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Parker Hannifin Czech Republica. Parker Hannifin Czech Republic S. Parker Hannifin De Mexico. Parker Hannifin De Mexico S. Parker Hannifin Dinsutrial S. The simultaneous stimulation of both 5-HT 1A and 5-HT 7 receptors, with opposing effects on adenylate cyclase in the same cell layer, is not expected to modify IOP. The agonism on these subtype receptors presumably increases the ciliary body blood flow, amplifying the metabolic activities of the ciliary processes, with an enhanced production of aqueous humor.

In fact, recently, it has been demonstrated that intravenous administration of fluoxetine significantly raises IOP in rabbits. This effect occurs via serotonin plasma levels augmentation, confirmed by elevated excretion of 5-hydroxyindolacetic acid in urine, and is strongly inhibited by topical administration of ketanserin, one of the most selective 5-HT 2A receptors antagonist [ 51 , 64 , 66 , 87 ]. The answer of the ciliary body to a direct via 5-HT 7 receptors or an indirect via 5-HT 2A receptors stimulation activity consists in an increase of the aqueous humor inflow.

When the outflow pathway are not able to drainage the aqueous humor overproduction IOP shall raise, according to the Goldmann equation [ 52 ]. The empirical correlation of this statement is in the evidence that fluoxetine administration to patients surely unaffected by glaucoma causes a transient This event has been observed in young adult depressed, otherwise healthy, subjects after the first exposure to SSRIs, but no data are actually available regarding the long-term effect of these compounds on IOP.

In other words, it has not yet been established whether the chronic assumption of SSRIs is responsible for a iatrogenic IOP shift towards highest levels, with a consequent overload of the autoregulation system. This last mechanism can work by influencing only the F component of the Goldmann equation rate of aqueous humor formation , whereas it is well known that the role played by the C component facility of aqueous humor outflow , which decreases with aging, is also crucial for the IOP modulation.

After SSRIs intake the ocular autoregulation system is able to ensure an equilibrium among the components affecting IOP homeostasis in the most part of depressed patients. This probably occurs just in the youngest subjects. On the contrary, in elderly patients the amount of plaque material at the level of the cribriform layer of the trabecular meshwork, derived from the sheaths of the elastic-like fibers, increases with age, inducing a parallel physiological increase in the outflow resistance.

Moreover, in comparison to normal eyes, this material is significantly greater in cases of POAG and of intermittent narrow-angle glaucoma [ 83 ], suggesting that the enhanced resistance to the outflow observed in elderly patients and, at highest extent, in the subjects suffering from the two above mentioned forms of glaucoma, represents one of the mechanism leading to IOP increase.

These mechanisms, at least theoretically, explain how the SSRIs intake can affect the IOP homeostasis and how the IOP ocular autoregulation system in elderly subjects, such as - independently from age - in glaucomatous patients or in eyes with primary or secondary peculiar structural configuration of the irido-corneal angle, could be not able to ensure the maintenance of IOP within individual acceptable physiological limits.

In , Ahmad firstly described a year-old man with acute angle-closure glaucoma occurred after five-week oral fluoxetine administration [ 4 ]. To date, other similar dramatic observations secondary to the intake of this specific SSRI have not been recorded. However, six cases of angle-closure glaucoma attack, induced by paroxetine administration, have been reported in the Literature [ 12 , 18 , 46 , 71 , 79 , 80 ].

In the first three case reports, this adverse ocular reaction occurred in patients whose ages ranged from 70 to 91 years, an atypical life-period for the occurrence of acute-angle glaucoma, as confirmed by epidemiological studies [ 16 ]. In these elderly phakic patients, the lens status per se , in presence of an ocular biometric predisposition, synergistically interacting with paroxetine-induced passive mydriasis via 5-HT 7 receptors , easily can determine the glaucomatous attack [ 46 , 71 , 80 ].

The other three cases were observed in younger subjects with normal lens, but affected by hyperopia [ 12 , 18 , 79 ], an ascertained risk factor for intermittent angle closure or acute angle-closure glaucoma [ ]. The interval between the onset of paroxetine administration and the development of the ocular adverse reaction was fairly different among these patients, ranging from few days to several weeks.

There is only one case of acute attack of glaucoma reported in the Literature secondary to the use of fluvoxamine [ 69 ]. In this year-old woman with a narrow-angle glaucoma, the exacerbation of the ocular disease became evident immediately after she started the antidepressive treatment. The two cases reported after citalopram administration have occurred in relatively young women, who were unaffected by neither cataract nor hyperopia [ 39 , 86 ].

The mechanisms by which citalopram has been responsible of the acute attack has not been completely ascertained. About the causal relationship, it could be proposed that citalopram may directly act on the iris or ciliary body muscle through serotonergic or cholinergic mechanisms, or both.

