Bacterial vaginosis is one of the major contributors of vaginal infections during pregnancy and accounts for 40% of these cases. Generally, bacterial vaginosis is associated with several obstretic complications like pre-term labor and delivery, untimely rupture of membranes, postpartum endometrisis, and chorioamnionitis (Wang et. al., 2010, p.444). Metronidazole has traditionally been used as the drug of choice in the treatment of bacterial vaginosis because it is an agent of the nitroimidazole antibiotic family. This drug has been used for several decades because it efficiency in treating the condition ranges between 80 and 90% and can be administered across all pregnancy stages while tolerated by pregnant women. The ability of the drug to achieve the high levels of efficacy is attributed to the fact that it can be found in the cord blood, fetal tissue, and amniotic fluid in high concentrations.
The authors of the article reported the findings of two early studies conducted on the administration of the drug to pregnant women diagnosed with bacterial vaginosis. One of the studies was conducted during pregnancy after a single intravenous of the drug while the other was performed after single or multiple oral doses were administered between 8 and 14 weeks of pregnancy. Both studies demonstrated that pharmacokinetic stricture of the drug in pregnant women is similar to those of healthy volunteers. The analyses also showed that after nearly 34 weeks of gestation, pregnancy-induced increases in the plasma volume that could have an impact on metronidazole distribution reach their maximum.
In light of the findings of the study, the pharmacokinetic parameters of this drug would vary during the middle and late stages of pregnancy because of the distinctive pharmacologic properties of the drug such as extremely low plasma protein binding. This is likely to occur in these stages during pregnancy as compared with the non-pregnant state due to increases in mean plasma volume by approximately the third trimester. Furthermore, plasma concentrations of this drug during early stages of pregnancy were higher as compared to during middle and late gestation periods. Following the adjustment for the weight normalized dose, the maximum plasma drug concentration at early periods of pregnancy did not vary from those identified at middle and late stages of pregnancy. Notably, the degree of drug distribution and approval was not impacted by various gestation periods when the other pharmacokinetic parameters did not vary significantly between groups.
While the study or article does not include non-pregnant controls and measures, it presents profound information regarding the pharmacokinetics of the use of the drug in pregnant women with bacterial vaginosis. Together with the reliance of antimicrobial efficacy on attainable concentrations, the use of this drug in treatment of bacterial vaginosis and related obstretic complications during pregnancy demonstrates the need for extra information on the drug’s distribution during middle and late pregnancy periods.
Prostate-specific Antigen (PSA):
There are numerous concerns on whether prostate-specific antigen (PSA) is an ideal tumor cell maker. Generally, tumor makers are substances that are created by cancer cells and/or other cells of the human body in reaction to some non-cancerous conditions or cancer (“Tumor Makers,” 2011). These substances are usually found in urine, stool, blood, tissues, or some bodily fluids of certain patients with cancer. The tumor makers are commonly used to help diagnose cancer, forecasts a patient’s reaction to some cancer therapies, examine a patient’s reaction to treatment, and determined the likelihood of the return of cancer. According to Handy (2009), tumor maker provide a simply invasive, cost-effective data source valuable for evaluating disease course, determining prognosis, and helping in treatment preparation (p.99).
On the other hand, prostate-specific antigen (PSA) is a protein brought by ordinary prostate cells and engages in the dissolution of the seminal fluid coagulum and plays a crucial role in fertility (Brosman, Kim, Goluboff & Talavera, 2012). Becker & Lilja (1997) state that prostate-specific antigen is a serine protease generally expressed in the human prostate and responsible for the proteolysis of gel-forming proteins in human semen (p.117). Prostate-specific antigen is one of various candidates used as universal tumor antigen in different tumor types. Before the identification of specific tumor antigen, these antigens were mainly derived from tumor cells as lysates or irradiated cell lines obtained from allogeneic or autologous tumors (Academic Press, 2011, p.185).
In modern oncology, prostate-specific antigen is an ideal tumor cell maker since it closely approximates the perfect tumor maker (Resnick & Thompson, 2000, p.353). The state of prostate-specific antigen as an ideal tumor cell maker is attributed to the fact that it nearly meets the criteria of the perfect tumor maker. PSA is produced exclusively by tumor cells, identifiable in any patient with the disease, and provides special information associated with staging or anatomic disease extent. The other attribute that make the antigen an ideal tumor cell maker include the fact that it permits for earlier identification of treatment failure resulting in early salvage treatment.
Prostate-specific antigen is sensitive in determining persistent or recurrent disease after treatment and has had significant effect on every aspect of prostate-cancer patient care. The efficacy of the antigen as an ideal tumor cell maker is evident in the fact that there is currently no better technique than prostate-specific antigen for evaluating prostate cancer patients after treatment. Prostate-specific antigen is the ideal tumor cell maker despite its shortcomings and is commonly used to screen for cancer in general population (“Tumor Makers,” 2013).
References:
Academic Press. (2011). Genomics in cancer drug discovery and development. San Diego, CA:
Elsevier Inc.
Becker, C. & Lilja, H. (1997, January 3). Individual Prostate-specific Antigen (PSA) Forms As
Prostate Tumor Makers. Clinica Chimica Acta, 257(1), 117-32.
Brosman, S.A., Kim, E.D., Goluboff, E.T. & Talavera, F. (2012). Prostate-specific Antigen
Testing. Retrieved February 28, 2014, from http://emedicine.medscape.com/article/457394-overview
Handy, B. (2009). The Clinical Utility of Tumor Makers. Lab Medicine, 40(2), 99-103.
Retrieved February 28, 2014, from http://labmed.ascpjournals.org/content/40/2/99.full
Resnick, M.I. & Thompson, I.M. (2000). Advanced therapy of prostate disease, volume 1.
Hamilton, Ontario: B.C. Decker Inc.
“Tumor Makers.” (2011, December 7). National Cancer Institute Fact Sheet. Retrieved from National Cancer Institute website: http://www.cancer.gov/cancertopics/factsheet/detection/tumor-markers
“Tumor Makers.” (2013, October 30). American Cancer Society. Retrieved February 28, 2014,
from http://www.cancer.org/treatment/understandingyourdiagnosis/examsandtestdescriptions/tumormarkers/tumor-markers-how-t-m-used
Wang et. al. (2010, May 27). Pharmacokinetics of Metronidazole in Pregnant Patients with Bacterial Vaginosis. The Journal of Maternal-Fetal and Neonatal Medicine, 24(3), 444-448.
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