The combined oral contraceptive pill (OCP)
is one of the most widely taken medicines in the healthy
population. It is also one of the most widely researched
drugs. We are now entering an era when women are using
the OCP for a longer duration and later in life.
The pill contains oestrogen and progestin. Regarding
choice of the oestrogen, ethinyl oestradiol is almost the
automatic choice as mestranol is rarely used. The most
important established hazard of OCP use are the
cardiovascular adverse effects. These are now known to be
due to dose-related stimulation of thrombosis by
oestrogen. The previous belief throughout the 1980s was
that the androgenic metabolic effect of the progestins
was the critical factor. In search of compounds with
minimal androgenic effects the pharmaceutical industry
succeeded in launching 3 new progestins ¾ desogestrel,
gestodene and norgestimate ¾ the so called 3rd
generation progestins, which were hailed as
lipid-friendly progestogens altering the HDL / LDLratio
favourably. One must be cautions regarding the clinical
significance of subtle changes before they are
championed. The cause of increased venous and arterial
cardiovascular disease, including myocardial infraction,
in OCP users is thrombosis (oestrogen-related) and not
atherosclerosis as shown in the large US Nurses’
Study. Past use of OCP does not increase heart attacks,
as would have been the case had atherosclerosis been the
reason.
The dose of oestrogen in OCP is therefore critical.
Ethinyl oestradiol 20 - 35 m g should be the universal
dose. If we lower the dose below 20 m g, there might be
breakthrough bleeding and possible loss of efficacy as
well. No 20 m g pills are however available in India and
this dose should certainly suit elderly women.
Regarding choice of the progestin, the oral progestin
potency is no longer a consideration in prescribing
because potency of the various progestins has been
accounted for by appropriate dose adjustment. Much has
been written in the past about matching pills to
particular hormonal profiles. Today we do not have
strongly progestogenic or oestrogenic pills.
The 3rd generation progestins have recently been
incriminated in the increased (twice that of users of
older progestins) risk of venous thromboembolism. The
Lancet published 3 articles in December, 1995 and the
British Medical Journal published another in January,
1996 confirming the risk. Germany, Norway and the United
Kingdom, are the only three countries where desogestrel
or gestodene containing OCPs are regarded as second
choice pills. The findings of the 4 studies were however
criticised for their design, biased prescription and
confounding factors. None of these studies were
prospective or randomised. Other European countries and
US Food and Drug Administration (FDA) have not affirmed
these findings. While the controversy rages on, the
progestins should be used in lowest effective doses. Thus
the pill should contain no more than 1mg norethisterone
or 150 m g of levonorgestrel or desogestrel.
While the principal mechanism of action of the combined
pill is undoubtedly suppression of ovulation, the concept
of pill free interval (PFI) must be clearly
understood. The 7 day PFI (at the end of 21 days of pill
taking) in some women is enough to start folliculogenesis
and 25% of women will have follicles 10 mm in diameter.
Beyond 7 days the follicles are further developed and
ready to take off and ovulate. Restarting the pill may
not inhibit ovulation if started late.
To start OCP, the first pill should be taken no later
that the third day of the next cycle. If it is started on
the 5th day (as some manufacturer’s literature
suggests) some other mode of protection, such as condom,
should be used for the first 7 days. It is important that
the start of the next packet never be delayed beyond 7
days and it should never be restarted from the 5th day of
the withdrawal bleeding.
The pill can be started immediately after an abortion
(spontaneous or induced) in either the first or the
second trimestar and it should be started within first 7
days post-abortion for assured protection. Following a
delivery, a women can begin OCP use after the second or
third post-partum week if she is not breast feeding. The
pill however should not be used by nursing mothers as it
has a detrimental effect on breast milk volume and
composition which may adversely affect the infant’s
health and growth.
The most critical time for loss of protection is when a
pill is omitted at the beginning or end of a cycle
because this tends to increase the PFI. The management of
the missed pill is shown in the following flow chart
based on the British National Formulary recommendations.
As per World Health Organization (WHO) recommendations of
1997, back-up is needed only if 2 or more pills are
missed. If the woman has diarrhoea or vomiting (within 1
hour after taking the tablet) back-up may be advisable.
If vomiting is severe or diarrhoea persists for more than
24 hours (then 2 pills have been missed), a back-up
method will be needed.
