Vitamin K Epoxide Reductases
International Normalized Ratio
Drug Dosage Calculations
Aryl Hydrocarbon Hydroxylases
A placebo-controlled study of interaction between nabumetone and acenocoumarol. (1/76)AIMS: The use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients treated with oral anticoagulants is generally discouraged due to the risk of interactions that could increase the risk of bleeding complications. Available data suggest the NSAID, nabumetone, does not produce such an interaction. We investigated whether nabumetone would interact with acenocoumarol, an oral anticoagulant widely used in some European countries. METHODS: A double-blind, randomized, placebo-controlled study was conducted evaluating nabumetone (1-2 g daily for up to 4 weeks) in osteoarthritis patients with thromboembolic risk previously stabilized on acenocoumarol. The primary efficacy end point was the proportion of patients whose International Normalized Ratio (INR) remained within established margins and whose acenocoumarol dose was not changed. Fifty-six patients were randomized to receive nabumetone (n=27) or placebo (n=29). RESULTS: Eighteen patients in each group (67% for nabumetone and 62% for placebo) completed the study without showing INR or acenocoumarol dose changes, and were considered as study successes. Nine patients (33%) with nabumetone and 11 (38%) with placebo were considered study failures in the intention-to-treat analysis (one patient on nabumetone and four on placebo did not complete the study due to reasons not related to INR and acenocoumarol dose changes). No significant differences were found between groups with regard to study successes. There were two minor bleeding complications, one in each group. Six patients per group presented with eight adverse experiences in each group. CONCLUSIONS: Treatment with nabumetone did not alter INR levels compared with placebo in patients stabilized on oral acenocoumarol who require NSAID therapy. These results suggest that nabumetone does not produce a clinically relevant interaction with acenocoumarol. In orally anticoagulated patients without other associated risk factors, treatment with nabumetone for up to 4 weeks does not require increased monitoring of INR levels. (+info)
Prediction of pharmacokinetic drug/drug interactions from In vitro data: interactions of the nonsteroidal anti-inflammatory drug lornoxicam with oral anticoagulants. (2/76)CYP2C9 is involved in the metabolism of the oral anticoagulants warfarin, phenprocoumon, and acenocoumarol. It is also responsible for the 5'-hydroxylation of the nonsteroidal anti-inflammatory drug lornoxicam. Therefore, lornoxicam and the oral anticoagulants are potential inhibitors of their metabolism. Their inhibitory potency was investigated in microsomes from six human livers. An approach to predict pharmacokinetic interactions of lornoxicam from in vitro inhibition data was developed. Where possible, the forecasts were verified by comparison with data from clinical interaction studies. The following increases in steady-state plasma concentrations or areas under the plasma concentration-time curve of the oral anticoagulants by concomitant lornoxicam medication were predicted (values in parentheses are for healthy volunteers): (S)-warfarin, 1. 58-fold (1.32-fold for racemate); racemic-acenocoumarol, 1.28-fold (1.09-fold); (R)-acenocoumarol, 1.10-fold (1.0-fold); racemic-phenprocoumon, 1.11-fold (1.18-fold); and (S)-phenprocoumon, 1.13-fold (1.24-fold). Lornoxicam 5'-hydroxylation was competitively inhibited in vitro by both phenprocoumon (K(i) = 1.2 +/- 0.4 microM) and acenocoumarol (K(i) = 5.5 +/- 3.5 microM). The present results indicate that relatively close predictions of the interactions of lornoxicam with oral anticoagulants from in vitro data are possible under the assumption that hepatic lornoxicam concentrations are similar to its total plasma concentrations. The degree of pharmacokinetic interactions exhibited by oral anticoagulants and lornoxicam is dependent on the respective contribution of CYP2C9 to their total clearance. (+info)
