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PubMed1981

Factors influencing serum protein binding of lidocaine in humans.

Several factors that may affect protein binding of lidocaine in human serum were studied in normal volunteers. Evidence was obtained for the presence of two classes of lidocaine binding sites with strikingly different affinity constants (k) and capacities (nP); k1 equals 1.3 x 10(5)M(-1), n1P1 equals 1.7 x 10(-5)M, and k2 equals 6.4 x 10(1)M(-1), n2P2 equals 6.9 x 10(-3)M. The low affinity binding sites are probably on serum albumin, whereas the high affinity site may be located on alpha 1 acid glycoprotein. At a lidocaine serum concentration of approximately 1.4 microgram/ml, it was observed that acidosis (pH 7.4 leads to 7.2) caused lidocaine-free fraction to increase from 0.29 to 0.36 (p less than 0.01) and that the addition of the lidocaine metabolites 3-hydroxylidocaine, 4-hydroxylidocaine, monoethylglycinexylidide, and glycinexylidide had no effect on the binding of lidocaine. Bupivacaine, disopyramide, and quinidine (in concentrations that are observed clinically) caused a significant increase (p less than 0.01) in the free fraction of lidocaine in serum (23%, 21%, and 34%, respectively. Interestingly, N-depropyl disopyramide, dihydroquinidine, procainamide, N-acetyl procainamide, and propranolol had no effect on lidocaine binding.

Acecainide↗
PubMed1981

Bioavailability of N-acetylprocainamide from mixed diet in rats.

The purpose of this study was to determine the bioavailability of N-Acetylprocainamide (NAPA) from mixed diet in rats. Six groups of 8 male Charles River CD rats received NAPA-HCl as follows: Group I, an intravenous dose (mean 21 mg) of 14C-labelled drug. Group II, in a solution given by oral gavage with and without feed (50 mg) in a two-way crossover fashion. Groups III-VI, incorporated in diet (42-68 mg). Urine and feces were collected for 48 hours and assayed for NAPA and procainamide by a specific HPLC method. On the average, 73% of the drug was eliminated unchanged in urine. Only a small percentage (3-4%) of the intact drug was recovered in feces after intravenous or oral administration. There were no detectable levels of procainamide in urine and feces. The absolute bioavailability of NAPA from oral solution with and without feed was 87 and 90%, respectively, and from the mixed diet was 84-92%. There was no statistically significant difference between the bioavailability of NAPA from solution in fasted and fed rats or from NAPA-mixed diet, indicating that the absorption of the drug in rats was not affected by food. The relative bioavailability of the drug from mixed diet ranged from 94-103%.

Acecainide↗
PubMedDate not supplied

[Effects of several anti-arrhythmia agents on excitability and conduction depressed by digitalis agents].

Digitalis intoxication is characterized by the appearance of most of the types of severe arrhythmias described and also by important disturbances of cardiac excitability and impulse propagation. Most of the antiarrhythmic agents that are used in the treatment of these conditions also depress excitability and impulse propagation. These characteristics are frequently responsible of severe complications. The purpose of this paper is to determine the type of interactions that exist between digitalis and some antiarrhythmic agents, and compare them with the effects of magnesium. The experiments were done in several groups, of dogs anesthetized with pentobarbital and with the chest open. Excitability, conduction time and functional refractory period were determined using the classical methods. The protocol used consisted in the comparison of the actions of toxic doses of digitalis on excitability and conduction times of the atrial and ventricular tissues, under control conditions and in the presence of therapeutic doses of procainamide, lidocaine and magnesium. The results showed that procainamide worsened the depression of excitability and conduction produced by digitalis intoxication, while lidocaine does not add to the digitalis effects and in some cases it produces a partial improvement of these parameters. Magnesium completely reverts the effects on excitability and conduction. These results provide us with rational pharmacological bases for the treatment of digitalis intoxication and suggest that magnesium could be very useful in the management of patients with severe digitalis intoxication.

Animals↗
PubMed1981

[The influence of several membrane stabilizing drugs on the induced hereditary myotonia--a methodic way to test the effectiveness of drugs on myotonia (author's transl)].

