LOSARTAN
Drugs in Pregnancy and Lactation.
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Name: LOSARTAN
Class: Antihypertensive
Risk Factor: CM*
Fetal Risk Summary
Losartan is a selective angiotensin II receptor antagonist that is used, either alone or in combination with other antihypertensive agents, for the treatment of hypertension. Losartan, and its active metabolite, block the vasoconstrictor and aldosterone-secreting effects of angiotensin II by preventing angiotensin II from binding to AT1 receptors.
Reproduction studies have been conducted in pregnant rats (1,2 and 3). At oral doses greater than 3 times the maximum recommended human dose of 100 mg on a body surface area basis (MRHD), reduced body weight, delayed physical and behavioral development, mortality, and renal toxicity were observed in rat fetuses and neonates (1,2 and 3). These adverse effects were attributed to exposure during late pregnancy (gestational days 15–20) and/or during lactation (1,2). A later study, however, found that the amounts of losartan and its active metabolite crossing to the rat fetus were much higher than those excreted in milk, suggesting that the renal toxicity was due to transplacental exposure (4). The irreversible renal abnormalities in the newborn pups included dilatation of the renal pelvis, edema of the renal papilla, medial hypertrophy of intracortical arterioles, chronic renal inflammation, and irregular scarring of the renal parenchyma (2).
In fertility and reproductive performance studies, a significant decrease in fetal implants in rats was noted at a maternally toxic oral dose, approximately 24 times the MRHD. No effects on implants/pregnant female, percent post-implantation loss, or live pups/litter at parturition were observed at an oral dose approximately 12 times the MRHD (1,2 and 3).
A study published in 1999 compared the effects of losartan (an AT1 receptor blocker) to an investigational agent, PD123319 (an AT2 receptor inhibitor), on the developing fetal rat heart (5). Both agents markedly decreased newborn cardiac collagen content, suggesting that angiotensin II receptors are involved in the development of cardiac tissue during gestation (5). The hearts, however, appeared normal in size, shape, and structure. Compared to controls, PD123319 had no effect on birth weight, whereas losartan caused intrauterine growth retardation.
It is not known if losartan or its active metabolite crosses the human placenta to the fetus. Both the drug and its active metabolite cross the rat placenta in significant amounts only during late gestation (1,4). Moreover, the amounts in the rat fetal plasma were significantly higher than those found in maternal milk during lactation (4). In sheep at 125–132 days' gestation (mean 130 days), a bioassay indicated that losartan (10 mg/kg IV) did not cross the placenta (6). The significance of this finding for humans is unknown because the sheep placenta is epitheliochorial whereas the human placenta is hemomonochorial (6). However, because the molecular weight of losartan potassium (about 461) is low enough, passage to the human fetus should be expected.
A postmarketing safety surveillance study of losartan, published in 1999, described the outcomes of four human pregnancies (7). Three of the pregnancies were exposed to the drug in the 1st trimester and the fourth pregnancy was diagnosed about 2 months after stopping the drug. In the first case, the woman became pregnant while taking losartan and the drug was discontinued at approximately 8 weeks' gestation. Because of worsening renal failure, dialysis was required during pregnancy. She delivered a growth-retarded infant at 29 weeks who died at 9 days of age. In the second case, losartan was stopped 6 weeks after the last menstrual period. The woman delivered prematurely at 30 weeks because of preeclampsia. The infant was reported to be doing well. The third pregnancy ended with a spontaneous abortion (no specific embryo data) at 6 to 8 weeks' gestation while the woman was receiving losartan. Finally, a spontaneous abortion (no specific embryo data) occurred at 6 weeks' gestation in a woman who had stopped losartan about 2 months before the pregnancy was diagnosed. Because of the timing of the exposures, none of the outcomes appear to be related to the use of losartan. They are probably a consequence of the women's severe hypertension.
