also reduced by the sulfhydryl reagent N-ethylmaleimide, by the carboxyl group blockerN,N′-dicyclohexylcarbodiimide, and by bafilomycin A1, a potent inhibitor of V-type H+-ATPases. Bafilomycin A1 blocked pH i recovery in parasites subjected to an intracellular acidification and reduced the rate of acidification of a weakly buffered solution by parasites under resting conditions. The data are consistent with the hypothesis that the malaria parasite, like other parasitic protozoa, has in its plasma membrane a V-type H+-ATPase, which serves as the major route for the efflux of H+ ions.