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PubMed1983

[Serum level of digoxin and digitoxin and glomerular filtration rate in hyper- and hypothyroidism].

In a comparative prospective study the serum levels of digoxin and digitoxin and the glomerular filtration of the kidneys were determined radioimmunologically in thyroid function disorders using the endogenous creatinine clearance and the 51Cr-EDTA clearance. Compared to a euthyroid control group 17 patients with hyperthyroidism showed a decreased and 5 patients with hypothyroidism showed a largely toxic digoxin level, both groups being on a maintenance therapy of 0.25 mg digoxin b. i. d. During an oral maintenance therapy of daily 0.1 mg digitoxin unchanged therapeutic serum levels were found in 35 hyperthyroid and 18 hypothyroid patients when compared to a euthyroid control group. Assessment of clearances showed that glomerular filtration rates were clearly increased in the hyperthyroid and lowered in the hypothyroid patients. Renewed assessment of the clearance in four hyperthyroid patients and three with hypothyroidism after thyroid recompensation showed a marked decrease of clearance values in hyperthyroidism and an increase in hypothyroidism. Increased clearance values in hyperthyroidism were associated with lowered digoxin serum levels. In contrast, lowered clearance values in hypothyroidism were accompanied by increased serum digoxin levels. There was no such association detectable for digitoxin.

Adult↗
PubMed1978

Relation between plasma and red-cell electrolyte concentrations and digoxin levels in children.

We determined alterations in plasma and red-cell electrolyte concentrations associated with digoxin administration in 11 children in heart failure, 24 nontoxic patients receiving maintenance digoxin and 11 children in whom digoxin toxicity developed. Twenty normal children served as controls. Digoxin therapy was associated with a mean (+/- S.E.M.) increase in red-cell sodium from a pretreatment level of 6.2 +/- 0.7 meq per liter to 11.9 +/- 1.2 meq per liter and a decrease in red-cell potassium from 105.4 +/- 1.4 to 99.5 +/- 1.9 meq per liter (P less than 0.001). The red-cell sodium levels of toxic patients exceeded those of nontoxic patients whereas the potassium concentrations were lower (P less than 0.001). Toxic patients manifested significantly higher ratios of red-cell sodium to red-cell potassium (0.213 +/- 0.003) than nontoxic patients (0.085 +/- 0.008; P less than 0.001). Changes in red-cell electrolytes are sensitive indicators of digoxin affects.

Adolescent↗
PubMed2002

Modulation of steady-state kinetics of digoxin by haplotypes of the P-glycoprotein MDR1 gene.

OBJECTIVE: We investigated the effect of polymorphisms in the P-glycoprotein (P-gp) MDR1 gene on steady-state pharmacokinetics of digoxin in Caucasians. According to earlier data, homozygous TT of the exon 26 complementary deoxyribonucleic acid (cDNA) 3435C>T polymorphism was associated with low P-gp expression in the human intestine. METHODS: Eight healthy male homozygous carriers of the wild-type exon-26 3435C>T (CC), 8 heterozygous subjects (CT), and 8 homozygous mutant (TT) subjects were selected. Seven further MDR1 polymorphisms were determined. Digoxin was administered orally twice daily on the first two study days; on days 3 to 5, 0.25 mg was given in the morning. On day 5, kinetic parameters were analyzed for genotype-phenotype and haplotype-phenotype relationships. RESULTS: The area under the plasma concentration-time curve from time zero to 4 hours [AUC(0-4)] (P =.042) and C(max) (P =.043) values of digoxin were higher in subjects with the 3435TT genotype than in those with the 3435CC. No influence of other single nucleotide polymorphisms (SNPs) on digoxin parameters was detected. Comparison of genotypes deduced from SNPs 2677G>T (exon 21) and 3435C>T revealed significant differences for AUC(0-4) (P =.034) and C(max) (P =.039), which were substantiated by haplotype analysis. Haplotype 12 (2677G/3435T), which had a frequency of 13.3% in a randomly drawn Caucasian sample (n = 687), was associated (Mann-Whitney test) with higher AUC(0-4) values (P =.009) than were found in noncarriers (mean +/- SD, 5.7 +/- 0.9 microg. h/L [n = 7] versus 4.8 +/- 0.9 microg. h/L [n = 17]). Haplotype 11 (2677G/3435C) had lower AUC(0-4) values (P =.013) compared with those of noncarriers (mean +/- SD, 4.7 +/- 0.9 microg. h/L [n = 16] versus 5.6 +/- 0.9 microg. h/L [n = 8]). Results of haplotype analysis match data of other MDR1 studies. CONCLUSION: Haplotype 12 codes for high values of AUC(0-4) and C(max) of orally administered digoxin. Analysis of MDR1 haplotypes is superior to unphased SNP analysis to predict MDR1 phenotype.