In a 2001 case report, anhydramnios was diagnosed at 31 weeks' gestation in a 31-year-old woman with periarteritis nodosa (8). Hypertension had developed at 17 weeks' gestation and losartan, 50 mg/day, had been started. Therapy was changed to methyldopa (750 mg/day), but 2 days later the woman noticed no fetal movements. Ultrasound confirmed intrauterine fetal death and she delivered a stillborn 1592-g male infant the next day. The infant had facial and limb deformities characteristic of oligohydramnios. At autopsy, pulmonary hypoplasia and hypoplastic skull bones with wide sutures were observed, but no other apparent abnormalities, including the kidneys and urinary tract, were noted. The anhydramnios and resulting fatal fetal abnormalities were attributed to losartan (8).
The antihypertensive mechanisms of action of losartan and angiotensin converting enzyme (ACE) inhibitors are very close. That is, the former selectively blocks the binding of angiotensin II to AT1 receptors, whereas the latter prevents the formation of angiotensin II itself. Therefore, use of this drug during the 2nd and 3rd trimesters may cause teratogenicity and severe fetal and neonatal toxicity that is identical to that seen with ACE inhibitors (e.g., see Captopril or Enalapril). Fetal toxic effects may include anuria, oligohydramnios, fetal hypocalvaria, intrauterine growth retardation, prematurity, and patent ductus arteriosus. Anuria-associated oligohydramnios may produce fetal limb contractures, craniofacial deformation, and pulmonary hypoplasia. Severe anuria and hypotension, that is resistant to both pressor agents and volume expansion, may occur in the newborn following in utero exposure to losartan. Newborn renal function and blood pressure should be closely monitored.
[*Risk factor DM if used in 2nd or 3rd trimesters.]
Breast Feeding Summary
No reports describing the use of losartan during human lactation have been located. The drug and its active metabolite are found in the milk of lactating rats (1). Because the molecular weight (about 461) of losartan potassium is low enough, excretion into human breast milk should also be expected. The effects of this exposure on a nursing infant are unknown. The American Academy of Pediatrics, however, considers ACE inhibitors, a closely related group of antihypertensive agents, to be compatible with breast feeding (see Captopril or Enalapril).
References
- Product information. Cozaar. Merck, 2001.
- Spence SG, Allen HL, Cukierski MA, Manson JM, Robertson RT, Eydelloth RS. Defining the susceptible period of developmental toxicity for the AT1-selective angiotensin II receptor antagonist losartan in rats. Teratology 1995;51:367–82.
- Spence SG, Cukierski MA, Manson JM, Robertson RT, Eydelloth RS. Evaluation of the reproductive and developmental toxicity of the AT1-selective angiotensin II receptor antagonist losartan in rats. Teratology 1995;51:383–97.
- Spence SG, Zacchei AG, Lee LL, Baldwin CL, Berna RA, Mattson BA, Eydelloth RS. Toxicokinetic analysis of losartan during gestation and lactation in the rat. Teratology 1996;53:245–52.
- Lamparter S, Sun Y, Weber KT. Angiotensin II receptor blockade during gestation attenuates collagen formation in the developing rat heart. Cardiovascular Res 1999;43:165–72.
- Stevenson KM, Gibson KJ, Lumbers ER. Comparison of the transplacental transfer of enalapril, captopril and losartan in sheep. Br J Pharmacol 1995;114:1495–1501.
- Mann RD, Mackay F, Pearce G, Freemantle S, Wilton LV. Losartan: a study of pharmacovigilance data on 14 522 patients. J Hum Hyperten 1999;13:551–7.
- Saji H, Yamanaka M, Hagiwara, Ijiri R. Losartan and fetal toxic effects. Lancet 2001;357:363.
Q&A about Losartan
I am working in the desert, and the only available losartan potassium here in "COZAAR". Since both medicines are losartan potassium, could I take "COZAAR" 50mg if ever I run out of "LIFEZAR" 50mg. "LIFEZAR" is a brand name of losartan potassium in the Philippines. Thanks.
I'am a hammer thrower, I take for blood pressure treatment COZAAR 50mg in the morning & NORVASC 5mg in the evening,& I would like to know if any or both of the above mentioned drugs might give a positive + result in the doping test
But it's more important to meet that quota when your consuming alcohol or drugs.
i need to know if it is like cozaar it was bought across and they said it was but it doesn't say cozaar it say "losartan potasico"
:http://www.ApprovedGenericPills.com
http://www.aclepsa.com/cozaar.shtml?id=6...
this will help.
aspirin to control my blood pressure. My question is about the side effects because lately I have noticed some itchy rashes in my body. Is it caused by taking losartan and atenolol at the same time? What are the other side effects of taking both medicines at the same time? I am now in the process of contacting my doctor through my wife but since I am working in a remote area, it might take some time before I get back an answer. Please help. Thanks.