Lastly, a case of a year-old woman who developed acute bilateral angle closure glaucoma with choroidal effusions while receiving escitalopram therapy has been recently described [ ]. Medication-induced uveal effusion causing angle closure has been well documented with the antiepileptic medication topiramate [ 50 ], and in this case the mechanism appears to be similar.

In fact, the ultrasonographic findings of choroidal effusion with ciliary body detachment during the acute attack with resolution of these findings once the attack was broken provide clear evidence that the mechanism of bilateral angle closure was related to uveal effusion. To date, no similar adverse events have been still documented after the administration of sertraline, although a significant increase in pupil diameter after administration has been documented with the use of these compounds.

Mydriasis occurs quite rapidly following a single acute dose of sertraline, reaching a maximum 5 h after first administration. Subsequently, mydriasis remained stable at this level throughout the treatment period [ , ]. In all these case reports, the Authors emphasized the role of passive mydriasis as precipitating event in the determinism of the acute angle-closure glaucoma [ 4 , 12 , 18 , 39 , 46 , 69 , 71 , 79 , 80 , 86 , ]. In fact, the sympathomimetic noradrenergic action, stimulating the dilator pupil muscle, produces an active mydriasis which, together with the serotonergic passive one, is able to reinforce the crowding at the level of the iridocorneal angle.

This triggering mechanical phenomenon can bring iris tissue into closer proximity with the functional trabecular meshwork, the structure that normally allows aqueous humor to escape from the eye. The incidence of ocular side effects induced by SSRIs is probably underestimated because the IOP increase in the course of intermittent angle closure and, some more, in misdiagnosed forms of POAG is, respectively, pauci- or asymptomatic.

Thus, it is not quite hazardous to hypothesize that the significant incidence of unspecified visual disturbances, reported by Preskorn in a comparative study on SSRIs tolerability [ 69 ], could be attributed - at least in some cases - to IOP modifications.

Increased plasma levels of serotonin may be a factor or, more probably, a co-factor in the development of optic nerve head perfusional disorders, either synergistically with an IOP level higher than the eye can tolerate individual critical IOP or independently from IOP with a direct vascular dysfunction of the posterior ciliary arteries. In the course of chronic antidepressive treatment with SSRIs, multiple transient vasospasms at the level optic nerve head vessels may directly produce hemodynamic alterations that, time to time, could progressively induce a manifest optic ischemic neuropathy.

In atherosclerotic individuals, the susceptibility to develop this kind of vascular disorder becomes highest because serotonin, enhancing platelet aggregation on the atheromata, can also indirectly trigger vasospasm of ocular arteries [ 60 ]. At the level of brain microcirculation it has been ascertained that serotonin is implicated in its regulation; significant changes in the status of 5-HT neurons of SNC have, in fact, vascular repercussion in specific brain regions.

This implies that neuronal serotonin release constitutes the basis of normal blood flow regulation that, when dysfunctional, may lead to inadequate blood supply to the brain [ 31 ]. In coronary arterial district, the role of serotonin in vasoconstriction or even vasospasm has been recently indicated as possible co-factor in the occurrence of myocardial ischemia in patients with acute coronary syndromes [ 53 ].

The recently recorded escitalopram-induced uveal effusion [ ] and sertraline presumed maculopathy [ ] may be due to this blood flow dysfunction secondary to SSRIs administration. Although AACG is an uncommon disease, risk factors have been identified. Women are more likely to develop AACG than men. Persons older than 50 years are at slightly increased risk, as are individuals with hyperopia. Those with a personal or family history of angle-closure glaucoma are at increased risk for the disease.

There are some evidences supporting this datum: i peripheral anterior chamber depth is less wide in women than in men and, with aging, it tends to be progressively reduced; ii the different prevalence of depression between the two sexes, with a female: male ratio in adulthood [ 68 ]. Moreover, independently by sex, hyperopic eyes have a predisposition to a reduced wide of the angle, with a consequent enhanced risk for glaucoma acute attack [ 17 , 32 ].

The frequency of hyponatremia is around 8 per 1, among elderly women. The risk of developing hyponatraemia, a potentially fatal condition that is typically asymptomatic until it becomes severe, appears to be highest during the first few weeks of treatment. SIADH is more likely in some populations, including people who are elderly or who take diuretics [ ]. A dose-dependent elevation of IOP has been reported in rabbits after injections of vasopressin into the 3 rd ventricle. This IOP elevation was blocked by the pretreatment with the V 1 receptor antagonist.

A worldwide prospective analysis revealed that, during the next two decades, the incidence of these psychiatric diseases in the general population is destined to progressively grow [ 93 ]; thus, unavoidably, the agreeable effectiveness-tolerability-safety profile of the SSRIs will result in a more extensive prescription of these antidepressants by psychiatrists and also non-psychiatrists. Until the real involvement of SSRIs on IOP increase and optic nerve head changes shall not be well-ascertained, it is difficult to draw final conclusions on the more reasonable clinical management of depressed patient under SSRIs treatment.