The therapeutic effectiveness of several membrane stabilizing drugs was investigated on experimentally induced myotonia by 2,4-Dichlorophenoxyacetate (2,4-D) and in 20 patients with myotonia congenita. Procainamide and quinine showed a better antimyotonic effect in-vitro- as well as in-vivo-experiments on the cold blood muscle and the rat than Sparteine sulfate and Tachmaline (Ajmalin). The two last-mentioned drugs had nearly the same effect. Because of these experimental results only procainamide and sparteine sulfate were clinically used. Quinine was not used because of the well known side-effects. Mention is made of the fact, that the therapeutic effect depends on the dose or the concentration. The results support not only the theoretic considerations on the pathogenesis of myotonia but also recommend to carry out further pharmacological investigations with this method.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1984

[Effect of membrane-effective drugs (anti-arrhythmia agents) on acoustically evoked brain-stem potentials].

Lidocaine, Mexiletine, Procainamide, and Phenytoin were administered intravenously to anaesthesized rabbits. BERA alterations showed two different patterns. If the intoxication dose was exceeded, amplitude depression, threshold elevation, desynchronization, and severe cumulative prolongation of all latencies and interpeak latencies appeared. Below this dose Lidocaine and Mexiletine induced a single, reversible, dose related, cumulative prolongation of all latencies and interpeak latencies. Procainamide induced counterrelated shiftings of interpeak latencies I-III and III-V, whereas Phenytoin showed no influence. One should, therefore, take into account these effects when BERA is used clinically, since otherwise serious errors can occur. On the other hand, there are diagnostic and therapeutic aspects for the tinnitus patient.

Animals↗
PubMed1981

Drug-polymer combinations. Part 1: The preparation of sustained release drugs by combination with ion exchanging resins.

The preparation of procainamide and propranolol resinates is described. By in vivo experiments with propranolol resinate as model substance the release rate as a function of crosslinking degree and particle size is studied. An in vitro test is carried out to compare the performance as prolonged release preparation of a resinate, e.g. procainamide resinate, with the action of the pure drug and of a Durette formulation.

Delayed-Action Preparations↗
PubMedDate not supplied

The influence of selected antiarrhythmic drugs on the hemodynamic parameters in rabbits during anesthesia. Part I. Propofol anesthesia.

Cardiac arrhythmia can be a serious complication during general anesthesia. On the other hand, there is a need for general anesthesia of patients suffering from cardiac arrhythmias and using antiarrhythmic drugs. The aim of the present experiments was to establish the way in which procainamide, N-acetyl-procainamide, verapamil and propranolol influence hemodynamic parameters of rabbits during propofol anesthesia. The experiments were performed on rabbits. Heart rate was counted from ECG. Blood pressure was measured directly in the carotid artery. Cardiac output, stroke volume, and total peripheral resistance were estimated using the method of human Cr51 albumin dilution. Hepatic blood flow was estimated after single injection of 99mTc/Sn Hepida. Renal blood flow was estimated after a single injection of 125J-hippurate. Propofol decreases renal and hepatic blood flows, decreases blood pressure and peripheral vascular resistance. Propranolol given alone or in combination with propofol decreases hepatic blood flow. The administration of antiarrhythmic drugs during propofol anesthesia decreases renal blood flow. Propofol decreases blood pressure in rabbits as a result of decreased peripheral vascular resistance. It also decreased RBF and HBF. Disadvantages of interactions of propofol and antiarrhythmic drugs concern mainly with RBF and HBF. Propranolol (given alone or in combination with propofol) strongly decreases HBF. NAPA given during P anesthesia exerts a weaker effect on HBF. The administration of antiarrhythmic drugs during propofol anesthesia decreases RBF. The strongest disadvantageous action is exerted by propranolol, the slightest one--by verapamil.

Anesthetics, Intravenous↗
PubMedDate not supplied

The influence of selected antiarrhythmic drugs on the hemodynamic parameters in rabbits during anesthesia. Part II. Thiopental anesthesia.

