Cholecystokinin-Induced Duodenogastric Bile Reflux Increases the Severity of Indomethacin-Induced Gastric Antral Ulcers in Re-fed Mice.

BACKGROUND/AIMS: We examined the involvement of cholecystokinin (CCK) in the exacerbation of indomethacin (IND)-induced gastric antral ulcers by gastroparesis caused by atropine or dopamine in mice. METHODS: Male mice were fed for 2 h (re-feeding) following a 22-h fast. Indomethacin (IND; 10 mg/kg, s.c.) was administered after re-feeding; gastric lesions were examined 24 h after IND treatment. In another experiment, mice were fed for 2 h after a 22-h fast, after which the stomachs were removed 1.5 h after the end of the feeding period. Antral lesions, the amount of gastric contents, and the gastric luminal bile acids concentration were measured with or without the administration of the pro- and antimotility drugs CCK-octapeptide (CCK-8), atropine, dopamine, SR57227 (5-HT3 receptor agonist), apomorphine, lorglumide (CCK1 receptor antagonist), ondansetron, and haloperidol alone and in combination. RESULTS: IND produced severe lesions only in the gastric antrum in re-fed mice. CCK-8, atropine, dopamine, SR57227 and apomorphine administered just after re-feeding increased bile reflux and worsened IND-induced antral lesions. These effects were significantly prevented by pretreatment with lorglumide. Although atropine and dopamine also increased the amount of gastric content, lorglumide had no effect on the delayed gastric emptying provoked by atropine and dopamine. Both ondansetron and haloperidol significantly inhibited the increase of bile reflux and the exacerbation of antral lesions induced by atropine and dopamine, respectively, but did not affect the effects of CCK-8. CONCLUSIONS: These results suggest that CCK-CCK1 receptor signal increases bile reflux during gastroparesis induced by atropine and dopamine, exacerbating IND-induced antral ulcers.

Hypertensive emergency secondary to atropine / Emergencia hipertensiva secundaria a atropina

Atropine, a competitive antagonist of acetylcholine muscarinic receptors, is commonly used to treat severe bradycardia by blocking parasympathetic activity. We present a rare case of hypertensive emergency following atropine administration, with only one previous report in the literature. A 78-year-old woman with essential hypertension and hypercholesterolemia was admitted to the cardiac intensive care unit for non-ST segment elevation myocardial infarction. During coronary angiography, an occlusion of the right coronary artery was identified. While removing the diagnostic catheter through the right radial artery, the patient experienced intense pain and discomfort, accompanied by a vasovagal reflex characterized by bradycardia and hypotension. Intravenous atropine (0.5mg) was administered, leading to a rapid rise in heart rate with frequent ventricular ectopy. Subsequently, a progressive and exaggerated elevation in arterial blood pressure occurred, peaking at 294/121mmHg approximately 10min after atropine administration. The patient developed hypertensive acute pulmonary edema, successfully treated with intravenous nitroglycerine (10mg) and furosemide (60mg). Blood pressure normalized after approximately 14min. The exact mechanism of atropine-induced hypertensive emergency remains unknown. While hypertensive emergencies with atropine are exceedingly rare, healthcare professionals should be aware of this potential effect and be prepared for prompt intervention.(AU)

La atropina, un antagonista competitivo de los receptores muscarínicos de acetilcolina, se utiliza comúnmente para tratar la bradicardia severa al bloquear la actividad parasimpática. Presentamos un caso raro de emergencia hipertensiva después de la administración de atropina, con solo un informe previo en la literatura. Una mujer de 78 años con hipertensión esencial e hipercolesterolemia fue ingresada en la unidad de cuidados intensivos cardíacos por infarto agudo de miocardio sin elevación del segmento ST. Durante la angiografía coronaria, se identificó una oclusión de la arteria coronaria derecha. Mientras se retiraba el catéter diagnóstico a través de la arteria radial derecha, la paciente experimentó un intenso dolor y malestar, acompañado de un reflejo vasovagal caracterizado por bradicardia e hipotensión. Se administró atropina intravenosa (0,5 mg), lo que provocó un rápido aumento de la frecuencia cardíaca con frecuente ectopia ventricular. Posteriormente, ocurrió una elevación progresiva y exagerada de la presión arterial, alcanzando un máximo de 294/121 mmHg aproximadamente 10 minutos después de la administración de atropina. La paciente desarrolló edema pulmonar agudo hipertensivo, tratado con éxito con nitroglicerina intravenosa (10 mg) y furosemida (60 mg). La presión arterial se normalizó después de aproximadamente 14 minutos. El mecanismo exacto de la emergencia hipertensiva inducida por atropina sigue siendo desconocido. Aunque las emergencias hipertensivas con atropina son excepcionalmente raras, los profesionales de la salud deben estar al tanto de este efecto potencial y estar preparados para intervenir rápidamente.(AU)

Hypertensive emergency secondary to atropine.

