International Journal of Inflammation, Cancer and Integrative Therapy
Open Access

Although statins are a potent and often used class of cholesterollowering drugs, it is yet unknown how they can affect cancer risk. Statins work by inhibiting HMG-CoA reductase, which stops HMG-Coo from being converted to mevalonate and lowers levels of mevalonate and its byproducts [1]. Numerous of these products are essential for vital cellular activities, and statins' disruption of these processes in cancerous cells may prevent tumour start, development, and metastasis [1]. According to recent findings, people using statins to control their cholesterol have a lower incidence of cancer and that statins cause cell death in certain epithelial malignancies. This has been seen in a number of organs, including the breast, colon, lungs, and liver [1].

The risk of female reproductive organ cancer has been examined in seven observational studies to far. In their biggest cohort analysis, Yu et al. assessed 550 instances of gynecologic cancer and discovered that Statin users had a clinically meaningful, but not statistically significant, lower risk of endometrial cancer than non-users [2]. Results from a case control study of newly discovered gynecologic cancers were published. In 430 individuals, they discovered a substantial inverse relationship between the duration of statin usage and the risk of endometrial cancer as well as a considerably increased survival rate when statins were started just after the diagnosis [3].

Statins may reduce the chance of developing gynecologic malignancies and may have an impact on survival, even if their utility in the chemoprevention of gynecologic malignancy has not been shown [3]. Bisphosphonates [4], anti-hyperglycemic drugs [5], and antiinflammatory drugs [6] have all been shown to enhance outcomes andact as chemo-preventative agents in a variety of tumour locations [7,8]. All studies conducted to date have all participants with a diagnosis of gynecologic cancer without comparing clinico-pathologic variables that affect survival and recurrence rates. The impact of statin usage on the clinical and pathologic aspects of endometrial cancer that raise the likelihood of recurrence and necessitate adjuvant therapy has not yet been studied.

Materials and methods

Review of all patients who underwent hysterectomy for endometrial cancer at UC Davis Medical Center over a seven-year period was approved by the institutional review board. Less than two years of electronic medical data, non-endometrioid histology, or ambiguous pathology reports were disqualified from analysis. 400 FIGO Stage I EC were found after the identification of 764 patients and the evaluation of pathology data. Any high intermediate risk characteristic, such as Grade 2 or 3 histology, higher than 50% myoinvasion, or lymph vascular space invasion, was used to identify cases.

Results

We found 400 individuals with FIGO Stage I illness out of the 764 endometrial cancer patients who had hysterectomy with or without staging. Of the entire cohort, 114 (28.5%) were taking a statin at the time of diagnosis, and 75 (18.8%) had at least one high intermediate risk characteristic. Thirty-one percent of our patients had a BMI above 30, 74 percent were under 70, 21 percent had been diagnosed with diabetes, and 36 percent had been diagnosed with hypertension. Even after adjusting for patient age, parity, diabetes, obesity, hypertension, metformin usage, NSAID use, and bisphosphonate use, statin use at the time of hysterectomy was related with higher high risk characteristics (OR 2.4, 95 percent CI 1.3-4.3). Metformin usage was linked to more HIR characteristics, although the association was not statistically significant (OR 1.6, 95 percent CI 0.7-3.5). A protective impact against high-risk characteristics was suggested by concurrent NSAID and bisphosphonate use, however this was not significant. For both groups, the average follow-up period was 35 months. In the Statin users, the rate of patients who recurred was non-significantly higher (10.5 percent (12/114) vs 6.3 percent (18/286) in the non-users. (p=0.15) Statin users had a mean months to recurrence of 20.8 months compared to 28.1 months for non-users (p=0.26).

Discussion

In our single institution retrospective case-control analysis, statin usage more than doubled the chance of FIGO stage I endometrioid endometrial cancer patients having high-risk characteristics at the time of hysterectomy. Additionally, statin users had an increased recurrence rate, which is consistent with a patient group at higher risk. We could have discovered a group of patients who are more likely to have a poor prognosis. Finasteride reduced the incidence of prostate cancer by 25%, according to the Prostate Cancer Prevention Experiment, a randomised placebo-controlled trial [9, 10]. However, the finasteride group had a higher incidence of high-grade prostate cancer (6.5 vs. 5.1%), with a relative risk of high-grade tumour of 1.67 [95 percent CI, 1.44 to 1.93]; P=0.005 [11]. The incidence of low-grade prostate cancer in males may be decreased because to the reduction in dihydrotestosterone associated with finasteride treatment. Their findings may indicate that androgen may not be necessary for the advancement of all high-grade prostate tumours.

Acknowledgement

Not applicable.

Conflict of Interest

Author declares no conflict of interest.

1. Rothnie KJ, Müllerova H, Smeeth L, Quint JK (2018) Natural history of chronic obstructive pulmonary disease exacerbations in a general practice-based population with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 198:464-71.

Indexed at, Google Scholar, Crossref

2. Lavorini F, Magnan A, Dubus JC, Voshaar T, Corbetta L, et al. (2008) Effect of incorrect use of dry powder inhalers on management of patients with asthma and COPD. Respir Med 102:593-604.

Indexed at, Google Scholar, Crossref

3. Zaccone EJ, Undem BJ (2016) Airway vagal neuroplasticity associated with respiratory viral infections. Lung 194:9-25.

Indexed at, Google Scholar, Crossref

4. Tashkin DP, Celli B, Senn S, Burkhart D, Kesten S, et al. (2008) A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med 359:1543-54.

Indexed at, Google Scholar, Crossref

5. Vestbo J, Edwards LD, Scanlon PD, Yates JC, Agusti A, et al. (2011). Changes in forced expiratory volume in 1 second over time in COPD. N Engl J Med 365:1184-1192.

Indexed at, Google Scholar, Crossref

6. Sanchez-Salcedo P, Divo M, Casanova C, Pinto-Plata V, de-Torres JP et al. (2014) Disease progression in young patients with COPD: rethinking the Fletcher and Peto model. Eur Respir J 44:324-331.

Indexed at, Google Scholar, Crossref

7. Tantucci C, Modina D (2012) Lung function decline in COPD. Int J Chronic Obstruct Pulm Dis 7:95-99.

Indexed at, Google Scholar, Crossref

8. Oga T, Nishimura K, Tsukino M, Sato S, Hajiro T, et al. (2007) Longitudinal deteriorations in patient reported outcomes in patients with COPD. Respir Med 101:146-153.

Indexed at, Google Scholar, Crossref

9. Sethi S, Yin J, Anderson PK (2014) Lung flute improves symptoms and health status in COPD with chronic bronchitis: A 26 week randomized controlled trial. Clin Trans Med 3:1-8.

Indexed at, Google Scholar, Crossref

10. Elhawary A, Ismail NA, Esawy MM, Shabana MA (2020) Efficacy and safety of a new acoustic device, the lung flute, for sputum induction and lung physiotherapy. Egypt J Chest Dis Tuberc 69:259-65.

Google Scholar

11. Valipour A, Fernandez-Bussy S, Ing AJ, Steinfort DP, Snell G, et al. (2020) Bronchial Rheoplasty for Treatment of Chronic Bronchitis. Twelve-Month Results from a Multicenter Clinical Trial. Am J Respir Crit Care Med 202:681-689.

Indexed at, Google Scholar, Crossref