Is a ‘rest period’ advisable for women on OCP
after some length of time? There is a popular
misconception that stopping the pill occasionally will
reverse the metabolic side effects. This is not the case
¾ the only result may be an unwanted pregnancy. The
other myths that need to be dispelled include:
All women should
discontinue the pill at 35 years. Selected
healthy non-smoking women without risk factors
can be prescribed low dose pills upto the age of
50 years provided they are carefully monitored.
Pills can be taken
for 5 - 8 years at most. As indicated above, low
risk women can use the pill till menopause
provided they are monitored.
Pills stunt growth in
adolescents. OCPs can be used at any age at which
the woman wants contraception. There is no lower
age limit and evidence does not support a role in
epiphyseal closure. Moreover they do not
compromise future fertility.
The typical failure
rate of the pill is 0.2%. The typical user
failure rate is 3% or more.
The list of
contraindications include asthma, peptic ulcer,
varicose veins, benign breast disease(e.g.
fibroademona), gestational diabetes, fibroid,
thyroid disease. These are no longer considered
contraindications.
Doctors alone can
prescribe the pill. As per WHO guidelines trained
providers other than doctors, including community
based distribution (CBD) workers, can initiate
and re-supply OCPs both in clinical and
non-clinical situations. The CBD workers should
use screening checklists to identify conditions
for which the woman can receive a limited supply
of OCPs or be referred to a clinic. Non-clinical
distribution is safe with sincere counselling.
Routine per-vaginal
(PV) and breast examination is a must in all
before starting OCPs. The PV examination can wait
if the menstrual history is all right. The breast
examination is mandatory only if the woman is
over 35 years age.
Routine Papanicoloau
(PAP) smears are essential before starting the
pill. No client should be denied the OCP if she
has not had a PAP smear done. However the
national policy on PAP smear screening should be
advised.
Test serum
cholesterol, glucose and liver function before
prescribing pills. These are not materially
related to either good routine preventive health
care or to the safe and effective use of the OCP.
Every balance sheet has a
debit column. The risks of the pill have been
overemphasised and the non-contraceptive benefits have
been down-played. But these considerably add to the value
of the pill. The non-contraceptive benefits include
prevention of ectopic pregnancies, endometrial carcinoma,
ovarian cancer, pelvic inflammatory disease, benign
breast disease, iron deficiency anaemia, functional
ovarian cysts. The pill also helps to improve
dysmenorrhoea, hirsutism, rheumatoid arthritis. To put
the risks of the OCP into proper perspective, I furnish a
list of ordinary life activities & events and the
odds of death from them in a year.
Activity/ Event
Annual risk of
death
Automobile
driving
1 in 6,000
Run over accident
1 in 17,000
Playing football
1 in 25,000
Home accident
1 in 33,000
OCP use in
non-smoker
1 in 63,000
Having a baby in
developing countires
1 in 200
References
Population Reports
1996; 24 (2): 2-6.
Hatcher RA, Rinehart
W, Blackburn R, Geller JS. The Essentials of
Contraceptive Technology. Baltimore: Population
Information Program - Center for Communication
Programs (The Johns Hopkins School of Public
Health), 1997.
Loudon N, Glasier A,
Gebbi A, eds. Handbook of Family Planning &
Reproductive Health Care. 3rd ed. London:
Churchill Livingstone, 1995.
Speroff L, Darney P.
A Clinical Guide for Contraception. 2nd ed.
Baltimore: Williams & Wilkins, 1996.
Poulter NR, Chang CL,
Farley TMM, Meirik O, Marmot MG. Venous
thromboembolic disease and combined oral
contraceptives: results of an international
multicentric case control study (WHO
collaborative study of cardiovascular disease and
steroid hormone contraception. Lancet 1995; 346:
1575-82.
Farley TMM, Meirik O,
Chang CL, Marmot MG, Poulter NR. Effect of
different progestogens in low oestrogen oral
contraceptives on venous thromboembolism. Lancet
1995; 346: 1582-8.
Jick H, Jick SS,
Gurewich V, Myers MW, Vasilakis C. Risk of
idiopathic cardiovascular death and non-fatal
venous thromboembolism in women using oral
contraceptives with differing progestogen
components. Lancet 1995; 346: 1589-93.
Spitzer WO, Lewis MA,
Heinmann LAJ, Thorogood M, MacRae KD.
Transnational research group on oral
contraceptives and the health of young women -
Third generation oral contraceptives and risk of
venous thromboembolic disorders: an international
case-control study. British Medical Journal 1996;
312: 83-8.
Combined oral
contraceptives. British National Formulary 1997;
(34 - Sep, 1997): 345-50.
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