If a tablet contains 50 mg losartan potassium and 12.5 mg hydrochlorothiazide how many tablets do I take in one day.
DOSAGE AND ADMINISTRATION
Hypertension Dosing must be individualized.
The usual starting dose of losartan is 50 mg once daily, with 25 mg recommended for patients with intravascular volume depletion (e.g., patients treated with diuretics) and patients with a history of hepatic impairment
Losartan can be administered once or twice daily at total daily doses of 25 to 100 mg. If the antihypertensive effect measured at trough using once-a-day dosing is inadequate, a twice-a-day regimen at the same total daily dose or an increase in dose may give a more satisfactory response.
Hydrochlorothiazide is effective in doses of 12.5 to 50 mg once daily and can be given at doses of 12.5 to 25 mg as HYZAAR. To minimize dose-independent side effects, it is usually appropriate to begin combination therapy only after a patient has failed to achieve the desired effect with monotherapy.
The side effects of losartan are generally rare and apparently independent of dose; those of hydrochlorothiazide are a mixture of dose-dependent (primarily hypokalemia) and dose-independent phenomena (e.g., pancreatitis), the former much more common than the latter.
Therapy with any combination of losartan and hydrochlorothiazide will be associated with both sets of dose-independent side effects.
Replacement Therapy: The combination may be substituted for the titrated components.
Dose Titration by Clinical Effect: A patient whose blood pressure is not adequately controlled with losartan monotherapy (see above) or hydrochlorothiazide alone, may be switched to HYZAAR 50-12.5 (losartan 50 mg/hydrochlorothiazide 12.5 mg) once daily. If blood pressure remains uncontrolled after about 3 weeks of therapy, the dose may be increased to two tablets of HYZAAR 50-12.5 once daily or one tablet of HYZAAR 100-25 (losartan 100 mg/hydrochlorothiazide 25 mg) once daily. A patient whose blood pressure is not adequately controlled with losartan 100 mg monotherapy (see above) may be switched to HYZAAR 100-12.5 once daily. If blood pressure remains uncontrolled after about 3 weeks of therapy, the dose may be increased to two tablets of HYZAAR 50-12.5 once daily or one tablet of HYZAAR 100-25 (losartan 100 mg/hydrochlorothiazide 25 mg) once daily.A patient whose blood pressure is inadequately controlled by 25 mg once daily of hydrochlorothiazide, or is controlled but who experiences hypokalemia with this regimen, may be switched to HYZAAR 50-12.5 (losartan 50 mg/hydrochlorothiazide 12.5 mg) once daily, reducing the dose of hydrochlorothiazide without reducing the overall expected antihypertensive response. The clinical response to HYZAAR 50-12.5 should be subsequently evaluated, and if blood pressure remains uncontrolled after about 3 weeks of therapy, the dose may be increased to two tablets of HYZAAR 50-12.5 once daily or one tablet of HYZAAR 100-25 (losartan 100 mg/hydrochlorothiazide 25 mg) once daily.The usual dose of HYZAAR is one tablet of HYZAAR 50-12.5 once daily. More than two tablets of HYZAAR 50-12.5 once daily or more than one tablet of HYZAAR 100-25 once daily is not recommended. The maximal antihypertensive effect is attained about 3 weeks after initiation of therapy.Use in Patients with Renal Impairment: The usual regimens of therapy with HYZAAR may be followed as long as the patient's creatinine clearance is >30 mL/min. In patients with more severe renal impairment, loop diuretics are preferred to thiazides, so HYZAAR is not recommended.
