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At least 19 recordsLinked to original sources
PubMed1975

Drug-biomolecule interactions: drug toxicity and vitamin coenzyme depletion.

Thirteen pyridine compounds, phenylbutazone, and three salicylates were studied for their effects upon the turnover of 7-14C-nicotinamide dinucleotides in the mouse. The compounds were administered at equitoxic doses (LD25) to 7-14C-nicotinic acid- (niacin) pretreated mice, and the induced excretion of urinary-14C was analyzed in terms of total 14C and percentage of total 14C as known metabolites of nicotinic acid. Of the 17 compounds, 12 afforded significant alterations in the total 14C excreted and five of these caused alterations in the disposition of the 7-14C-nicotinamide endogenously liberated from the 7-14C-nicotinamide adenine dinucleotide pool. Comparative depletions of 14C from brain, lungs, liver, and kidneys were studied with 10 of the pyridine compounds. Several tissues were found to be the sources of the urinary-14C, with the lungs being the most accessible source. Some compounds had effects at doses less than the LD25's, as shown by increased hexobarbital sleeping time in acute experiments with rats. These pyridine compounds were initially considered to act at the level of the nicotinamide dinucleotides in the normal biosynthetic pathway (nicotinic acid site) and/or at the level of glycohydrolase (nicotinamide site). In view of the inclusion of nicotinic acid, nicotinamide, salicylic acid, and phenylbutazone in this correlation between toxicity and 7-14C-nicotinamide mobilization, it is not necessary that the formation of compounds analogous to the nicotinamide dinucleotides plays a significant role in the toxic manifestations of the nicotinamide analogs. The displacement of 7-14C-nicotinamide dinucleotides from their corresponding apoenzymes with subsequent metabolism of the dinucleotides could explain the noted increased 7-14C-nicotinamide dinucleotide turnover and depletion which led to the toxic effects.

Animals↗
PubMed1978

Drug interactions with antihypertensive drugs.

Drug interactions with antihypertensive drugs can be either beneficial or hazardous. The hazardous interactions are relatively infrequent but must be shown so they can be avoided. Those of most importance involve interaction with guanethidine-type agents and tricyclic antidepressants, amphetamine-type anorexiants or phenolpropanolamine-type common cold remedies; combined use of potassium retaining diuretics with potassium supplements; and incautious use of diuretics with cardiac glycosides. The beneficial interactions are the basis for modern antihypertensive therapy and can be of major help if logically applied to therapeutic problems.

Adrenergic beta-Antagonists↗
PubMed1979

[Drug interactions].

Beneficial and adverse interactions between drugs may occur in any process that influences the pharmacokinetic and pharmacodynamic behaviour of a given drug and thus affects its therapeutic or toxic effects. Many additional "patient factors" and "drug factors" influence clinical occurrence and severity of adverse drug interactions. In dealing with drug interactions and their consequences, a uniform mode of classifying and reporting drug interactions based on clinical relevance appears to be the prime necessity. A number of adverse drug interactions commonly occurring during cardiovascular therapy are discussed.

Anti-Arrhythmia Agents↗
PubMed1979

[Drug interaction on antitumor drugs I. Antitumor activity of cyclophosphamide in mice consecutively administered aminopyrine, chlorpromazine, or morphine (author's transl)].

Antitumor activity and lethality of cyclophosphamide alone and in combination with several drugs were investigated in male ddY mice. The antitumor activity was estimated by weighing the solid tumor on the 15th day after Ehrlich ascites cell inoculation. Pentobarbital induced sleeping time for monitoring the activity of hepatic drug-metabolizing enzymes was defined as the time between the loss and the recovery of the righting reflex. Consecutive administration of pentobarbital shortened the pentobarbital sleeping time and increased the antitumor activity after cyclophosphamide. On the contrary, a single administration of SKF 525A or cycloheximide prolonged the pentobarbital sleeping time significantly and decreased the antitumor activity after cyclophosphamide. Consecutive administration of aminopyrine, or chlorpromazine shortened the pentobarbital sleeping time and increased the antitumor activity after cyclophosphamide. These results indicate that aminopyrine and chlorpromazine may increase the levels of the hepatic drug-metabolizing components and may activate cyclophosphamide by conversion to an active form. Effect of a consecutive administration of morphine on the pentobarbital sleeping time and the antitumor activity was uncertain in individual cases. On the other hand, aminopyrine, chlorpromazine, or morphine in consecutive administration increased the lethality of cyclophosphamide.

Aminopyrine↗
PubMed1975

Pharmacokinetic mechanisms of drug interactions.

Many patients require multiple-drug therapy, often under the supervision of several physicians, this increasing the risk of adverse drug effects. While drug interactions cannot always be conveniently categorized, familiarity with basic pharmacologic and pharmacokinetic principles permits the clinician to anticipate and avoid many of the more common and serious drug interactions. Most serious drug interactions involve one of the four pharmacokinetic processes governing drug behavior within the body: absorption, distribution, metabolism, and renal clearance. Knowledge of whether a drug is a weak acid or a weak base is clinically useful because it can alert the physician to the propensity for certain types of drug interactions.

Aged↗
PubMed1979

Drug interactions and side effects of hypolipidemic drugs.

The side effects and drug interactions of clofibrate, cholestyramine and nicotinic acid are reviewed because these hypolipidemic drugs are given for preventive and only rarely curative reasons and because these drugs have been given for many years and often concomitantly with other drugs.

Blood Coagulation↗
PubMed1978

Potential anticoagulant drug interactions in ambulatory patients.