The knowledge of individual tolerability, angle-closure predisposition and critical IOP could be goals no so difficult to realize. In fact, although in the course of a search utilizing Medline, we have found only eleven papers documenting cases of acute angle-closure glaucoma related to SSRIs administration [ 4 , 12 , 18 , 39 , 46 , 69 , 71 , 79 , 80 , 86 , ], the World Health Organization Adverse Drug Reactions database contains several other reports of undefined glaucoma associated with the different marketed SSRIs.

This discrepancy further confirms the suspicious that the recording of pauci- or asymptomatic side effects, like POAG, is underestimated. Thus, because experimental and clinical findings indicate that SSRIs affect pupil diameter, aqueous humor dynamics and optic nerve blood flow, the following recommendations should be taken into account:.

Read article at publisher's site DOI : Br J Clin Pharmacol , 86 10 , 27 Apr Front Cell Neurosci , , 03 May J Psychopharmacol , 32 11 , 25 Sep Cited by: 1 article PMID: J Ocul Pharmacol Ther , 34 , 25 Jan Cited by: 0 articles PMID: To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.

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Recent history Saved searches. Costagliola C ,. Francesco Parmeggiani Search articles by 'Francesco Parmeggiani'. Parmeggiani F ,. Semeraro F ,. Adolfo Sebastiani Search articles by 'Adolfo Sebastiani'. Sebastiani A. Affiliations All authors 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. The primary SSRIs pharmacological action's mechanism consists in the presynaptic inhibition on the serotonin reuptake, with an increased availability of this amine into the synaptic cleft.

Free full text. Curr Neuropharmacol. PMID: Author information Article notes Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Go to:. Key words: Fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram, intraocular pressure, side effects. Open in a separate window. The biosynthesis of serotonin from the amino acid tryptophan. Cornea The presence of functional serotonergic receptors in the rabbit cornea was firstly postulated by Neufeld and co-workers [ 98 ].

Iris and Ciliary Body Serotonin is present in mammalian iris-ciliary body complex ICB at higher concentration that in non-mammalian species [ 5 , 45 , 73 , , ]. Lens The presence of serotonin and its receptors in the lens has not been extensively investigated, even is it has been ascertained that 5-HT is both synthesized in situ and transported from the aqueous humor.

Retina Although 5-HT is found in the mammalian retina only at low levels, considerable evidence suggests that it plays a role in visual processing. Vascular Structures Before considering the interactions among serotonin, vascular compartments controlling the blood supply to the eye, and their hemodynamic characteristics, it is important to highlight that several structural differences exist between the extraocular vessels and the intraocular microvessels.

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Ocular Pharmacol. Krupin T, Civan MM. Physiologic basis of aqueous humor formation. The glaucomas: clinical science. Louis: Mosbly-Year Book Inc; Lane RM. SSRIs and hyponatraemia. Cataractogenesis in rats induced by in utero exposure to RG , a 5-HT 3 antagonist. Late bilateral acute angle-closure glaucoma after administration of paroxetine in a patient with plateau iris configuration. Acute angle-closure glaucoma and paroxetine. Lieberman E, Stoudemire A. Use of tricyclic antidepressants in patients with glaucoma.

Assessment and appropriate precautions. A novel adenylyl cyclase activating serotonin receptor 5-HT 7 implicate din the regulation of mammalian circadian rhythms. Quantitative analysis of 'plaque material' in the inner- and outer wall of Schlemm's canal in normal- and glaucomatous eyes. Exp, Eye Res.

Mallorga P, Sugrue MF. The ciliary body: the third organs found to synthesize indoleamines in humans. Bilateral symptomatic angle closure associated with a regular dose of citalopram, an SSRI antidepressant. Ocular hypotensive effect of topical ketanserin in timolol users. Graefes Arch Clin. Topical application of serotonin or the 5-HT 1 -agonist 5-CT intraocular pressure in rabbits. Analysis of pre- and postsynaptic factors of the serotonin system in rabbit retina.

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Changes in responsiveness of the beta-adrenergic and serotonergic pathways of the rabbit corneal epithelium. Olver JM. Angioarchitecture of the human optic nerve and perioptic area. In: Bisantis C, Carella G, editors. Vascular system of the optic nerve and perioptic area.

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Osborne NN, Chidlow G. Do beta-adrenoceptors and serotonin 5-HT 1A receptors have similar functions in the control of intraocular pressure in the rabbit? Osborne NN, Ghazi H. A hypothesis to explain ganglion cell death caused by vascular insults at the optic nerve head: possible implication for the treatment of glaucoma.

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