Atropine, a competitive antagonist of acetylcholine muscarinic receptors, is commonly used to treat severe bradycardia by blocking parasympathetic activity. We present a rare case of hypertensive emergency following atropine administration, with only one previous report in the literature. A 78-year-old woman with essential hypertension and hypercholesterolemia was admitted to the cardiac intensive care unit for non-ST segment elevation myocardial infarction. During coronary angiography, an occlusion of the right coronary artery was identified. While removing the diagnostic catheter through the right radial artery, the patient experienced intense pain and discomfort, accompanied by a vasovagal reflex characterized by bradycardia and hypotension. Intravenous atropine (0.5mg) was administered, leading to a rapid rise in heart rate with frequent ventricular ectopy. Subsequently, a progressive and exaggerated elevation in arterial blood pressure occurred, peaking at 294/121mmHg approximately 10min after atropine administration. The patient developed hypertensive acute pulmonary edema, successfully treated with intravenous nitroglycerine (10mg) and furosemide (60mg). Blood pressure normalized after approximately 14min. The exact mechanism of atropine-induced hypertensive emergency remains unknown. While hypertensive emergencies with atropine are exceedingly rare, healthcare professionals should be aware of this potential effect and be prepared for prompt intervention.

Age-related results over 2 years of the multicenter Spanish study of atropine 0.01% in childhood myopia progression.

To evaluate the age-related efficacy and safety of atropine 0.01% eye drops over 2 years for myopia control in a multicentric pediatric Spanish cohort. A non-controlled, interventional, prospective multicenter study was conducted as an extension of the Spanish Group of Atropine Treatment for Myopia Control Study (GTAM 1). Children aged 6-14 years with myopia from - 2.00 to - 6.00 D, astigmatism < 1.50 D and documented annual myopic progression of at least - 0.50 D under cycloplegic examination were recruited. From the original cohort of 105 participants, 92 children who had been receiving atropine 0.01% eye drops once nightly in each eye for 1 year continued their participation in this extended study (GTAM 2). All the patients underwent a standardized quarterly follow-up protocol, which included measurements of best-corrected visual acuity (BCVA), cycloplegic autorefraction, axial length (AL), anterior chamber depth (ACD), and pupil diameter. The study sample was divided into three age groups: 6-8, 9-11, and 12-14 years old. The mean change in cycloplegic spherical equivalent (SE) and axial length (AL) during the 24 months of follow-up was analyzed. Correlations between SE and AL, as well as the distribution of annual progression, were evaluated. Adverse effects were recorded using a specific questionnaire. Finally, 81 children completed the follow-up and were included in the analysis. Over the 2-year period, the mean changes in SE and AL were - 0.88 ± 0.60 D and 0.49 ± 0.25 mm, respectively. Additionally, 51 patients (63%) experienced SE annual progression lower than - 0.50 D. The correlation between the progression of SE and AL during the total period of treatment was mild (r = - 0.36; p < 0.001). There were no differences between the first and the second year of treatment in the progression of SE (- 0.42 ± 0.41 D versus - 0.45 ± 0.39 D; p = 0.69) or AL (0.25 ± 0.16 mm versus 0.23 ± 0.14 mm; p = 0.43). Older patients (12-14 years old) showed less AL progression than younger children (6-8 years old): 0.36 ± 0.18 mm versus 0.59 ± 0.30 mm; p = 0.01. Adverse effects were mild, infrequent, and decreased over time. On average, the myopia progression in control groups from other published biannual studies exceeded that observed in our study. Over 2 years, atropine 0.01% demonstrated a safe treatment for controlling myopia progression in a multicentric cohort of Spanish children. The effect remained stable during this period. Older patients exhibited a more favorable response in terms of AL enlargement. However, further studies are needed to investigate the age-related effect of low-dose atropine in the Caucasian population.