Animals↗
PubMed2000

A prospective, randomized controlled trial comparing the efficacy and safety of sotalol, amiodarone, and digoxin for the reversion of new-onset atrial fibrillation.

STUDY OBJECTIVE: A prospective, randomized controlled trial of new-onset atrial fibrillation was conducted to compare the efficacy and safety of sotalol and amiodarone (active treatment) with rate control by digoxin alone for successful reversion to sinus rhythm at 48 hours. METHODS: We prospectively randomly assigned 120 patients with atrial fibrillation of less than 24 hours' duration to treatment with sotalol, amiodarone, or digoxin using a single intravenous dose followed by 48 hours of oral treatment. Patients had ECG monitoring for 48 hours, and time of reversion, adequacy of rate control, and numbers of adverse events were compared. After 48 hours, those still in atrial fibrillation underwent cardioversion according to a standardized protocol. After 48 hours of therapy and attempted cardioversion, the number of patients whose rhythms had successfully reverted were compared. RESULTS: There was a significant reduction in the time to reversion with both sotalol (13. 0+/-2.5 hours, P <.01) and amiodarone (18.1+/-2.9 hours, P <.05) treatment compared with digoxin only (26.9+/-3.4 hours). By 48 hours, the active treatment group was significantly more likely to have reverted to sinus rhythm than the rate control group (95% versus 78%, P <.05; risk ratio 5.4, 95% confidence interval [CI] 1.5 to 19.2 ). In those patients whose rhythms did not revert to sinus rhythm, there was superior ventricular rate control in the sotalol group at both 24 and 48 hours compared with those who received either amiodarone or digoxin. There were also fewer adverse events in the active treatment group compared with the rate control group. CONCLUSION: Immediate pharmacologic therapy for new-onset atrial fibrillation with class III antiarrhythmic drugs (sotalol or amiodarone) improves complication-free 48-hour reversion rates compared with rate control with digoxin.

Aged↗
PubMed2000

Specificity of the stress electrocardiogram during adenosine myocardial perfusion imaging in patients taking digoxin.

BACKGROUND: In patients taking digoxin, the exercise electrocardiogram has a lower specificity for detecting coronary artery disease. However, the effect of digoxin on adenosine-induced ST-segment depression is unknown. The purpose of this study was to evaluate the specificity of the electrocardiogram during adenosine myocardial perfusion imaging in patients taking digoxin. METHODS: Between May 1991 and September 1997, patients (n = 99) taking digoxin who underwent adenosine stress imaging with thallium-201 or technetium-99m sestamibi and coronary angiography within 3 months were retrospectively identified. Exclusion criteria included prior myocardial infarction, coronary artery angioplasty or bypass surgery, left bundle branch block, paced ventricular rhythm, or significant valvular disease. Twelve-lead electrocardiograms were visually interpreted at baseline, during adenosine infusion, and during the recovery period. The stress electrocardiogram was considered positive if there was > or =1 mm additional horizontal or downsloping ST-segment depression or elevation 0.08 seconds after the J-point compared with the baseline tracing. RESULTS: ST-segment depression and/or elevation occurred in 24 of 99 patients. There were only 2 false-positive stress electrocardiograms, yielding a specificity of 87% and positive predictive value of 92%. All 8 patients with > or =2 mm ST segment depression had multivessel disease by coronary angiography. CONCLUSIONS: ST-segment depression or elevation during adenosine myocardial perfusion imaging in patients taking digoxin is highly specific for coronary artery disease. Marked (> or =2 mm) ST-segment depression and/or ST-segment elevation is associated with a high likelihood of multivessel disease.

Adenosine↗
PubMed2004

Isolation and characterization of a digoxin transporter and its rat homologue expressed in the kidney.

