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Methyldopa.Pdf DN Iliodromiti_Layout 1 16/04/2010 15:00 Page 1 DRUG NOTES Methyldopa S Iliodromiti*, F Mackenzie, RS Lindsay Introduction Figure 1. Mechanism of action of methyldopa Methyldopa (α-methyl-3, 4-dihydroxy- L-phenylalanine) was synthesised and α-methylnorepinephrine shown to be a potent inhibitor of renocortical DOPA decarboxylase by Sourkes in 1954. Stein et al. presented α2 receptor Pons the chemical characteristics of DBH Synapse methyldopa in 1955 and in 1960 Brainstem Sjoerdsma et al. demonstrated its antihypertensive action in humans. Medulla In the 1970s, methyldopa was consid- Methyldopa ered an effective antihypertensive agent, especially in the elderly, Spinal cord patients with renal insufficiency, and Inhibition of pregnancy. The side effect profile of adrenergic methyldopa, along with the launch of neuronal outflow newer antihypertensives, resulted in Vasodilatation Blood vessels methyldopa being removed from first line treatment in hypertension in the Methyldopa is metabolised by dopamine β hydroxylase (DBH) to its active metabolite developed countries. Despite these α-methylnorepinephrine. This acts as an agonist at the pre-synaptic α2 adrenergic changes, methyldopa remains a safe receptors in the brainstem, resulting in a reduced adrenergic neuronal outflow through alternative for treatment of hyperten- the peripheral nervous system causing vasodilation and reduced blood pressure. sion in pregnancy. It is still a first line therapy for primary hypertension in cardiac function and does not excreted by the kidneys with a half- the developing countries due to its usually reduce glomerular filtration life for the drug of two hours. low cost. rate, renal blood flow or filtration Methyldopa crosses the placenta fraction. Plasma concentrations of and the blood brain barrier with Pharmacology norepinephrine fall in association active transfer. Methyldopa is also Methyldopa is an analogue of DOPA with the reduction in arterial pres- eliminated into breast milk, (3, 4 dihydroxyphenylanine). The sure and this reflects the decrease although the concentrations are antihypertensive effect of methyldopa in sympathetic tone. Although renin thought to be too small to be harm- is probably through its active metabo- secretion is decreased, this is not ful to the baby. lite, α-methylnorepinephrine. This the prime mechanism of action of Although its side effect profile is acts as an agonist at presynaptic methyldopa. extensive, severe adverse effects due α2 adrenergic receptors in the brain- When administered orally, to methyldopa have been infrequent stem and results in the inhibition methyldopa is absorbed by an active and the side effects are minimised if of adrenergic neuronal outflow. amino acid transport. After a single the daily dose is kept below 1g. The attenuation of norepinephrine therapeutic dose, the hypotensive Drowsiness is one of the common release in the brainstem reduces the effect occurs in two or more hours; side effects but it is usually transient; output of vasoconstrictor adrenergic its maximal effect is in six to eight headache or weakness may be noted signals to the peripheral sympathetic hours, and continues with diminish- as early and transient symptoms as nervous system, leading to blood ing intensity for 18–24 hours. The well. It can cause positive Coombs pressure (BP) reduction. Methyldopa maximum hypotensive effect after test in up to 20% of patients. It can reduces both supine and standing repeated doses may not occur potentially cause hepatotoxicity and BP with infrequent symptomatic though until the second day. On it should be avoided in history of postural hypotension. discontinuation, the BP returns to active hepatic disease or discontin- Methyldopa reduces vascular pretreatment levels in 24–48 hours. ued if there is persistent elevation resistance, has no direct effect on Methyldopa and its metabolites are of transaminases. Methyldopa can S Iliodromiti, Ptychio Iatrikes of Athens, RS Lindsay, MBChB, FRCP(Glasg), BSc, *Correspondence to: S Iliodromiti, Specialty trainee PhD, Consultant Physician and Reader in Princess Royal Maternity Unit, Glasgow F Mackenzie, MBChB, MRCOG, Diabetes and Endocrinology, Princess Royal Royal Infirmary, 16 Alexandra Parade, Consultant Obstetrician Maternity Unit, Glasgow Royal Infirmary, Glasgow G31 2ER, UK; e-mail: Princess Royal Maternity Unit, Glasgow and BHF Glasgow Cardiovascular Research [email protected] Royal Infirmary, Glasgow, UK Centre, University of Glasgow, Glasgow, UK 166 Pract Diab Int May 2010 Vol. 27 No. 4 Copyright © 2010 John Wiley & Sons DN Iliodromiti_Layout 1 16/04/2010 15:00 Page 2 DRUG NOTES Methyldopa aggravate pre-existing – or cause – conducted in the USA showed that Key points depression. Less frequent adverse women