Oral steroidal contraceptives patient

Oral contraceptives have their most significant effect on endocrine parameters. Blood cortisol, thyroxine, protein-bound iodine, T3 uptake, and urinary free cortisol are elevated. Urinary 17,21-dihydroxy steroids, 17-ketosteroids, and estrogens are decreased. There is no effect on urinary catecholamines or VMA (Table 10) (LIO). The effect of thyroid functions tests is due to the administered hormone stimulating an increase in the production of thyroid-binding globulin which in turn binds 1-thyroxine. The lowering of free thyroxine stimulates the anterior pituitary to produce thyrotropin, which in turn stimulates the thyroid to produce more thyroxine. Since the additional thyroxine is bound to the extra protein, there is an equilibrium and the patient remains clinically euthyroid, but the protein-bound iodine and the thyroxine are elevated. 

A review by Rase . summarizes. studies on the effects of certain hormones on vitamin B(, nutrition in humans, on the biochemical interrelationship between steroid hormones and pyridoxal phasphate-dependent enzymes, and on the role of vitamin B(, in regulating hypothalamus-pituitary functions. Some of these studies have important clinical implications. The use of estrogen-containing oral contraceptives has been investigated as a factor leading to an abnormality of tiyptophan metaboli.sm. This abnormality resembles dietary vitamin B deficiency and responds favorably to treatment with the vitamin. For some time, there has been clinical interest in the relationship between certain hormones and vitamin B function because abnormal urinary excretion of tiyptophan metabolites was observed during pregnancy and in patients with hyperthyroidism. 

Some women may require small increases or decreases in their dosage of antidiabetic while taking oral contraceptives or HRT, but it is unusual for the control of diabetes to be seriously disturbed. Irrespective of diabetic control, HRT or oral contraceptives should be used with caution in patients with diabetes because of the increased risk of arterial disease. PiogUtazone, rosiglitazone and repaglinide do not appear to alter the pharmacokinetics of contraceptive steroids, and ethinylestradiol/levonoi estrel do not appear to have an important effect on the pharmacokinetics of repaglinide. 

Rofecoxib increases contraceptive steroid levels to a small extent, and would not therefore be expected to reduce contraceptive efficacy. Etoricoxib raises ethinylestradiol levels by 50 to 60%, and also appears to raise the levels of conjugated oestrogens in HRT. Celecoxib appears to have no effect on combined oral contraceptive levels. One case of pulmonary embolism has been reported in a patient taking valdecoxib with a combined oral contraceptive. 

Although data are limited, the minor to modest possible ineieases in frov-atriptan, naratriptan, sumatriptan and zoimitriptan pharmacokinetics described are not likely to produce clinically relevant adverse effects. Almotriptan, rizatriptan and sumatriptan do not appear to have any clinically important effect on levels of contraceptive steroids. The significance of the single case report of ischaemic colitis associated with concurrent use of naratriptan and a combined oral contraceptive is unclear. Note that ischaemic colitis has, rarely, been reported with naratriptan itself The manufacturers have found no cases of ischaemic colitis in approximately 450 women on oral contraceptives and taking naratriptan for prophylaxis for 5 to 6 days. However, caution may be needed with concurrent use in those patients with risk factors for ischaemic colitis, such as those with a history of abdominal surgery, low blood pressure, diabetes, cardiovascular disease or stroke. 

Enzyme inducers that increase the metabolism of contraceptive steroids might also be expected to reduce the efficacy of menopausal HRT. An isolated case describes reduced efficacy of oral conjugated oestrogens in a patient taking phenytoin. 

Two further cases of hepatocellular carcinoma associated with anabolic steroid therapy have been reported. One was a child with Fanconi s anaemia, who was treated with anabolic steroids for 50 months (2 ). The other also occurred in a patient with Fanconi s anaemia following 4 years medication with androgenic, anabolic steroids (3 ). Examination of the livers of 2 patients with acquired aplastic anaemia who had been treated with similar compounds for 3 months prior to death revealed generalized parenchymal hyperplasia in one and widespread nodular hyperplasia in the other. Since 1971, 10 cases of hepatocellular carcinoma during medication with anabolic steroids have been reported in the literature. The prognosis is poor with a survival time of less than a year. The similar medical history indicates but does not prove a cause-effect relationship between disease and medication. The data must, however, be viewed alongside that pointing to hepatic tumours as complications of treatment with other types of steroids, notably the oral contraceptives. 

Srivastava, M. C., Oakley, N. W., Tompkins, C. V., Sonksen, P. H. and Wynn, V. (1975) Insulin metabolism, insulin sensitivity and hormonal responses to insulin infusion in patients taking oral contraceptive steroids. Europ. J. din. Invest. (Berl.), 5, 425. 

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