Digoxin, which is one of the most commonly prescribed drugs for the treatment of heart failure, is mainly eliminated from the circulation by the kidney. P-glycoprotein is well characterized as a digoxin pump at the apical membrane of the nephron. However, little is known about the transport mechanism at the basolateral membrane. We have isolated an organic anion transporter (OATP4C1) from human kidney. Human OATP4C1 is the first member of the organic anion transporting polypeptide (OATP) family expressed in human kidney. The isolated cDNA encodes a polypeptide of 724 aa with 12 transmembrane domains. The genomic organization consists of 13 exons located on chromosome 5q21. Its rat counterpart, Oatp4c1, is also isolated from rat kidney. Human OATP4C1 transports cardiac glycosides (digoxin, K(m) = 7.8 microM and ouabain, K(m) = 0.38 microM), thyroid hormone (triiodothyronine, K(m) = 5.9 microM and thyroxine), cAMP, and methotrexate in a sodium-independent manner. Rat Oatp4c1 also transports digoxin (K(m) = 8.0 microM) and triiodothyronine (K(m) = 1.9 microM). Immunohistochemical analysis reveals that rat Oatp4c1 protein is localized at the basolateral membrane of the proximal tubule cell in the kidney. These data suggest that human OATP4C1/rat Oatp4c1 might be a first step of the transport pathway of digoxin and various compounds into urine in the kidney.

Amino Acid Sequence↗
PubMed1988

Variable region framework differences result in decreased or increased affinity of variant anti-digoxin antibodies.

Rare spontaneous variants of the anti-digoxin antibody-producing hybridoma 40-150 (Ko = 5.4 x 10(9) M-1) were selected for altered antigen binding by two-color fluorescence-activated cell sorting. The parent antibody binds digoxin 890-fold greater than digitoxin. The variant 40-150 A2.4 has reduced affinity for digoxin (Ko = 9.2 x 10(6) M-1) and binds digoxin 33-fold greater than digitoxin. A second-order variant, derived from 40-150 A2.4 (designated 40-150 A2.4 P.10), demonstrated partial regain of digoxin binding (Ko = 4.4 x 10(8) M-1). The altered binding of the variant 40-150 A2.4 was accounted for by a point mutation resulting in substitution of arginine for serine at position 94 in the heavy chain variable region. Antibody 40-150 A2.4 P.10 also contains this arginine but owes its enhanced antigen binding to deletion of two amino acids from the heavy chain amino terminus. This unusual sequence alteration in an immunoglobulin framework region confers increased affinity for antigen.

Amino Acid Sequence↗
PubMed2003

Hypothalamic digoxin and hemispheric chemical dominance--relation to the pathogenesis of senile osteoporosis, degenerative osteoarthritis, and spondylosis.

The isoprenoid pathway produces three key metabolites: i) digoxin (a membrane sodium-potassium ATPase inhibitor which can regulate intracellular calcium/magnesium ratios), ii) dolichol (which regulates N-glycosylation of proteins), and iii) ubiquinone (a free radical scavenger), all of which are important in bone and joint metabolism. The pathway was assessed in senile osteoporosis, spondylosis, and osteoarthritis. Digoxin could possibly play a role in the genesis of cerebral dominance because it can regulate multiple neurotransmitter systems. The pathway was also assessed in individuals of differing hemispheric dominance for comparison and to find out the role of cerebral dominance in the pathogenesis of these diseases. The plasma/serum-activity of HMG CoA reductase, magnesium, digoxin, dolichol, ubiquinone, and tryptophan/tyrosine catabolic patterns, as well as RBC Na(+)-K+ ATPase activity, were measured in the above mentioned groups. The glycoconjugate metabolism, free radical metabolism, and membrane composition were also studied. The pathway was upregulated with increased digoxin synthesis in patients with spondylosis and osteoarthritis. In this group of patients, the glycoconjugate levels and dolichol levels were increased and lysosomal stability reduced. The ubiquinone levels were low and free radicals increased in spondylosis and osteoarthritis. On the other hand, in senile osteoporosis, the isoprenoid pathway was downregulated and digoxin synthesis reduced. The glycoconjugate and dolichol levels were low and lysosomal stability increased. The ubiquinone levels were increased and free radical production increased in senile osteoporosis. The significance of these changes in the pathogenesis of osteoarthritis, spondylosis, and osteoporosis is discussed. The hyperdigoxinemic state is seen in osteoarthritis and spondylosis and in right hemispheric dominance. The hypodigoxinemic state is seen in left hemispheric dominance and senile osteoporosis. Hemispheric dominance plays a crucial role in deciding the predisposition to bone and joint diseases. Right hemispheric chemical dominance predisposes to spondylosis and osteoarthritis. Left hemispheric chemical dominance predisposes to osteoporosis.

Digoxin↗
PubMed2003

Hypothalamic digoxin, hemispheric chemical dominance, and inflammatory bowel disease.

