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In recent years, an increasing amount of attention has been paid to medicinal products as possible risk factors in the development of eye diseases. The frequency of diagnosed drug-induced uveitis is growing yearly, which can be attributed to the appearance of new drugs - biological agents (immune checkpoint inhibitors, BRAF and MEK inhibitors, vascular endothelial growth factor inhibitors, tumor necrosis factor-α inhibitors), as well as systemic bisphosphonates and some antiviral drugs. The time interval between the beginning of the drug use and the appearance of uveitis symptoms varies from several days to months. Common symptoms include eye pain, photophobia, the appearance of floating opacities, and reduced vision associated with active inflammatory changes in the retina and optic nerve and outcomes of those inflammations. Timely diagnosis, cancellation of the drug that caused uveitis and appointment of adequate anti-inflammatory therapy in most cases effectively stops the symptoms of the disease, which determines the relevance of attention to the prevalence, pathogenesis, diagnosis and treatment of drug-induced uveitis.

Glaucoma is seen as a heterogeneous group of diseases characterized by optical neuropathy with associated visual field loss; one of the main risk factors for its development is increased intraocular pressure (IOP). In the case of drug-induced glaucoma (DIG), patients develop elevated IOP, optic neuropathy and visual field defects associated with the use of certain drugs. Corticosteroids are one of the most well-known classes of drugs that can cause an increase in IOP through the open-angle mechanism. Drug-induced glaucoma, which develops similarly to open-angle glaucoma, can also be caused by some non-steroidal anti-inflammatory agents, antibodies to the endothelial growth factor, etc. Classes of drugs that can cause angle-closure glaucoma include topical anticholinergic or sympathomimetic drops, tricyclic antidepressants, monoamine oxidase inhibitors, antihistamines, antiparkinsonian drugs, antipsychotic drugs, antispasmodics. Products containing sulfa group drugs can cause DIG due to a different closing angle mechanism involving a forward rotation of the ciliary body. It is important for medical practitioners to be aware of this unwanted drug reaction in order to prevent, detect and treat DIG. In the case of drug-induced increase in IOP, if the underlying disease allows discontinuation of drugs, this measure usually leads to normalization of IOP. In cases when the patient's IOP does not normalize after discontinuation of steroids or when they must continue to take corticosteroids, the administration of topical drugs for the treatment of glaucoma should be considered.

Drug-induced dysphonia is a non-life-threatening adverse drug reaction, however, this complication can significantly worsen the quality of life of patients, especially those in voice-speaking professions. The aim of the work was to search for information about the prevalence, etiology, pathogenesis, and features of treatment and prevention of drug-induced dysphonia. In the case of some drugs, the true prevalence may be higher than described in the literature, due to the fact that dysphonia is in most cases mild, reversible and, in comparison with other undesirable drug reactions, rarely attracts the attention of both the patient and practitioners.

One type of non-allergic non-infectious rhinitis is represented by a heterogeneous group of rhinitis medicamentosa, which can be divided into several pathogenetic types. The most common rebound nasal congestion associated with the use of topical decongestants. Excessive use of intranasal decongestants leads to a decrease in the number of alpha-adrenoreceptors on the surface of cell membranes and uncoupling their connection with the G-protein and the development of tachyphylaxis. To prevent the development of rebound nasal congestion caused by topical decongestants, it is important to limit the frequency of their use. In most cases, the duration of the use of vasoconstrictor drugs should be limited to 5-7 days, according to Patient information leaflets for the drugs. However, in patients who have had a history of episodes of rebound nasal congestion, which develops including the previously indicated periods, the duration of decongestant therapy should be limited to 3 days. Rhinitis associated with local inflammation is caused by the intake of acetylsalicylic acid (ASA) or other non-steroidal anti-inflammatory drugs. Currently, the so-called "aspirin triad" is well known - a combination of bronchial asthma, rhinosinusitis (often polyposis) and intolerance to ASA. Neurogenic rhinitis develops due to the use of drugs that violate vascular tone, for example, antihypertensive drugs or type 5 phosphodiesterase inhibitors. Drug-induced rhinitis has a significant impact on the patient's quality of life: nasal congestion, rhinorrhea, secondary night apnea, insomnia as a result of nasal breathing disturbances, headaches, irritability, weakness after sleepless nights disturb patients to a large extent. Timely diagnosis and withdrawal of a provocative drug, the use of topical corticosteroids in case of severe rhinitis are the basis of the treatment of rhinitis medicamentosa. In severe cases, there is a need, including surgical treatment, such as, for example, submucosal laser destruction of the lower nasal concha.

Drug-induced optic neuropathy is a group of disorders in which medications cause degeneration of the optic nerve. The true prevalence of drug-induced neuropathy has not been studied, although the percentage of patients who develop optic nerve damage is known for individual medications. The common pathophysiological mechanisms are believed to be mitochondrial damage and imbalance of intracellular and extracellular free radical homeostasis. Typical symptoms of drug-induced neuropathy are reduced visual acuity in the central area, which is often bilateral, visual field disturbances, dyschromatopsia, and edema of the optic nerve head. Early detection of drug-induced optic neuropathy can potentially prevent or minimize serious complications. For patients who develop drug-induced optic neuropathy, treatment is based on timely diagnosis and cancellation of the provoking drug. In most patients, vision usually recovers a few weeks or months after discontinuation of previous therapy, but there have been cases of irreversible vision loss. In addition to withdrawal of the drug that caused optic nerve lesion, treatment of drug-induced neuropathy may include use of drugs and treatment methods prescribed by neurologists for peripheral neuropathy, however, such treatment is seldom based on evidence.

The ability of drugs to have an ototoxic effect has been studied for a long time, however, the true prevalence of this undesirable phenomenon is unknown, which is due to the use of various audiological protocols, a wide range of reactions to drugs in different ethnic groups, and most importantly, the lack of caution with regard to otological symptoms due to their reversibility or lack of immediate threat to life. Drug-induced ototoxicity is a functional disorder of the inner ear (cochlea and/or vestibular apparatus) or eighth pair of cranial nerves. Pharmacotherapy, associated with the development of ototoxic drug reactions, may remain undervalued for a long time, often until irreversible hearing impairment is formed. The most frequently prescribed drugs that cause ototoxic phenomena include anticancer drugs, antibacterial drugs of the aminoglycoside group, loop diuretics, calcium channel blockers, non-steroidal anti-inflammatory drugs, antimalarial drugs, salicylates, etc. Monitoring the degree of hearing impairment before and during therapy is important in preventing the development of drug-induced ototoxicity and makes it possible to consider alternative treatment regimens in a timely manner. It is in this connection that the role of participation in the appointment of rational pharmacotherapy to patients with a potential risk of developing otological phenomena of a clinical pharmacologist and audiologist undoubtedly increases.