The aim of the study was to investigate the combined influence of thiopental and antiarrhythmic drugs: procainamide, N-acetylprocainamide, verapamil or propranolol on hemodynamic parameters in rabbits: arterial blood pressure, heart rate, cardiac output, stroke volume, peripheral vascular resistance, renal and hepatic blood flows. Propranolol used during thiopental anesthesia deepened the decrease of hepatic and renal blood flow resulting from the action of the anesthetic drug. Verapamil in a dose that did not change hepatic blood flow caused significant decrease of that parameter during thiopental anesthesia. Other hemodynamic changes observed after administration of antiarrhythmic drugs during thiopental anesthesia are essentially similar to those resulting from the action of antiarrhythmic drugs alone. The administration of procainamide or N-acetylprocainamide during thiopental anaesthesia in rabbits had no significant influence on hemodynamic changes evoked by thiopental alone. Verapamil injected to rabbits together with thiopental caused a significant decrease of blood flow in the liver, which was not observed after thiopental alone or verapamil alone. Propranolol injection together with thiopental caused a decrease of blood pressure, heart rate, cardiac output but an increase of vascular peripheral resistance, which was similar to the action of propranolol alone. Propranolol administered during thiopental anesthesia caused a significant decrease of the renal and hepatic blood flow, more marked than after the injection of that beta-blocker alone.

Anesthetics, Intravenous↗
PubMed2006

St. John's wort does not interfere with therapeutic drug monitoring of 12 commonly monitored drugs using immunoassays.

St. John's wort, a popular herbal remedy for depression, is known to interact with many Western drugs because of the ability of its components to induce liver enzymes. Lower concentrations of various drugs due to increased clearance have been reported. Because immunoassays are commonly used in clinical laboratories for therapeutic drug monitoring, we studied the potential interference of St. John's wort with commonly monitored therapeutic drugs. Drug-free serum pools were supplemented with St. John's wort to achieve in vitro St. John's wort concentrations mimicking in vivo concentrations after both recommended use and overdose. Concentrations of digoxin, tricyclic antidepressants (TCAs), phenytoin, carbamazepine, theophylline, valproic acid, quinidine, phenobarbital, procainamide, and N-acetyl procainamide were measured in serum. Pooled serum specimens from patients who were taking a particular drug were also supplemented in vitro with concentrations of St. John's wort to investigate whether observed concentrations changed after supplementation with St. John's wort. The effect of St. John's wort on cyclosporine and tacrolimus (FK 506) was studied in whole blood. We found no significant interference from St. John's wort with any assay studied. Moreover, when drug-free serum was supplemented with very high concentrations of hypericin (2 microg/mL) and hyperforin (2 microg/mL) pure standard, we observed no apparent drug level with any immunoassay. The presence of both hypericin and hyperforin was also confirmed by thin layer chromatography (TLC) in both preparations of St. John's wort. We conclude that immunoassays may be used to measure levels of therapeutic drugs in patients who self-medicate with St. John's wort.

Antidepressive Agents, Tricyclic↗
PubMed1985

Recognition of fetal arrhythmias by echocardiography.

Fetal arrhythmias were detected in 33/198 high risk pregnancies from 21 weeks to term. Using the two-dimensional echocardiographic image of the fetal heart as a guide, the M-mode beam was directed to define the motion of the ventricular and atrial walls and atrioventricular valve or semilunar valves. Atrial contraction was defined either by the atrial wall motion or from the A-point of the atrioventricular valve. Ventricular contraction was defined by closure of the atrioventricular valve (C-point), the onset of ventricular wall contraction, or from the semilunar valve opening. Ladder diagrams of the sequence of atrial and ventricular activation were constructed to define the temporal sequence of these events. Premature atrial contractions were present in 12. In one fetus this arrhythmia converted into supraventricular tachycardia while in the other 11 fetuses the course was benign. Two fetuses had premature ventricular contractions. Supraventricular tachycardia was noted in five fetuses. One with hydrops at 29 weeks returned to sinus rhythm following maternal administration of procainamide. A second hydropic fetus with paroxysmal atrial tachycardia and hydrops failed to respond to digitalis, propranolol, procainamide, verapamil, or amiodarone, and died shortly after cesarean section. Two mature fetuses had tachycardia close to term and were treated after cesarean section. One fetus with runs of atrial tachycardia died in utero. Three fetuses had complete heart block, two of whom were from mothers with connective tissue diseases. In four fetuses, there was bradycardia of less than 100/minute lasting more than 30 seconds, but these episodes disappeared in 2 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1977

Effect of shear mixing on in vitro drug release of capsule formulations containing lubricants.

