Oral contraceptives carcinogenicity

For the sake of simplicity the carcinogenic effects of estrogens in all formulations, including the combined oral contraceptives, are included here. 

In a review of the earliest studies of hepatocellular carcinoma, it was concluded that oral contraceptives may not interact with other hepatic carcinogens, and that if they do not interact they may not measurably enhance the risk of liver cancer in parts of the world where hepatitis B virus is endemic and hepatocellular carcinoma is common (86). Others have since suggested a positive association between parity or gravidity and hepatocellular carcinoma, which needs to be further explored (87). 

The carcinogenic effects of oral contraceptives are covered in the monograph on estrogens. 

Carcinogenicity Oral contraceptives have been shown to decrease the incidence of endometrial and ovarian cancer. Their ability to induce other neoplasms is controversial. The production of benign tumors of the liver that may rupture and hemorrhage is rare. 

SAFETY PROFILE Suspected human carcinogen producing Mver tumors. An experimental teratogen. Human systemic effects by ingestion dyspnea, nausea or vomiting, and fever. Experimental reproductive effects. Used as an oral contraceptive. When heated to decomposition it emits acrid smoke and irritating fumes. 

Public concern has focused on the possible carcinogenic effects of drugs and other chemicals. Long-term chronic toxicity studies in a variety of species have been started in the hope of minimizing potential risk of cancer in man. However, the results of such studies are difficult, sometimes impossible, to interpret. Yet their economic impact can be enormous, as shown by the withdrawal of cyclamates when bladder cancer was observed in a limited number of rodents. Inevitably drugs will be affected too already the safety of certain oral contraceptives has been questioned because of possible carcinogenic effects in the breasts of dogs after extended use. 

Subsequently, studies with microsomes, antibodies, and purified P450 3A4 quickly indicated that nifedipine was not the only substrate other substrates included other dihydropyridines , steroids quinidine , the oral contraceptive 17a-ethynylestradiol , and the carcinogen afla-toxin B, (ref [714]). With more studies and the application of recombinant systems, the repertoire of substrates expanded rapidly . 

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