Pancreatic cancer risk of Hormonal Contraception

Incidence rates for pancreatic cancer are consistently lower in women than in men. Previous studies suggested that reproductive factors, particularly parity, may reduce pancreatic cancer risk in women. During a study on 115,474 women (follow-up: 22 years), 243 cases of pancreatic cancer were identified.

Compared with nulliparous women, the relative risk of pancreatic cancer was 0.86 for women with 1-2 births, 0.75 for 3-4 births, and 0.58 for those with 5 or more births, after adjusting for other factors. The analysis for linear trend indicated a 10% reduction in risk for each birth.

Other reproductive factors and exogenous hormone use were not significantly, related to pancreatic cancer risk ⁽¹²¹⁾.

Compared with women who were premenopausal at baseline, postmenopausal women were at significantly increased risk of pancreatic cancer (odds ratio = 2.44). Age at first live birth, parity, age at menarche, use of oral contraceptive, and use of hormone replacement therapy (HRT) were not associated with altered pancreatic cancer risk in studies population.
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However, among parous women, later age at first full-term pregnancy ,significantly increases the risk of this cancer (adjusted OR = 4.05).

Other than the increased risk among postmenopausal women, this cohort study provides little support for associations with hormonal factors. Additional prospective data are needed.

However, growing epidemiological evidence that aspects of reproductive history and hormonal exposure are associated with risk of this disease could induce to support the hypothesis that pancreatic cancer is, at least in part, an estrogen-dependent disease ⁽¹²²⁾. Prolonged lactation and increased parity seem associated with a reduced risk for pancreatic cancer ⁽¹²³⁾.

In a parallel fashion, risk of pancreatic cancer was decreased for women with intact ovaries compared to those who had oophorectomy: hazard ratio was 0.70. These results indicate that older age at menopause are associated with reduced pancreatic cancer risk, but further research is warranted. ⁽¹²⁴⁾.

It was observed no association between any other reproductive factors examined (age at first birth, menarche, or menopause; type of menopause; diethylstilbestrol (DES) use; or duration of oral contraceptive or estrogen replacement therapy use) and pancreatic cancer mortality ⁽¹²⁵⁾. In summary, literature data support the observation that high parity is associated with lower risk of pancreatic cancer but do not show a linear trend with increasing parity.

Furthermore, we find no evidence that other reproductive factors are associated with pancreatic cancer mortality. ⁽¹²⁶⁾. It is of interest to report that clinically attainable concentrations of Medroxyprogesterone acetate can inhibit the growth of some human pancreatic carcinoma cells, in vitro, by inducing apoptosis, probably through their PR, in association with the phosphorylation of bcl-2 .