The influence of shear mixing on the in vitro dissolution properties of several experimental capsule formulations containing lubricants was investigated. The studies were carried out in 2.8-liter laboratory V-blender equipped with a high-speed intensifier bar, using nitrofurantoin and procainamide hydrochloride as active drugs, powdered lactose and starch as excipients, and magnesium stearate and magnesium lauryl sulfate as lubricants. These studies revealed a pronounced inhibitory effect on drug dissolution due to shear in powder mixtures containing magnesium stearate; even at the maximum lubricant level of only 2%, high mixing markedly altered the in vitro dissolution rate. In systems with magnesium lauryl sulfate, the shear effect was less pronounced (nitrofurantoin blends) or absent (procainamide hydrochloride blends). The poor dissolution characteristics noted with magnesium stearate--shear combinations seem to result from the formation of a hydrophobic film around the powder mass, preventing wetting and deaggregation.

Capsules↗
PubMed1988

Efficacy of phenytoin in suppressing inducible ventricular tachyarrhythmias.

We examined the efficacy of phenytoin in 69 of 87 consecutive patients undergoing serial electrophysiologic studies for inducible sustained ventricular tachycardia or fibrillation (VT/VF). In general, during the initial session lidocaine and procainamide were tested immediately after baseline electrophysiologic evaluation, followed by phenytoin and quinidine during the next two sessions, and then by additional drugs as needed. Once a successful drug was identified, all testing was stopped. Drugs that had failed in prior empiric trials were not tested. Twenty-five of the 87 patients (28.7%) had success in 258 serial drug tests. Sixty-nine patients were tested on phenytoin (mean serum level 13.4 +/- 5.0 mg/L), 52 after oral loading, and 17 after intravenous loading; the remaining 18 had either had prior successful testing with other drugs (9 patients) or had prior empiric failures with phenytoin (9 patients) or had prior empiric failures with phenytoin (9 patients). Nine of the 69 phenytoin trials were successful (13.0%), compared to 8 of 57 trials (14.0%) with procainamide, 4 of 37 trials (10.8%) with quinidine, and 0 of 41 trials (0%) with lidocaine. All nine patients who had successful phenytoin trials tolerated chronic doses adequate to maintain serum phenytoin levels equivalent to those measured during successful drug testing. For the 25 patients with successful drug trials, the mean follow-up was 14.5 +/- 9.8 months, and the actuarial incidence or recurrent VT/VF was 7 +/- 5% at 12 months. For the nine patients who had success with phenytoin the mean follow-up was 18.4 +/- 11.7 months, and the 12-month actuarial recurrence was 0%. Phenytoin is a well tolerated drug whose efficacy appears similar to most standard antiarrhythmic agents. If our results are confirmed in a larger, randomized study, routine testing with phenytoin should be considered.

Anti-Arrhythmia Agents↗
PubMed1992

Slow-to-fast transformation of denervated soleus muscle of the rat, in the presence of an antifibrillatory drug.

The myofibrillar changes of rat denervated soleus muscle were studied in the presence and in the absence of an antifibrillatory drug. After bilateral sciaticotomy, a concentrated solution of procainamide hydrochloride was steadily released, by way of a miniosmotic pump, in the space between the soleus and the gastrocnemius muscles of one leg. Fibrillation activity of soleus muscles was checked electromyografically at 3- to 5-day intervals. On the 21st day following denervation the muscles were excised, stained for adenosine triphosphatase activity and analysed for myosin heavy chain (MHC) isoforms. In the denervated-procainamide-treated muscles fibrillation was consistently (-75% on average) depressed in comparison to the contralateral denervated muscles. Type 1 (slow) fibres and MHC isoform were also significantly reduced, to the advantage of type 2A (fast) fibres and MHC isoform. The results support the view that denervation inactivity, like other kinds of muscle inactivity, favours the expression of fast type myofibrillar isoforms, and that this effect is counteracted, at least partially, by the spontaneous activity of the denervated muscle.

Animals↗
PubMed1994

Impairment of raw 264.7 macrophage function by antiarrhythmic drugs.