receiving methyldopa were reactions include orthostatic hyper- as likely as women in the no-treat- • Methyldopa is effective in tension, congestive heart failure, ment group to develop pre-eclamp- lowering blood pressure but, due bradycardia, vomiting, colitis, sia (OR=1.21; 95% CI 0.55–2.65) but to its side effect profile, has pancreatitis, diarrhoea, constipa- there was a decreased risk of devel- limited use out of pregnancy tion, mouth dryness, bone marrow oping severe hypertension.3 • In pregnancy, including in depression, haemolytic anaemia, In the management of gesta- patients with diabetes, Parkinsonism and nasal congestion. tional hypertension, one trial com- methyldopa may be used, but pared methyldopa with labetalol labetalol is now recommended as Use of methyldopa out of and found that fewer women first line for use in moderate pregnancy who received labetalol developed hypertension, and labetalol, A recent Cochrane review has sum- proteinuria (RR=0.04; 95% CI nifedipine or hydralazine as first marised randomised control trial 0.003–0.73). Compared to placebo, line in severe hypertension (RCT) evidence in the use of methyldopa has been shown to methyldopa outwith pregnancy.1 In prolong the duration of pregnancy methyldopa is not the ideal drug for a meta-analysis of trials predomi- by eight days and decrease the post-natal treatment due to its exten- nantly published in the 1970s and incidence of severe hypertension. sive side effect profile, in particular early 1980s, the authors concluded When nifedipine was compared with the risk of causing or exacerbating that methyldopa (500–2250mg methyldopa in gestational hyperten- depression. daily) lowers systolic and diastolic sion, Apgar scores were better Methyldopa has been used suc- BP by a mean of 13mmHg (95% CI for infants of women receiving cessfully in pregnancies complicated 6–20)/8mmHg (95% CI 4–13). methyldopa. More women required with diabetes, but the data are lim- They also noted that no RCT treatment for acute hypertension in ited and based mainly on small evidence was available assessing the nifedipine group (RR=1.67; 95% observational studies. the clinical impact of methyldopa CI 1.16–2.40).3 Methyldopa has no clinically therapy on end points such as Only one RCT has compared significant effect on glucose toler- mortality, stroke, cardiovascular dis- methyldopa to placebo in women ance and therefore no anticipated ease or heart failure – reflecting the with pre-eclampsia. Women receiv- adverse interaction with diabetes. reduction in clinical use of the drug ing methyldopa were significantly in the developed world prior to the less likely to develop severe pre- Conclusion advent of large end point trials in eclampsia compared to women on Methyldopa has for many years been hypertension. There are no RCTs bed rest without treatment the first line therapy for hyperten- for the use of methyldopa in patients (RR=0.18; 95% CI 0.06–0.55).3 sion in pregnancy; labetalol has now with diabetes. The management of severe hyper- taken that role but methyldopa tension (systolic BP >160mmHg and remains a safe alternative to con- Use of methyldopa in diastolic BP >110mmHg) has been sider in pregnant women with pregnancy evaluated by several trials and sum- chronic hypertension, gestational Methyldopa crosses the placenta marised in a Cochrane review. There hypertension or pre-eclampsia. and achieves fetal concentrations were no significant differences in out- Other agents are preferred for use similar to maternal serum levels. comes but few useful comparisons as in severe hypertension (with or with- Despite this, there is no obvious to the choice of antihypertensive.4 out pre-eclampsia), post-natal hyper- association with congenital abnor- The Royal College of Obstetricians tension and out of pregnancy. malities but mild hypotension has and Gynaecologists’ preferred thera- been reported in neonates in the peutic agents for severe hypertension Conflict of interest statement first two days of life. The long-term in pregnancy are labetalol, nifedipine There are no conflicts of interest. safety of methyldopa in pregnancy or hydralazine (Green-top guideline was reported by Cockburn et al. in number 10a). The recent draft NICE References The Lancet in 1982.2 guideline (full guideline April 2010) 1. Mah GT, Tejani AM, Musini VM. Methyldopa for primary hypertension. Hypertension in pregnancy can on the management of hypertension Cochrane Database Syst Rev 2009. be classified as: (a) chronic, (b) ges- during pregnancy suggests that 2. Cockburn J, Moar VA, Ounsted M, et al. tational, (c) pre-eclampsia, and (d) labetalol should be considered the Final report of study on hypertension chronic hypertension with superim- first line agent for treatment of both during pregnancy:
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