The isoprenoid pathway produces three key metabolites--endogenous digoxin, dolichol, and ubiquinone. It was considered pertinent to assess the pathway in inflammatory bowel disease (ulcerative colitis and regional ileitis). Since endogenous digoxin can regulate neurotransmitter transport, the pathway and the related cascade were also assessed in individuals with differing hemispheric dominance to find out the role of hemispheric dominance in its pathogenesis. All the patients with inflammatory bowel disease were right-handed/left hemispheric dominant by the dichotic listening test. The following parameters were measured in patients with inflammatory bowel disease and in individuals with differing hemispheric dominance: (1) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (2) tryptophan/tyrosine catabolic patterns; (3) free-radical metabolism; (4) glycoconjugate metabolism; and (5) membrane composition and RBC membrane Na+-K+ ATPase activity. Statistical analysis was done by ANOVA. In patients with inflammatory bowel disease there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, and low ubiquinone and elevated free radical levels. There was also an increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was an increase in cholesterol:phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in these groups of patients. Inflammatory bowel disease is associated with an upregulated isoprenoid pathway and elevated digoxin secretion from the hypothalamus. This can contribute to immune activation, defective glycoprotein bowel antigen presentation, and autoimmunity and a schizophreniform psychosis important in its pathogenesis. The biochemical patterns obtained in inflammatory bowel disease is similar to those obtained in left-handed/right hemispheric dominant individuals by the dichotic listening test. But all the patients with peptic ulcer disease were right-handed/left hemispheric dominant by the dichotic listening test. Hemispheric chemical dominance has no correlation with handedness or the dichotic listening test. Inflammatory bowel disease occurs in right hemispheric chemically dominant individuals and is a reflection of altered brain function.

Adult↗
PubMed1987

The effect of long-term administration of digoxin on plasma androgens and sexual dysfunction.

The effect of long-term administration of digoxin on sexual dysfunction was investigated in correlation to plasma androgens level. The patients of the experimental (digoxin-treated) and control (without digoxin) groups were of similar cardiac functional capacity and age (25-40 years) and were randomly selected from the rheumatic heart disease patients. A subjective assessment of sexual behavior was carried out, using parameters such as sexual desire, sexual excitement, and frequency of sexual relations. Personal interviews and questionnaires were also used for the evaluation of sexual behavior. The findings support various reports concerning digoxin effect on plasma levels of testosterone (the difference in the mean was significant). The effect on plasma levels of androstenedione and dehydroepiandrosterone in the experimental group as compared to the control group were not significant. Tests used to evaluate the changes in sexual behavior, showed a significant decrease in sexual desire, sexual excitement phase (erection) and frequency of sexual relations in the digoxin-treated group.

Adult↗
PubMed2002

Hypothalamic digoxin-mediated model for subacute sclerosing panencephalitis.

The isoprenoid pathway including endogenous digoxin was assessed in subacute sclerosing panencephalitis (SSPE). This was also studied for comparison in patients with right hemispheric and left hemispheric dominance. The following parameters were measured in patients with SSPE and in individuals with right hemispheric, left hemispheric and bihemispheric dominance-(a) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (b) tryptophan/tyrosine catabolic patterns; (c) free-radical metabolism; (d) glycoconjugate metabolism; and (e) membrane composition and RBC membrane Na(+)-K(+) ATPase activity. The isoprenoid pathway was upregulated with increased digoxin synthesis in patients with SSPE and in those with right hemispheric dominance. In this group of patients: (a) the tryptophan catabolites were increased and the tyrosine catabolites reduced; (b) the dolichol and glycoconjugate levels were elevated; (c) lysosomal stability was reduced; (d) ubiquinone levels were low and free-radical levels increased; and (e) the membrane cholesterol:phospholipid ratios were increased and membrane glycoconjugates reduced. On the other hand, in patients with left hemispheric dominance the reverse patterns were obtained. The upregulated isoprenoid pathway and hypothalamic digoxin are involved in the pathogenesis of SSPE. SSPE occurs in right hemispheric chemically dominant individuals and a pathogenetic model for SSPE implicating hypothalamic digoxin is proposed.

Adolescent↗
PubMed2000

Falsely elevated digoxin level of 45.9 ng/mL due to interference from human antimouse antibody.