The effect of the antiarrhythmic drugs lidocaine, quinidine and procainamide on macrophage function was investigated in RAW 264.7 mouse monocytic macrophage cell. Cells stimulated by either zymosan or phorbol ester were found to generate both superoxide (O2-) and H2O2. The production of O2 was detected as superoxide dismutase inhibitable ferricytochrome c reduction. H2O2 production was monitored in both chemical and flow cytometric fluorescent assays. Although all three drugs inhibited both O2 and H2O2 release in a dose-dependent manner, only quinidine was found to have significant inhibitory effects. The amounts of quinidine required to cause a 50% inhibition in O2 production in zymosan and phorbol ester stimulated cells were found to be 250 microM and 300 microM, respectively and the amounts required to cause one-half optimum levels of H2O2 production in these cells were found to be 50 microM and 100 microM, respectively. The effect of these drugs on O2 producing NADPH oxidase was investigated and only procainamide was found to have a significant effect (p < 0.001) in inhibiting the oxidase activity. Lidocaine and quinidine had no significant effect on the activation of the respiratory burst oxidase. A sensitive and convenient 'differential phagocytosis' assay was devised on the basis of number of particles engulfed by individual phagocytes using flow cytometric techniques. It appears to be remarkably free of interference and was applied to investigate the role of antiarrhythmic drugs on the phagocytosis of fluorescent latex beads. All three antiarrhythmic drugs inhibited phagocytosis of latex beads in a dose dependent manner irrespective of the number of particles phagocitized by the cells. The results of these studies do not conclusively establish a mechanism of action of these drugs on the generation of O2 and H2O2 by stimulated macrophages; nevertheless, it is interesting that all three drugs inhibited the phagocytic activity.

Animals↗
PubMed1985

Canine digitalis arrhythmia as a model for detecting Na-channel blocking antiarrhythmic drugs: a comparative study using other canine arrhythmia models and the new antiarrhythmic drugs, propafenone, tocainide, and SUN 1165.

Antiarrhythmic effects of three new drugs, propafenone, tocainide, and SUN 1165, were examined using three canine ventricular arrhythmia models, i.e., digitalis, adrenaline and two-stage coronary ligation arrhythmias. The effects of procainamide, disopyramide, lidocaine, and phenytoin, class 1 antiarrhythmic drugs, on digitalis arrhythmia were also examined. The minimum effective plasma concentrations of all these drugs for each arrhythmia model were determined for a quantitative comparison. Propafenone and tocainide suppressed all the arrhythmias, while SUN 1165 suppressed digitalis and coronary ligation arrhythmias. The minimum effective plasma concentrations of propafenone for digitalis, adrenaline, 24-h coronary ligation, and 48-h coronary ligation arrhythmias were 1.8 +/- 0.7, 0.58 +/- 0.20, 3.5 +/- 0.3, and 3.6 +/- 0.9 micrograms/ml, respectively, and those of tocainide were 6.2 +/- 2.1, 23.7 +/- 9.0, 11.4 +/- 0.5, and 8.6 +/- 2.9 micrograms/ml, respectively (mean +/- standard deviation, n = 6-7). The minimum effective concentrations of SUN 1165 for digitalis, 24-h coronary ligation, and 48-h coronary ligation arrhythmias were 0.92 +/- 0.19, 2.5 +/- 0.4, and 1.2 +/- 0.4 micrograms/ml. The minimum effective concentrations for digitalis arrhythmias were 1.7 +/- 0.4 micrograms/ml for disopyramide, 10.1 +/- 2.4 micrograms/ml for procainamide, 3.5 +/- 1.6 micrograms/ml for lidocaine, and 11.3 +/- 3.0 micrograms/ml for phenytoin. Digitalis arrhythmia seems to be a useful model for detecting class 1 drugs, as it was suppressed by all the class 1 Na-channel blocking antiarrhythmic drugs, while class 2 beta adrenergic blockers and class 4 Ca-channel blockers had no effect. Also, not all the class 1 drugs suppressed coronary ligation and adrenaline arrhythmias.

Animals↗
PubMed1999

Negative chronotropic and inotropic effects of class I antiarrhythmic drugs assessed in isolated canine blood-perfused sinoatrial node and papillary muscle preparations.