Assessment of patient capability to self-adjust oral anticoagulant dose: a multicenter study on home use of portable prothrombin time monitor (COAGUCHECK). (3/76)BACKGROUND AND OBJECTIVES: Self-testing and self-monitoring with portable prothrombin time (PT) monitors has been shown to be feasible and safe. However the ability of patients on chronic oral anticoagulant therapy (OAT) to self-adjust their dose without specific training has never been properly evaluated. The aims of this study were to evaluate: 1) the ability of patients on chronic OAT to self-adjust their dose without specific training; 2) the integration of a portable PT monitor (Coagucheck, Roche Diagnostics, Germany) for home use into routine patient care in anticoagulation clinics. DESIGN AND METHODS: A nested case-control study was conducted in four centers of the Italian Federation of Anticoagulation Clinics (FCSA). Patients (n=78) on stable OAT for at least 6 months (cases: 47 men, 31 women, age range: 18-75 years) were enrolled on a volunteer basis after passing an Abbreviated Mental Test and providing informed consent. After three instruction sessions on the use of Coaguchek, subjects performed the PT test at home, communicated the INR results to the Center and suggested the dose adjustment and date for next control as they thought appropriate. However, they were requested to follow the prescription made by the Center. Controls (78 subjects) matched by age (+/- 5 years), sex and therapeutic range with the cases, were selected from among those who attended the anticoagulation clinics and managed by usual care. RESULTS: When compared with the dose prescribed by the Clinic, the dose suggested by warfarin and acenocoumarol users was equal to or within +/- 6% of the mean weekly dose in 80% and 82% of suggestions, respectively. Time spent in the therapeutic range during the study was the same (80%) for cases and controls. INTERPRETATION AND CONCLUSIONS: Selected patients on chronic anticoagulant therapy can acquire a satisfactory ability for self-adjustment of OAT dose without specific training. (+info)
Cytochrome P4502C9 is the principal catalyst of racemic acenocoumarol hydroxylation reactions in human liver microsomes. (4/76)The oral anticoagulant acenocoumarol is given as a racemic mixture. The (S)-enantiomer is rapidly cleared and is the reason why only (R)-acenocoumarol contributes to the pharmacological effect. The objective of the study was to establish the cytochrome P450 (CYP) enzymes catalyzing the hydroxylations of the acenocoumarol enantiomers. Of various cDNA-expressed human CYPs, only CYP2C9 hydroxylated (S)-acenocoumarol. Hydroxylation occurred at the 6-, 7-, and 8-position with equal K(m) values and a ratio of 0.9:1:0.1 for V(max). CYP2C9 also mediated the 6-, 7-, and 8-hydroxylations of (R)-acenocoumarol with K(m) values three to four times and V(max) values one-sixth times those of (S)-acenocoumarol. (R)-Acenocoumarol was also metabolized by CYP1A2 (6-hydroxylation) and CYP2C19 (6-, 7-, and 8-hydroxylation). In human liver microsomes one enzyme only catalyzed (S)-acenocoumarol hydroxylations with K(m) values < 1 microM. In most of the samples tested the 7-hydroxylation of (R)-acenocoumarol was also catalyzed by one enzyme only. The 6-hydroxylation was catalyzed by at least two enzymes. Sulfaphenazole could completely inhibit in a competitive way the hydroxylations of (S)-acenocoumarol and the 7-hydroxylation of (R)-acenocoumarol. The 6-hydroxylation of (R)-acenocoumarol could be partially inhibited by sulfaphenazole, 40 to 50%, and by furafylline, 20 to 30%. Significant mutual correlations were obtained between the hydroxylations of (S)-acenocoumarol, the 7-hydroxylation of (R)-acenocoumarol, the 7-hydroxylation of (S)-warfarin, and the methylhydroxylation of tolbutamide. The results demonstrate that (S)-acenocoumarol is hydroxylated by a single enzyme, namely CYP2C9. CYP2C9 is also the main enzyme in the 7-hydroxylation of (R)-acenocoumarol. Other enzymes involved in (R)-acenocoumarol hydroxylation reactions are CYP1A2 and CYP2C19. Drug interactions must be expected, particularly for drugs interfering with CYP2C9. Also, drugs interfering with CYP1A2 and CYP2C19 may potentiate acenocoumarol anticoagulant therapy. (+info)