Gastroparesis Worsens Indomethacin-Induced Gastric Antral Ulcers by Bile Reflux via Activation of 5-HT3 and Dopamine D2 Receptors in Mice.

BACKGROUND/AIMS: We examined the contributions of gastric emptying and duodenogastric bile reflux in the formation of gastric antral ulcers induced by NSAIDs in mice. METHODS: We used the murine re-fed indomethacin (IND) experimental ulcer model. Outcome measures included the appearance of gastric lesions 24 h after IND treatment and the assessment of gastric contents and the concentration of bile acids 1.5 h after re-feeding. The effects of atropine, dopamine, SR57227 (5-HT3 receptor agonist), apomorphine, ondansetron, haloperidol, and dietary taurocholate and cholestyramine were also examined. RESULTS: IND (10 mg/kg, s.c.) induced severe lesions only in the gastric antrum in the re-fed model. The antral lesion index and the amount of food intake during the 2-h refeeding period were positively correlated. Atropine and dopamine delayed gastric emptying, increased bile reflux, and worsened IND-induced antral lesions. SR57227 and apomorphine worsened antral lesions with increased bile reflux. These effects were prevented by the anti-emetic drugs ondansetron and haloperidol, respectively. The anti-emetic drugs markedly decreased the severity of antral lesions and the increase of bile reflux induced by atropine or dopamine without affecting delayed gastric emptying. Antral lesions induced by IND were increased by dietary taurocholate but decreased by the addition of the bile acid sequestrant cholestyramine. CONCLUSIONS: These results suggest that gastroparesis induced by atropine or dopamine worsens NSAID-induced gastric antral ulcers by increasing duodenogastric bile reflux via activation of 5-HT3 and dopamine D2 receptors.

Incidence of Adverse Events Induced by Atropine in Myopic Children: A Meta-Analysis.

A large number of studies have evaluated the efficacy of low-dose atropine in preventing or slowing myopic progression. However, it is challenging to evaluate the ocular safety from these studies. We aimed to evaluate the incidence of adverse events induced by atropine in children with myopia. We performed a systematic literature search in several databases for studies published until November 2022. The incidence of adverse events induced by atropine was pooled by a common-effect (fixed-effect) or random-effects model. Subgroup analyses were conducted according to drug doses, types of adverse events, and ethnicity. A total of 31 articles were ultimately included in the study. The overall incidence of adverse events for atropine was 5.9%, and the incidence of severe adverse events was 0.0%. The most commonly reported adverse events were photophobia (9.1%) and blurred near vision (2.9%). Other adverse events including eye irritation/discomfort, allergic reactions, headache, stye/chalazion, glare, and dizziness occurred in less than 1% of the patients. The incidence of atropine-induced adverse events varied depending on the drug doses. A lower dose of atropine was associated with a lower incidence of adverse events. There was no significant difference in the incidence of adverse events for low-dose atropine between Asian and White children. Our study suggests photophobia and blurred near vision are the most frequently reported adverse events induced by atropine. Low-dose atropine is safer than moderate- and high-dose atropine. Our study could provide a safe reference for ophthalmologists to prescribe atropine for myopic children.

Efficacy and safety of atropine in myopic children: A meta-analysis of randomized controlled trials.

PURPOSE: To evaluate the safety and efficacy of atropine for childhood myopia and further explore the optimal concentration of atropine, so as to provide more reference for clinical application. METHODS: PubMed, Embase, Cochrane Library and ClinicalTrials.gov were comprehensively searched for randomized controlled trials (RCTs) up to October 14, 2021. The efficacy outcomes were progression of spherical equivalent (SE) and axial length (AL). The safety outcomes included accommodation amplitude, pupil size and adverse effects. The meta-analysis was performed using Review Manager 5.3. RESULTS: Eighteen RCTs involving 3002 eyes were included. The results showed that at 6-36 months of treatment, atropine was effective in slowing the progression of myopia in children. At 12 months, the WMD of SE and AL of low-dose atropine was 0.25 diopters (D) and 0.1 millimeter (mm), moderate-dose atropine was 0.44 D and 0.16mm, high-dose atropine was 1.21 D and 0.82mm, respectively, compared with the control group. Similarly, at 24 months, low-dose atropine was 0.22 D and 0.14mm, moderate-dose atropine was 0.60 D, high-dose atropine was 0.66 D and 0.24mm, respectively. Interestingly, we also found that there was no significant difference in the effects of low-dose atropine on accommodation amplitude and photopic pupil size compared with the control group, and the rate of photophobia, allergy, blurred vision and other side effects was similar between the low-dose atropine group and the control group. In addition, atropine appears to be more effective in myopic children in China than in other countries. CONCLUSIONS: Atropine in various concentrations can effectively slow myopia progression in children, and its effect is dose-dependent, while low-dose atropine (0.01% atropine) appears to be safer.