The present study was designed to assess the negative chronotropic and inotropic effects of 10 class I antiarrhythmic drugs, using isolated canine blood-perfused sinoatrial node and papillary muscle preparations. Each drug showed negative chronotropic and inotropic effects in a dose-related manner. The potency of the suppressive effect on the sinoatrial automaticity was in the order of aprindine, quinidine, flecainide, lidocaine, mexiletine, cibenzoline, disopyramide, procainamide, tocainide, and phenytoin, while the effect on the ventricular contraction was in the order of aprindine, flecainide, cibenzoline, lidocaine, mexiletine, disopyramide, tocainide, phenytoin, quinidine, and procainamide. The differences in the suppressive effects could not necessarily be explained by their subclassification, based either on action potential duration or kinetic properties of dissociation or association with sodium channels. On the other hand, we found a good correlation between the negative inotropic effects of class I drugs in this study and the canine antiarrhythmic plasma concentrations for the digitalis- and coronary ligation-induced ventricular arrhythmia models in our previous studies. However, the negative chronotropic effects of the drugs showed a poor correlation with the antiarrhythmic plasma drug concentrations. The data shown in this paper may provide a convenient guideline for predicting acute cardiosuppressive effects of antiarrhythmic drugs, especially in patients with reduced cardiac function.

Animals↗
PubMed2005

Class I antiarrhythmics inhibit Na+ absorption and Cl- secretion in rabbit descending colon epithelium.

To clarify the mechanism of the diarrhea associated with the clinical use of antiarrhythmic drugs we assessed the effects of these agents on transepithelial Na+ absorption and Cl- secretion, on basolateral K+ conductance, and on the properties of single basolateral K+ channels of rabbit colon epithelium. Quinidine and propafenone, both at 10 microM, inhibited Na+ absorption by 27 and 38% respectively, compared with 50% with 5 mM Ba2+. The other tested class I antiarrhythmics disopyramide, mexiletine, lidocaine, and flecainide decreased Na+ current by 9-13%. Procainamide and the class III antiarrhythmics N-acetylprocainamide, sotalol, ibutilide, and amiodarone were no or were very weak inhibitors of Na+ absorption. Cl- secretion, stimulated with the adenosine analogue NECA (5'-N-ethylcarboxamide-adenosine), was reduced by 54% with quinidine and by 29% with propafenone compared with 100% with Ba2+. Mexiletine, lidocaine, and flecainide inhibited Cl- secretion by 10-23%, whereas the class III antiarrhythmics were no or were weak inhibitors. Those antiarrhythmics that inhibited Na+ and Cl- transport also reduced basolateral K+ conductance, determined in amphotericin B permeabilized epithelia. The activity of the high-conductance, Ca2+-activated, voltage-dependent K+ (BK(Ca)) channel, which is primarily responsible for basolateral K+ recycling during Na+ absorption, was inhibited by 10-30 microM quinidine or propafenone in the form of a rapidly dissociating block. Mexiletine and flecainide inhibited the single channel conductance at higher concentrations; disopyramide, lidocaine, and procainamide were ineffective. In conclusion, the present evidence suggests that the diarrhea caused by class I antiarrhythmic drugs such as quinidine and propafenone is a result of a reduction in basolateral K+ conductance and inhibition of BK(Ca) channels, thereby impeding transepithelial Na+ and water absorption.

Animals↗
PubMedDate not supplied

Medications used to manage supraventricular tachycardia in the infant a North American survey.

Supraventricular tachycardia is the most common pediatric arrhythmia, but there is no consensus and little evidence to guide its treatment. We sent a questionnaire to pediatric cardiologists in North America to assess the current practice pattern. Of 1534 surveys mailed, 352 (23%) were returned and 295 (19%) had complete data for analysis. In the acute setting, 11 different medications were chosen. The most commonly used in the infant without preexcitation were digoxin (42%), procainamide (21%), esmolol (13%), propranolol (10%), and amiodarone (8%). In the infant with preexcitation, propranolol (34%), procainamide (23%), esmolol (17%), amiodarone (11%), and digoxin (6%) were used. In the chronic setting, 8 different medications were chosen. The most commonly used in this scenario were digoxin (52%), propranolol (33%), amiodarone (4%), and sotalol (3%). In the infant with preexcitation, propranolol (70%), amiodarone (6%), digoxin (6%), atenolol (6%), and flecainide (5%) were used. Medication choices were influenced by additional electrophysiology training and preexcitation. Digoxin was used less in the setting of preexcitation. There are no comparative trials to explain the different medication choices. Although a number of medications may be efficacious, a randomized clinical trial is needed to offer further guidance.

Acute Disease↗