Patients with Hepatic Impairment: HYZAAR is not recommended for titration in patients with hepatic impairment because the appropriate 25 mg starting dose of losartan cannot be given. Severe Hypertension The starting dose of HYZAAR for initial treatment of severe hypertension is one tablet of HYZAAR 50-12.5 once daily (see CLINICAL PHARMACOLOGY, Pharmacodynamics and Clinical Effects). For patients who do not respond adequately to HYZAAR 50-12.5 after 2 to 4 weeks of therapy, the dosage may be increased to one tablet of HYZAAR 100-25 once daily. The maximum dose is one tablet of HYZAAR 100-25 once daily. HYZAAR is not recommended as initial therapy in patients with hepatic impairment because the appropriate 25 mg starting dose of losartan cannot be given. It is also not recommended for use as initial therapy in patients with intravascular volume depletion (e.g., patients treated with diuretics.
HYZAAR®50-12.5 (Losartan Potassium-Hydrochlorothiazide Tablets)
HYZAAR®100-12.5 (Losartan Potassium-Hydrochlorothiazide Tablets)
HYZAAR®100-25 (Losartan Potassium-Hydrochlorothiazide Tablets)
16 Hypertensive Patients with Left Ventricular Hypertrophy Treatment should be initiated with COZAAR 50 mg once daily. Hydrochlorothiazide 12.5 mg should be added or HYZAAR 50-12.5 substituted if the blood pressure reduction is inadequate. If additional blood pressure reduction is needed, COZAAR 100 mg and hydrochlorothiazide 12.5 mg or HYZAAR 100-12.5 may be substituted, followed by COZAAR 100 mg and hydrochlorothiazide 25 mg or HYZAAR 100-25. For further blood pressure reduction other antihypertensives should be added
HYZAAR may be administered with other antihypertensive agents. HYZAAR may be administered with or without food
I have read ATII stimulates cortisol release and i thought it may reduce serum cortisol levels.
This drug works by blocking the hormone angiotensin thereby relaxing blood vessels, causing them to widen. Losartan belongs to a class of drugs called angiotensin receptor blockers.
Common side effects:
Head PainLess Severe
Infrequent side effects:
Acute Infection of the Nose, Throat or SinusSevere
DizzySevere
Stuffy NoseLess Severe
BackacheLess Severe
Low EnergyLess Severe
DiarrheaLess Severe
Rare side effects:
VasculitisSevere
Hepatitis caused by DrugsSevere
Serious Muscle Tissue DamageSevere
Abnormal Liver Function TestsSevere
Life Threatening Allergic ReactionSevere
Giant HivesSevere
Low Amount of Sodium in the BloodSevere
High Amount of Potassium in the BloodSevere
Decreased Blood PlateletsSevere
Sinus Irritation and CongestionLess Severe
Redness of SkinLess Severe
Muscle PainLess Severe
Pain in Arms or LegsLess Severe
CrampsLess Severe
Abnormal Trouble SleepingLess Severe
Taste ProblemsLess Severe
CoughLess Severe
What are ACE inhibitors, and how do they work?
Angiotensin II is a very potent chemical that causes the muscles surrounding blood vessels to contract and thereby narrows the blood vessels. The narrowing of the vessels increases the pressure within the vessels and can cause high blood pressure (hypertension). Angiotensin II is formed from angiotensin I in the blood by the enzyme, angiotensin converting enzyme (ACE). ACE inhibitors are medications that slow (inhibit) the activity of the enzyme, which decreases the production of angiotensin II. As a result, the blood vessels enlarge or dilate, and the blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart. In addition, the progression of kidney disease due to high blood pressure or diabetes is slowed.
What are the side effects of ACE inhibitors?
ACE inhibitors are relatively well-tolerated by most individuals. Nevertheless, they are not free of side effects, and some patients should not use ACE inhibitors. ACE inhibitors usually are not prescribed for pregnant patients because they may cause birth defects. Individuals with severe kidney problems and people who have had a severe reaction to ACE inhibitors probably should avoid them. The most common side effects are cough, elevated blood potassium levels, low blood pressure, dizziness, headache, drowsiness, weakness, abnormal taste (metallic or salty taste), and rash. It may take up to a month for coughing to subside, and if one ACE inhibitor causes cough it is likely that the others will too. The most serious, but rare, side effects of ACE inhibitors are kidney failure, allergic reactions, a decrease in white blood cells, and swelling of tissues (angioedema).
Hope that helps!!!!!!!!