Low molecular weight heparin versus oral anticoagulants in the long-term treatment of deep venous thrombosis. (5/76)PURPOSE: The purpose of this study was to evaluate whether low molecular weight heparin (LMWH) could be equal or more effective than conventional oral anticoagulants (OAs) in the long-term treatment of deep venous thrombosis (DVT). METHODS: One hundred fifty-eight patients with symptomatic DVT of the lower limbs confirmed by means of duplex ultrasound scan were randomized to receive 3 to 6 months' treatment with nadroparine calcium or acenocoumarol. Quantitative and qualitative duplex scan scoring systems were used to study the evolution of thrombosis in both groups at 1, 3, 6, and 12 months. RESULTS: During the 12-month surveillance period, two (2.5%) of the 81 patients who received LMWH and seven (9%) of the 77 patients who received OAs had recurrence of venous thrombosis (not significant). In the LMWH group no cases of major bleeding were found, and four cases (5.2%) occurred in the OA group (not significant). The mortality rate was nine (11.1%) in the LMWH group and 7.8% in the OA group (not significant). The quantitative mean duplex scan score decreased in both groups during the follow-up and had statistical significance after long-term LMWH treatment on iliofemoral DVT (1, 3, 6, and 12 months), femoropopliteal DVT (1-3 months), and infrapopliteal DVT (first month). Duplex scan evaluation showed that the rate of venous recanalization significantly increased in the common femoral vein at 6 and at 12 months and during each point of follow-up in the superficial and popliteal veins in the LMWH group. Reflux was significantly less frequent in communicating veins after LMWH treatment (17.9% vs 32.2% in the OA group). The reflux rates in the superficial (22.4% in the LMWH group, 30.6% in OA group) and deep (13.4% vs 17.7%) venous system showed no significant differences between groups. CONCLUSIONS: The unmonitored subcutaneous administration of nadroparine in fixed daily doses was more effective than oral acenocoumarol with laboratory control adjustment in achieving recanalization of leg thrombi. With nadroparine, there was less late valvular communicating vein insufficiency, and it was at least as efficacious and safe as oral anticoagulants after long-term administration. These results suggest that LMWHs may therefore represent a real therapeutic advance in the long-term management of DVT. (+info)
Optimal oral anticoagulant intensity to prevent secondary ischemic and hemorrhagic events in patients after infrainguinal bypass graft surgery. Dutch BOA Study Group. (6/76)OBJECTIVES: The purpose of this study was to determine the optimal intensity of oral anticoagulation in patients who participated in a randomized trial of oral anticoagulants or aspirin after infrainguinal bypass graft surgery. METHODS: The distribution of patient-time spent in international normalized ratio (INR) classes of 0.5 INR unit was calculated assuming a linear change between successive measurements. INR-specific incidence rates of ischemic and hemorrhagic events were calculated as the ratio of the number of events at a certain INR category and the total patient-time spent in that class. The relationship between INR class and event rates was quantified by rate ratios calculated in a Poisson regression model. RESULTS: In 1326 patients (mean age, 69 years) 41,928 INR measurements were recorded in 1698 patient-years. Patients spent 50% of the total time within the target range of 3.0 to 4.5 INR. Most of the patient-time (60%) was spent between 2.5 and 3.5 INR. For each increasing class of 0.5 INR, the incidence of ischemic events (n = 154, INR data on event available in 49%) decreased by a factor of 0.97 (95% CI, 0.87-1.08). The incidence of major bleeding (n = 123, INR data on event available in 65%) increased significantly by a factor of 1.27 (95% CI, 1.19-1.34) for each increasing 0.5 INR category. The optimal target range was 3.0 to 4.0 INR, with an incidence of 3.8 events (0.9 ischemic and 2.9 hemorrhagic) per 100 patient-years. CONCLUSIONS: The target range of 3.0 to 4.0 INR is the optimal range of achieved anticoagulation intensity and is safe for the prevention of ischemic events in patients after infrainguinal bypass graft surgery. (+info)
Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators. (7/76)BACKGROUND: In patients with idiopathic deep venous thrombosis, continuing anticoagulant therapy beyond three months is associated with a reduced incidence of recurrent thrombosis during the period of therapy. Whether this benefit persists after anticoagulant therapy is discontinued is controversial. METHODS: Patients with a first episode of idiopathic proximal deep venous thrombosis who had completed three months of oral anticoagulant therapy (with warfarin, in 97 percent of the cases and acenocoumarol in 3 percent) were randomly assigned to the discontinuation of oral anticoagulants or to their continuation for nine additional months. The primary study outcome was recurrence of symptomatic, objectively confirmed venous thromboembolism during at least two years of follow-up. RESULTS: