Liver cancer risk of Hormonal Contraception

Liver cell adenomas are rare benign tumors whose incidence has been increasing since 1970 ⁽⁹¹⁾.

They generally occur in otherwise healthy women over age 30, who have used hormonal contraceptives (HCs) for five years or longer ^(92,93).

In fact,evidence proved the link between the raise of incidence of hepatic adenomas and the widespread and prolonged use of the"pill" ^{(94,95, 96)}.

Not rarely benign liver tumours are incidental findings on echography. Liver cell adenomas are not premalignant and may undergo reversible change after withdrawal of causative agents,such as oral contraceptives ^{(97,98,99 )}.

However, these tumors which regress when OC use stops, can reoccur if HC use is reinstituted or if pregnancy occurs ^(94,100).
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The most extensive complication of hepatic adenoma is intratumoral or intraperitoneal hemorrhage, which occurs in 50 to 60 per cent of patients ⁽¹⁰¹⁾.

The risk of developing adenoma is increased with duration of oral contraceptive use, and in larger tumors, the hemorrhagic risk is also increased in pill users ^(93,101).

Adenoma also occurs in people with Type Ia glycogen storage disease,and is associated with insulin dependent diabetes ⁽¹⁰¹⁾.

Some authors believe that liver cell adenomas are potentially premalignant and could degenerate into hepatocellular carcinoma but there is very few well documented reports of this transformation ^{(101,102,103 )}. Although a recent report shows that 10% of hepatic adenoma progress to hepatocellular carcinoma ⁽¹⁰²⁾.
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Really, seems that the transformation might be come from areas of dysplasia in the context of liver cell adenoma. In fact, liver adenoma can regress, while dysplasia is an irreversible, premalignant change and will eventually progress to hepatocellular carcinoma ^{(104,105,106)}.

It is generally believed that focal nodular hyperplasia (FNH) having a wider age distribution, is not associated with the use of oral contraceptives ^(107,108). However, a large proportion of women with FNH (50-75%) are HC users, as previous clinical observations affirmed ⁽¹⁰⁹⁾.
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However,in long-term HC users it was emphasized the need of surveillance with ultrasonography. It is known that sex hormones and anabolic –androgenic steroids are implicated in the development and progression of hepatic adenomas.

The human liver expresses estrogen and androgen receptors and, experimentally both androgens and estrogens have been implicated in stimulating hepatocyte proliferation and may act as liver tumor inducers or promoters. In humans, receptors are present and may mediate the action of sex steroids or androgenic steroids on hepatic adenomas and adiacent liver,but in less than one third of patients. This evidence may have theraepeutic implications .