CASE REPORT: We report the case of a 77-year-old man who was admitted to the intensive care unit with a serum digoxin level of 45.9 ng/mL. The patient was hemodynamically stable throughout his hospital course and did not require antidigoxin antibody fragments. The elevated digoxin level was determined by subsequent testing to be falsely elevated by interference from human antimouse antibodies in his serum. A repeat digoxin measurement using an assay not affected by human antimouse antibodies indicated a level of 1.3 ng/mL. Newer digoxin assays are not affected by human antimouse antibody interference, but clinicians should be aware of possible human antimouse antibody interference with older digoxin assays and in other tests utilizing mouse monoclonal antibody reagents.

Aged↗
PubMed1986

'Digoxin-like' substance in serum of elderly patients.

The Amersham Amerlex Radio-immunoassay was used to detect 'digoxin-like' substance in the sera of 37 elderly subjects, nine with renal impairment, 14 with hepatobiliary disease and 14 over-65-years-old controls with no renal or hepatic impairment. In the patients with hepatobiliary disease, digoxin-like substance was detected in 11 out of 14, the level being closely correlated with serum bilirubin (P less than 5.5 X 10(-10)) and significantly but less closely with serum alkaline phosphatase activity (P less than 10(-3)). While serum digoxin-like substance was detectable in seven out of nine patients with renal impairment, there was no correlation between the degree of renal impairment as reflected by blood urea and serum creatinine and serum digoxin-like activity. We suggest that in elderly subjects with renal impairment or hepatobiliary disease these findings should be borne in mind especially when considering digoxin toxicity.

Aged↗
PubMed1975

Significance of non-steady-state serum digoxin concentrations.

In order better to define the optimal time for sample collection, the authors examined the serial concentrations of digoxin in serum and urine of six hospitalized patients during the first 8 hours after administration of their maintenance doses of digoxin. Expressed as % of baseline value, mean serum digoxin concentrations 1/2, 1, 1 1/2, 2,4, 6, and 8 hours after administration of the drug were 167, 185, 228, 256, 175, 145, and 134%, respectively. Steady-state serum concentrations were not established until 6-8 hours after administration of the drug, and high serum values during the first 6 hours did not correlate with clinical and/or electrocardiographic evidence of digoxin toxicity. It is concluded that when serum digoxin levels are utilized as an index of digitalization or toxicity in patients on maintenance therapy, the blood samples should be drawn just prior to the daily dose and no sooner than 6 hours after administration of the drug.

Digoxin↗
PubMed1980

Digoxin- and digitoxin-induced changes in monophasic action potential of the right ventricle of the dog heart.

The effects of digitoxin and digoxin on right ventricular monophasic action potentials were studied in intact dogs during an 8 hour observation period. Pentobarbital anaesthesia was used, and monophasic action potential recordings were obtained with the suction electrode technique. Intravenous injection of 2.0 mg digitoxin to six dogs, 2.0 mg digoxin to two dogs and 1.0 mg digoxin to five dogs caused a rapid increase in the time taken for 90% repolarisation with return to control values after 20 to 30 min. A late increase in 50 and 90% repolarisation times was observed 2 to 4 h after digitoxin, while digoxin had no such effect. The late action potential prolonging effect was inversely correlated to serum concentrations in the early elimination phase (2 to 8 h after the injection) since it reached a maximum towards the end of the observation period. Digitoxin and digoxin thus differed in their late effects on ventricular monophasic action potentials in intact dogs and may possess different antiarrhythmic activity.

Action Potentials↗
PubMed1991

Endogenous plasma Na,K-ATPase inhibitory activity and digoxin like immunoreactivity after acute myocardial infarction.