The primary intention-to-treat analysis showed that of 134 patients assigned to continued oral anticoagulant therapy, 21 had a recurrence of venous thromboembolism (15.7 percent; average follow-up, 37.8 months), as compared with 21 of 133 patients assigned to the discontinuation of oral anticoagulant therapy (15.8 percent; average follow-up, 37.2 months), resulting in a relative risk of 0.99 (95 percent confidence interval, 0.57 to 1.73). During the initial nine months after randomization (after all patients received three months of therapy), 1 patient had a recurrence while receiving oral anticoagulant therapy (0.7 percent), as compared with 11 of the patients assigned to the discontinuation of oral anticoagulant therapy (8.3 percent; P=0.003). The incidence of recurrence after the discontinuation of treatment was 5.1 percent per patient-year in patients in whom oral anticoagulant therapy was discontinued after 3 months (95 percent confidence interval, 3.2 to 7.5 percent; average interval since discontinuation, 37.2 months) and 5.0 percent per patient-year in patients who received an additional 9 months of oral anticoagulant therapy (95 percent confidence interval, 3.1 to 7.8 percent; average interval since discontinuation, 29.4 months). None of the recurrences were fatal. Four patients had non-fatal major bleeding during the extended period of anticoagulant therapy (3.0 percent). CONCLUSIONS: In patients with idiopathic deep venous thrombosis, the clinical benefit associated with extending the duration of anticoagulant therapy to one year is not maintained after the therapy is discontinued. (+info)
Determination of coumarin-type anticoagulants in human plasma by HPLC-electrospray ionization tandem mass spectrometry with an ion trap detector. (8/76)BACKGROUND: Coumarin-type anticoagulants are used for the long-term treatment and prevention of thromboembolic disorders. The identification of these drugs is crucial in patients with an increased prothrombin time of unknown origin. The aim of this study was to develop a sensitive and specific method for the simultaneous determination of phenprocoumon, acenocoumarol, and warfarin in human plasma by HPLC-electrospray ionization tandem mass spectrometry. METHODS: After addition of the internal standard, p-chlorowarfarin, plasma samples were extracted using Oasis MCX solid-phase extraction cartridges. The compounds were separated on a Symmetry C18 column (Waters) with a mobile phase of acetonitrile-1 g/L formic acid (75:25 by volume) at a flow rate of 0.5 mL/min. RESULTS: Extraction and separation of the three drugs and the internal standard were accomplished in 9 min. The overall extraction efficiency was >89% for all three compounds. The limits of detection were 1 microg/L for phenprocoumon and warfarin and 10 microg/L for acenocoumarol. Regression analysis of the calibration data revealed good correlation (r(2) >or=0.995) for all compounds. Within-run accuracies for quality-control samples were +/- 1% to 7% of the target concentration, with CVs <9%. CONCLUSIONS: The proposed method enables the unambiguous identification and quantification of phenprocoumon, warfarin, and acenocoumarol in both clinical and forensic specimens. This method combines a new, rapid solid-phase extraction procedure with an extremely fast chromatographic analysis, which is especially advantageous for clinical laboratories. (+info)
Acenocoumarol is an anticoagulant medication that is used to prevent blood clots. It is a synthetic derivative of coumarin, a naturally occurring compound found in certain plants. Acenocoumarol works by inhibiting the enzyme vitamin K epoxide reductase, which is involved in the production of clotting factors in the liver. This leads to a decrease in the production of clotting factors, making it more difficult for blood to clot. Acenocoumarol is typically used to treat and prevent blood clots in people with conditions such as deep vein thrombosis (DVT), pulmonary embolism (PE), and atrial fibrillation (AF). It is also sometimes used to prevent blood clots after surgery or during pregnancy. Acenocoumarol is usually taken orally, and the dosage is adjusted based on the patient's response to the medication and their risk of bleeding. It is important to monitor the patient's blood levels of acenocoumarol and international normalized ratio (INR) while they are taking the medication, as these can help to ensure that the medication is working effectively and that the patient is not at risk of bleeding.