Computer-generated prescription drug purchase records for ambulatory patients receiving oral anticoagulants (OAC) were studied for concomitant use of other drugs which have been reported to induce clinically significant interactions. One third of 479 patients taking OAC were exposed to a potentially interacting drug at some time during this 6-month period. The percentage of patients with drug interaction exposure correlated directly with total drug use (p less than 0.0005). There were no significant differences when interaction exposure rates were compared in the cases of single : multiple pharmacy and single : multiple physician-patient groups. Warfarin was the most common anticoagulant (greater than 95%) and barbiturates the most common interacting drug.

Anticoagulants↗
PubMed1976

[Drug-drug interactions (author's transl)].

This short outline of drug-drug interactions does not claim to cover the entire field. The task of this paper is to illustrate the most important principles of drug-drug interactions by paradigms taken from the experience of the practitioner. One consequence of drug-drug interactions is the change in pharmacolinetic parameters important for the therapeutical effect of drugs in the organism. Very often the elucidation of the mechanisms of drug-drug interactions in man is impossible; therefore, for clinical pharmacologists experiments on animals remain the tool in order to gain more knowledge in this field.

Age Factors↗
PubMed1978

Drug interactions in rheumatoid disease--are they of any clinical importance?

Much of the literature on drug interactions over-emphasizes their importance. A review of the mechanisms of drug interactions and of the clinically important interactions involving drugs commonly used in rheumatology reveals that serious interactions are likely to be uncommon. A practical approach to this problem may be divided into three parts: 1. Be aware of the mechanisms of drug interactions as they may explain some unexpected finding occurring during drug treatment. 2. Remember that serious drug interactions are more likely to involve a drug which possesses a narrow therapeutic range (e.g. oral anticoagulants). 3. When indulging in polypharmacy attempt to ensure that such treatment has real benefits. This last point may be the most important for if it is proven that combined therapy has no advantages then the potential for drug interactions will be much reduced.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2025

Large-scale CRISPR screening in primary human 3D gastric organoids enables comprehensive dissection of gene-drug interactions.

Understanding how genes influence drug responses is critical for advancing personalized cancer treatments. However, identifying these gene-drug interactions in a physiologically relevant human system remains a challenge, as it requires a model that reflects the complexity and heterogeneity among individuals. Here we show that large-scale CRISPR-based genetic screens, including knockout, interference (CRISPRi), activation (CRISPRa), and single-cell approaches, can be applied in primary human 3D gastric organoids to systematically identify genes that affect sensitivity to cisplatin. Our screens uncover genes that modulate cisplatin response. By combining CRISPR perturbations with single-cell transcriptomics, we resolve how genetic alterations interact with cisplatin at the level of individual cells and uncover an unexpected link between fucosylation and cisplatin sensitivity. We identify TAF6L as a regulator of cell recovery from cisplatin-induced cytotoxicity. These results highlight the utility of human organoid models for dissecting gene-drug interactions and offer insights into therapeutic vulnerabilities in gastric cancer.

Humans↗
PubMedDate not supplied

Drug-drug interactions among residents in homes for the elderly: a pilot study.

This pilot study investigated epidemiologically the potential for clinically significant drug-drug interactions, a subclass of adverse drug responses, in two homes for the elderly. The agent (drugs), host (residents), and environment (rural and urban nursing homes) in the illness known as drug-drug interaction were studied. Drug profiles on 188 subjects were compiled and screened by computer. Of these, 100 (80 in the rural home and 20 in the urban home) had the potential for clinically significant drug-drug interactions. Laboratory diagnostic procedures essential to confirm the unintentional interaction of two or more drugs were beyond the scope of the study; therefore, physicians independently reviewed the records of 66 residents who could be interviewed, agreeing that 27 residents were potential drug-drug interactors. These subjects had twice as many drug products and three times as many pro re nata products prescribed for them as did subjects without the potential for drug-drug interaction. The possible cause of interaction found most frequently was digitalis combined with thiazide or furosemide. The results of this pilot study suggest several implications for practice within the research setting.

Aged↗
PubMed1979

Drug interactions with saralasin.

Diuretic and vasodilator drugs alter the BP response to saralasin causing drug interactions. Saralasin-induced BP reduction is related directly to PRA and intravascular volume. Diuretic agents deplete intravascular volume and elevate PRA, enhancing saralasin hypotension. Vasodilating agents increase PRA and may induce angiotensin dependence of BP. Thus, with potent vasodilators, saralasin can induce hypotension. Rebound hypertension has been reported after saralasin infusion in several patients with accelerated or malignant hypertension. Theoretically, this BP elevation could be related to sustained release of renin resulting from disinhibition of an intrarenal angiotensin receptor inhibitory to renin release. Since propranolol can block saralasin-induced renin release, angiotensin and beta-blockers could constitute a beneficial drug interaction.

Angiotensin II↗
PubMed1977

Drug interactions with oral sulphonylurea hypoglycaemic drugs.

The effect of the oral sulphonylurea hypoglycaemic drugs may be influenced by a large number of other drugs. Some of these combinations (e.g. phenylbutazone, sulphaphenazole) may result in cases of severe hypoglycaemic collapse. Tolbutamide and chlorpropamide should never be given to a patient without a prior careful check of which medicaments are already being given. Similarly, no drug should be given to a diabetic treated with tolbutamide and chlorpropamide without consideration of the possibility of interaction phenomena.

Allopurinol↗
PubMed1978

[Alcohol and drug interactions].

Alcohol appears to interact with many drugs in many different and complicated ways. The absorption and metabolism of drugs can be altered under the influence of acute or chronic alcohol intake, and it is possible that alcohol itself or its metabolic products may interfere with the effect of several drugs. These interactions are not only of biological interest but also of clinical importance, and the general practitioner should therefore be aware of them. The therapy of patients with chronic alcoholism is often complicated by such interactions, and it is thus important to know both the habits of the patient with respect to alcohol intake and possible interference with the drugs used.

Alcoholism↗