PURPOSE OF INVESTIGATION: The aim was to look for the presence of circulating factor(s) with Na,K-ATPase inhibitory properties and digoxin like immunoreactivity in patients after acute myocardial infarction. DESIGN: Venous blood samples were obtained when the patients were admitted and different methods were used to monitor the plasma concentrations of factor(s) with properties of digitalis. SUBJECTS - These were 26 patients of both sexes (mean age 57.7 years, range 40-72) during the first 24 h of a first transmural acute myocardial infarct, 11 male patients with unstable angina pectoris (52.5 years, 45-67), and 18 healthy male controls (25 to 50 years). MEASUREMENTS AND MAIN RESULTS: There was significant inhibition of ouabain sensitive Na,K-ATPase in intact erythrocytes in patients with myocardial infarction [1.4(SEM 0.15)mumol Pi.mg-1.h-1] compared with patients with unstable angina pectoris [3.1(0.4), p less than 0.01] and healthy controls [3.4(0.25), p less than 0.01]. In myocardial infarction complicated by ventricular fibrillation (n = 5) Na,K-ATPase activity was significantly lower than in the other 21 patients [0.95(0.2) and 1.55(0.11) mumol Pi.mg-1.h-1 respectively, p less than 0.05]. There was no change in erythrocyte Na,K-ATPase activity in myocardial infarction complicated by acute pulmonary oedema, nor was there any difference in activity in erythrocyte ghosts obtained from the patients with myocardial infarction v healthy controls, at 0.47(0.13) v 0.50(0.02) mumol Pi.mg-1.h-1. Boiled plasma supernatants obtained from the patients with myocardial infarction inhibited Na,K-ATPase in erythrocytes from healthy subjects. This inhibitory effect was antagonised by antidigoxin antibody. Plasma inhibitory potency was correlated with erythrocyte Na,K-ATPase activity in the patients with myocardial infarction (r = -0.65, p less than 0.001, n = 23). There was a 2.5-fold increase in plasma digoxin like immunoreactivity in the patients with myocardial infarction [1.65(0.5) ng.ml-1] using DELFIA fluoroimmunoassay as compared with five healthy controls [0.04(0.12), p less than 0.05] and nine patients with unstable angina [0.48(0.11), p less than 0.05]. There was no difference in plasma digoxin like immunoreactivity in myocardial infarction complicated or not by ventricular fibrillation, but there was very low digoxin like immunoreactivity in patients with myocardial infarction complicated by acute pulmonary oedema [0.26(0.08) ng.ml-1, n = 7]. There was no correlation between plasma digoxin like immunoreactivity and either plasma Na,K-ATPase inhibitory potency or erythrocyte Na,K-ATPase activity. CONCLUSIONS: The results show that plasma factor(s) with some of the properties of digitalis are increased in acute myocardial infarction.

Adult↗
PubMed1987

Minimal doses of digoxin: a new marker for compliance to medication.

A direct and objective method of measuring compliance to medication is presented. Digoxin is used as a marker in capsules of either gemfibrozil or placebo with a minimal dose of 4.4 micrograms twice a day. Compliance is estimated by measuring the ratio of urinary digoxin to creatinine concentration. By choosing two cut-off points of this ratio patients who are taking their capsules regularly and those who have taken no capsules at all could be distinguished from others. Reduced dosage was easily detected in the marker results. During regular intake of three quarters of the dose, 53% of the samples would have classified the patient to the good compliance group. With half of the dose, 24% of samples and with a quarter of the dose, 5% of samples would have classified the subject to good compliance. Since the digoxin marker was planned for compliance measurements in the Helsinki Heart Study, a primary prevention study of coronary heart disease, it was tested under the conditions of a clinical trial. Digoxin concentrations were measured using a routine method normally applied to serum but shown to be valid for urine. The results of the urinary assays were not affected by storage at room temperature, as occurs during postal transport of samples, nor were they affected by freezing, routinely used for the storage of samples in clinical trials. The results therefore suggest that the digoxin marker represents a particularly effective method to study compliance to medication during such long-lasting clinical investigations.

Clinical Trials as Topic↗
PubMed1987

Comparison of the digoxin marker with capsule counting and compliance questionnaire methods for measuring compliance to medication in a clinical trial.

During the last quarter of the third year of follow-up in the Helsinki Heart Study, compliance to medication was measured in 1739 patients with digoxin used as a marker substance, capsule counting and a compliance questionnaire. The estimates for good and poor compliers were found to be highly dependent on the method and the cut-off points chosen for the compliance allocation. The methods studied here were more reliable for the detection of poor rather than good compliance. In the poor compliance group, defined with the use of the digoxin marker, there was 39% of subjects who returned less than 5% of their capsule dosage or reported a deviation less than 5%. In the good compliance group, defined by the digoxin marker, only 11.8% of patients either returned or reported a deviation of at least 25% of their dose. The compliance was better when measured by the questionnaire than by capsule counting. The size of the poor compliance group, defined by the use of the digoxin marker, was as large as a group who had returned at least 27% of their capsule dose and a group who had reported a deviation of 11% or more from their dosing schedule. The size of the group allocated to the good compliance category by the use of the digoxin marker was equivalent in size to a group of patients who had returned less than 15% of their prescribed dose or reported a deviation of less than 6% from their prescription. When the strictest criteria for the combination of all three methods were used, 57% of subjects were classified as good and 31% as poor compliers to medication in the third year of the primary prevention trial designed to reduce the incidence of coronary heart disease.

Capsules↗