Phenprocoumon is a medication that is used to prevent blood clots. It is also known by the brand name Marcumar. It works by inhibiting the enzyme that converts vitamin K into its active form, which is necessary for blood clotting. This leads to a decrease in the production of clotting factors in the blood, making it less likely for blood clots to form. Phenprocoumon is typically prescribed for people who are at risk of developing blood clots, such as those who have had a previous blood clot or who are undergoing surgery. It is usually taken in the form of tablets, and the dosage is adjusted based on the individual's response to the medication.
Vitamin K epoxide reductases (VKORs) are a group of enzymes that play a critical role in the metabolism of vitamin K. Vitamin K is a fat-soluble vitamin that is essential for blood clotting and bone health. There are two main types of VKORs: VKORC1 and VKORC2. VKORC1 is primarily found in the liver and is responsible for the reduction of vitamin K epoxides, which are inactive forms of vitamin K. This reduction is necessary for the activation of vitamin K-dependent clotting factors, such as factor II, VII, IX, and X. VKORC1 is also the target of warfarin, a commonly used anticoagulant medication. VKORC2 is found in other tissues, such as the placenta and the brain, and may have additional functions beyond vitamin K metabolism. Both VKORC1 and VKORC2 are important for maintaining normal blood clotting and bone health. Disruptions in VKOR activity can lead to bleeding disorders or bone abnormalities. For example, mutations in the VKORC1 gene can cause vitamin K-dependent clotting factor deficiency, which can lead to bleeding disorders. Similarly, deficiencies in vitamin K can lead to bone abnormalities, such as osteoporosis.
Povidone-iodine is a topical antiseptic solution that contains a mixture of povidone (a water-soluble polymer) and iodine. It is commonly used in the medical field for wound care, skin antisepsis, and surgical preparation. Povidone-iodine is effective against a wide range of microorganisms, including bacteria, viruses, and fungi. It is available in various strengths and forms, including solutions, gels, and foams. When used properly, povidone-iodine is considered safe and effective for most skin surfaces and can help prevent the spread of infection.
Steroid 16-alpha-hydroxylase is an enzyme that plays a crucial role in the metabolism of steroids in the human body. It is responsible for converting certain steroids, such as testosterone and progesterone, into their corresponding 16-alpha-hydroxylated derivatives. This enzyme is primarily found in the liver and is involved in the biosynthesis of several important hormones, including cortisol, aldosterone, and androgens. It is also involved in the metabolism of certain drugs, such as oral contraceptives and anabolic steroids. Deficiency or dysfunction of steroid 16-alpha-hydroxylase can lead to a variety of medical conditions, including adrenal insufficiency, polycystic ovary syndrome, and certain forms of hypertension. In addition, mutations in the gene encoding this enzyme have been associated with certain inherited disorders, such as 16-alpha-hydroxylase deficiency and 11-beta-hydroxylase deficiency.
Aryl Hydrocarbon Hydroxylases (AHHs) are a group of enzymes that are involved in the metabolism of aromatic hydrocarbons, such as polycyclic aromatic hydrocarbons (PAHs) and halogenated aromatic hydrocarbons (HAHs). These enzymes are primarily found in the liver and are responsible for the oxidation of these compounds to their corresponding hydroxylated derivatives. AHHs play an important role in the detoxification of these compounds, as the hydroxylated derivatives are more water-soluble and can be more easily excreted from the body. In addition, the hydroxylation of aromatic hydrocarbons can also lead to the formation of reactive intermediates, such as quinones, which can be further metabolized or detoxified by other enzymes. AHHs are also involved in the metabolism of other compounds, such as certain drugs and hormones. Mutations in the genes encoding AHHs can lead to impaired metabolism of these compounds, which can result in toxicity or other health effects. In the medical field, AHHs are often studied in the context of their role in the metabolism of environmental pollutants and their potential health effects. For example, exposure to PAHs and HAHs has been linked to an increased risk of cancer and other health problems, and AHHs are thought to play a key role in this process.
Warfarin is an anticoagulant medication that is used to prevent blood clots from forming in the body. It is also used to treat blood clots that have already formed, such as deep vein thrombosis (DVT) or pulmonary embolism (PE). Warfarin works by inhibiting the production of vitamin K, which is necessary for the production of certain clotting factors in the blood. This helps to prevent blood clots from forming and can also help to dissolve existing clots. Warfarin is typically prescribed for people who are at risk of developing blood clots, such as those who have had a previous blood clot or who have certain medical conditions that increase their risk of blood clots. It is usually taken orally and requires regular monitoring of blood clotting levels to ensure that the dose is appropriate and to prevent bleeding complications.