[[A MULTICENTER SPANISH STUDY OF ATROPINE 0.01% IN CHILDHOOD MYOPIA PROGRESSION]].

Myopia, short-sightedness, is the most frequent cause of vision difficulty and its prevalence is expected to rise. Nowadays, the usage of atropine drops is effective for myopia progression control. Studies on the Asian population showed that atropine 0.01% is more efficient and safer than solutions that have a higher concentration. In this study, we report findings from a multicenter Spanish study that showed that atropine 0.01% decreases the progression of myopia in a pediatric population, with relatively few adverse effects. The results of this study may be relevant to doctors who treat children who have myopia, as well as to the children treated and their parents.

Effect of Low-Concentration Atropine Eyedrops vs Placebo on Myopia Incidence in Children: The LAMP2 Randomized Clinical Trial.

Importance: Early onset of myopia is associated with high myopia later in life, and myopia is irreversible once developed. Objective: To evaluate the efficacy of low-concentration atropine eyedrops at 0.05% and 0.01% concentration for delaying the onset of myopia. Design, Setting, and Participants: This randomized, placebo-controlled, double-masked trial conducted at the Chinese University of Hong Kong Eye Centre enrolled 474 nonmyopic children aged 4 through 9 years with cycloplegic spherical equivalent between +1.00 D to 0.00 D and astigmatism less than -1.00 D. The first recruited participant started treatment on July 11, 2017, and the last participant was enrolled on June 4, 2020; the date of the final follow-up session was June 4, 2022. Interventions: Participants were assigned at random to the 0.05% atropine (n = 160), 0.01% atropine (n = 159), and placebo (n = 155) groups and had eyedrops applied once nightly in both eyes over 2 years. Main Outcomes and Measures: The primary outcomes were the 2-year cumulative incidence rate of myopia (cycloplegic spherical equivalent of at least -0.50 D in either eye) and the percentage of participants with fast myopic shift (spherical equivalent myopic shift of at least 1.00 D). Results: Of the 474 randomized patients (mean age, 6.8 years; 50% female), 353 (74.5%) completed the trial. The 2-year cumulative incidence of myopia in the 0.05% atropine, 0.01% atropine, and placebo groups were 28.4% (33/116), 45.9% (56/122), and 53.0% (61/115), respectively, and the percentages of participants with fast myopic shift at 2 years were 25.0%, 45.1%, and 53.9%. Compared with the placebo group, the 0.05% atropine group had significantly lower 2-year cumulative myopia incidence (difference, 24.6% [95% CI, 12.0%-36.4%]) and percentage of patients with fast myopic shift (difference, 28.9% [95% CI, 16.5%-40.5%]). Compared with the 0.01% atropine group, the 0.05% atropine group had significantly lower 2-year cumulative myopia incidence (difference, 17.5% [95% CI, 5.2%-29.2%]) and percentage of patients with fast myopic shift (difference, 20.1% [95% CI, 8.0%-31.6%]). The 0.01% atropine and placebo groups were not significantly different in 2-year cumulative myopia incidence or percentage of patients with fast myopic shift. Photophobia was the most common adverse event and was reported by 12.9% of participants in the 0.05% atropine group, 18.9% in the 0.01% atropine group, and 12.2% in the placebo group in the second year. Conclusions and Relevance: Among children aged 4 to 9 years without myopia, nightly use of 0.05% atropine eyedrops compared with placebo resulted in a significantly lower incidence of myopia and lower percentage of participants with fast myopic shift at 2 years. There was no significant difference between 0.01% atropine and placebo. Further research is needed to replicate the findings, to understand whether this represents a delay or prevention of myopia, and to assess longer-term safety. Trial Registration: Chinese Clinical Trial Registry: ChiCTR-IPR-15006883.

Central anticholinergic syndrome secondary to atropine eye drops: A case study.

