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Arterial hypertension is one of the most common comorbidities in patients with cancer. Moreover, the treatment with anticancer agents can lead to the development of drug-induced arterial hypertension. The aim of this work is to systematize and analyze data about anticancer agents, the use of which can cause the development of drug-induced hypertension, about epidemiology, pathophysiological mechanisms, risk factors, clinical signs, diagnosis and differential diagnosis, treatment and prevention of hypertension associated with the use of anticancer drugs. It was found that anti-cancer drugs often contribute to the development of drug-induced hypertension. The mechanisms that determine the development of hypertension are diverse and may include the development of endothelial dysfunction, an increased arterial stiffness, capillary rarefaction, fluid and electrolyte imbalance, and genetic factors. It is important to remember about drugs that can cause drug-induced hypertension to reduce the risk of developing adverse reactions, and prevent cardiovascular disease. Treatment of drug-induced hypertension, caused by anticancer drugs, often requires immediate discontinuation of drugs, due to adverse reactions that are often life-threatening. In some situations, it is possible to reduce the dose of the drugs and / or prescribe antihypertensive drugs. Arterial hypertension is an important risk factor in the development of cardiovascular events, including stroke, coronary heart disease, heart failure.

Some drugs can lead to the development of drug-induced arterial hypertension. The aim of the work is to systematize and analyze the data about drugs that can cause the development of drug-induced hypertension, as well as on epidemiology, pathophysiological mechanisms, risk factors, clinical picture, diagnosis and differential diagnosis, treatment and prevention of drug-induced hypertension. As a result of data analysis, it was revealed that drugs: glucocorticosteroids, antineoplastic drugs, immunosuppressants, nonsteroidal anti-inflammatory drugs, antidepressants and some others are associated with the development of hypertension. The mechanisms of development of drug-induced arterial hypertension are not fully established and require further study. Drug-induced arterial hypertension is still one of the most common and often unrecognized adverse reactions. The clinical manifestations of drug-induced hypertension are not specific. The symptoms are associated with target organ damage or complications of hypertension and may include a headache, nausea, dizziness, blurred vision, anxiety, shortness of breath, etc. patients with previously well-controlled hypertension or cases of uncontrolled hypertension. Therefore, it is always necessary to pay attention to the patient’s history, pharmacological anamnesis, rapid increases in blood pressure in patients with previously well-controlled hypertension, or cases of uncontrolled hypertension.

Atrio-ventricular (AV) blockages are a serious violation of the heart rhythm. One of the reasons for the development of this pathology may be taking medications. This effect has a significant number of drugs used for the treatment of diseases of the cardiovascular system, central nervous system, general and local anesthetics, antineoplastic drugs, and many others. The main mechanism for the development of drug-induced AV blockades is the inhibition of AV node conduction. The most common risk factors for the development of drug-induced AV blockades are taking two and more drugs that have an inhibitory effect on AV conduction, the initial duration of the PQ interval more than 0.2 second, initial dysfunction of the AV node, increased plasma concentration of a potential inducer drug due to the presence of kidney and/or liver disease, drugdrug interactions, and specific risk factors for individual drugs. Special attention in solving this problem should be paid to both stopping the developed AV conduction disorder – medication or using an electric cardiostimulator, and its prevention. This article systematizes the literature data on drug-induced AV blockades in order to increase the awareness of practitioners and patients about their prevalence, risk factors, approaches to diagnosis, treatment and prevention.

Many classes of medications, such as antipsychotics, anticonvulsants, anticholinergics, and other commonly prescribed drugs, can cause cognitive impairment (CI). The negative effect of drugs on cognitive functions is due to the following pathophysiological mechanisms: a reduction in neuronal excitability, an increase in gamma-aminobutyric acid activity, and decreases in enzyme activity, the number of receptors, cerebral perfusion, as well as brain atrophy; moreover, a number of mechanisms have not been fully studied. An important role in the development of drug-induced CI is played by predisposing (senility or childhood, brain damage, chronic diseases, functional disorders, genetic causes, initial cognitive decline, polypragmasia), and precipitating (acute diseases, infections, metabolic disorders, dehydration, acute urinary retention, malnutrition, environmental influences, etc.) factors. The dose of a drug, the duration of its use is of absolute value. There is a need for the differential diagnosis of CI induced by drugs and CI directly related to the diseases, for which these drugs are prescribed. Drug-induced CI should be suspected if an association is established between a decline of cognitive functions and the start of drug intake. The treatment of this CI involves primarily dose withdrawal or reduction and the use of sustained-release dosage forms, if available. In some cases, cognitive training and/or special drug therapy may be required to correct the CI that has occurred. The measures to prevent drug-induced KI include the choice of the lowest-risk drugs, the use of current side-effect rating scales, in particular an anticholinergic burden scale.