Butanones, also known as methyl ethyl ketone (MEK) and butyl acetate, are organic compounds that are commonly used in the medical field as solvents and as ingredients in various medical products. MEK is a colorless liquid with a sweet, fruity odor that is used as a solvent in the production of pharmaceuticals, cosmetics, and other medical products. It is also used as a cleaning agent and as a solvent for removing paint and other coatings. Butyl acetate is a colorless liquid with a sweet, fruity odor that is used as a solvent in the production of pharmaceuticals, cosmetics, and other medical products. It is also used as a flavoring agent in food and beverages. Both MEK and butyl acetate are considered to be relatively safe when used in the proper concentrations and under controlled conditions. However, exposure to high concentrations of these compounds can cause irritation of the eyes, nose, and throat, as well as headaches, dizziness, and nausea. In some cases, prolonged or repeated exposure to these compounds may also cause more serious health effects, such as liver and kidney damage.
Hemorrhage is the medical term used to describe the loss of blood from a vessel or vessel system. It can occur due to a variety of reasons, including injury, disease, or abnormal blood vessel function. Hemorrhage can be classified based on the location of the bleeding, the amount of blood lost, and the severity of the condition. For example, internal hemorrhage occurs within the body's organs or tissues, while external hemorrhage occurs outside the body, such as through a wound or broken skin. The severity of hemorrhage can range from mild to life-threatening, depending on the amount of blood lost and the body's ability to compensate for the loss. In severe cases, hemorrhage can lead to shock, which is a life-threatening condition characterized by low blood pressure and inadequate blood flow to the body's organs and tissues. Treatment for hemorrhage depends on the cause and severity of the bleeding. In some cases, simple measures such as applying pressure to the wound or elevating the affected limb may be sufficient to stop the bleeding. In more severe cases, medical intervention such as surgery or blood transfusions may be necessary to control the bleeding and prevent further complications.
Vitamin K antagonist
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- Acenocoumarol is an anticoagulant that functions as a vitamin K antagonist (like warfarin ). (wikidoc.org)
- Warfarin or acenocoumarol is better in the anticoagulant treatment of chronic atrial fibrillation? (wikidoc.org)
- Side bar - in the Netherlands, the vitamin K antagonists acenocoumarol or phenprocoumon are much more commonly used than warfarin . (medscape.com)
- Similar to other coumarin derivatives, the anticoagulant effects of acenocoumarol are mediated via inhibition of vitamin K epoxide reductase, which impairs gamma carboxylation of glutamic acid residues of the precursor proteins of factors II, VII, IX, and X. (superiortoxicology.com)
- Acenocoumarol is used for short-term anticoagulation needs but is not approved for use in the USA. (superiortoxicology.com)
Vitamin K antagonist1
- The aim of this study was to assess the effectiveness and safety of dabigatran (direct thrombin inhibitor) vs. acenocoumarol (vitamin K antagonist) in patients with atrial fibrillation (AF) in daily clinical practice. (medscape.com)
- [ 5-8 ] However, in different parts of the world, other coumarin derivatives are widely used such as acenocoumarol and phenprocoumon. (medscape.com)
- Efficiency and effectiveness of the use of an acenocoumarol pharmacogenetic dosing algorithm versus usual care in patients with venous thromboembolic disease initiating oral anticoagulation: study protocol for a randomized controlled trial. (cdc.gov)
- In total, 920 consecutive AF patients were enrolled (442 dabigatran, 478 acenocoumarol), of which 2 × 383 were available for analysis after propensity score matching. (medscape.com)
- The mean calculated stroke risk according to the CHA 2 DS 2 -VASc score was 3.5%/year in dabigatran vs. 3.7%/year acenocoumarol-treated patients. (medscape.com)
- Conclusion In 'real-world' patients with AF, dabigatran appears to be as effective, but significantly safer than acenocoumarol . (medscape.com)
- 15. [Significance of cytochrome P450 2C9 genotype for the bleeding complications in patients treated with acenocoumarol]. (nih.gov)
- There is a consensus that maternal acenocoumarol therapy during breastfeeding poses little risk to the breastfed infant. (nih.gov)