Atropine eye drops are frequently used in the treatment of keratitis and during ophthalmic surgery. We described a rare complication of central anticholinergic syndrome secondary to atropine eye drops.

Efficacy of 0.01% low dose atropine and its correlation with various factors in myopia control in the Indian population.

We aimed to evaluate the efficacy and safety of low-dose atropine compared to placebo in the Indian population and also to study the impact of various modifiable and non-modifiable factors on myopia progression (MP) and drug efficacy (DE). It was a single-centre prospective placebo-controlled interventional study. 43 participants aged 6-16 years with progressive myopia received 0.01% atropine in the right eyes (treatment) and placebo in the left eyes (control) for 1-year. The main outcome measures were annual MP and axial length elongation (ALE) in treatment and control eyes and their percentage difference between two eyes (drug efficacy). Secondary outcome measures were the occurrence of any adverse events and the correlation of MP, ALE, and DE with various factors. 40 participants (80 eyes) completed the follow-up. After 1-year, MP was 0.25 D (IQR 0.13-0.44) and 0.69 D (IQR 0.50-1.0) (p < 0.001) in treatment and control respectively (63.89% reduction) with respective ALE of 0.14 mm (IQR 0.05-0.35) and 0.32 mm (IQR 0.19-0.46) (p < 0.001) (44.44% reduction). No adverse events were noted. Reduction in MP and ALE was statistically significant in all children irrespective of age-group, baseline MP, family history, screen-time, near and outdoor-time. The strongest determinants of annual MP were age (Treatment: r = - 0.418, p = 0.007; Control: r = - 0.452, p = 0.003) and baseline MP (Treatment: r = 0.64, p = 0.000; Control: r = 0.79, p = 0.000). Screen-time in control eyes was associated with greater ALE (r = 0.620, p = 0.042). DE was higher when outdoor time exceeded 2 h/day (p = 0.035) while the efficacy was lower with prolonged near activities (p = 0.03), baseline fast-progressors (p < 0.05) and history of parental myopia (p < 0.05). 0.01% atropine is effective and safe in retarding MP and ALE in Indian eyes.

Anticholinergics and serious adverse events in pediatric procedural sedation: A report of the pediatric sedation research consortiums.

BACKGROUND: Pediatric sedation is a clinical activity with potential for serious but rare airway adverse events, particularly laryngospasm. Anticholinergic drugs, atropine and glycopyrrolate, are frequently used with the intention to improve sedation safety by virtue of their antisialagogue effects. AIMS: The objective of this study is to describe the current practice of anticholinergic use in pediatric sedation and to compare the frequency of serious sedation-related adverse events in patients who received anticholinergics to those who did not. METHODS: We examined prospectively collected data from the Pediatric Sedation Research Consortium database. Patient characteristics, procedure type, sedation provider, sedatives, location of sedation, anticholinergic administered, adverse events, and airway interventions were reported. Propensity score matching and multivariable logistic regression were used to test whether any association exists between anticholinergic use and serious sedation-related adverse events. RESULTS: Anticholinergics were administered in 7.1% (n = 18 707) of all cases (n = 263 883) reported between November 2011 and October 2017. When anticholinergics were used, atropine was used in 22% (n = 4111) and glycopyrrolate in 78.1% (n = 14 601) of sedations. Use of anticholinergics was more common in patients with well-described risk factors for airway adverse events: active/history of upper respiratory infection, history of reactive airway disease/asthma, and exposure to smoke. However, infants and ASA 3 patients were not associated with higher rate of anticholinergic use. Anticholinergic use was independently associated with an increase in the odds of serious adverse events, OR 1.8 (95% CI 1.6-2.1), especially airway adverse events. CONCLUSIONS: In this large Pediatric Sedation Research Consortium study, we found the use of anticholinergic adjuvants independently associated with greater odds of serious adverse events, especially airway adverse events, after adjusting for well-known sedation risk factors using propensity score matching and multivariate analysis.

Safety and efficacy of 0.02% and 0.01% atropine on controlling myopia progression: a 2-year clinical trial.

Four hundred myopic children randomly received atropine 0.02% (n = 138) or 0.01% (n = 142) in both eyes once-nightly or only wore single-vision spectacles (control group) (n = 120) for 2 years. Spherical equivalent refractive error (SER), axial length (AL), pupil diameter (PD), and amplitude of accommodation (AMP) were measured every 4 months. After 2 years, the SER changes were - 0.80 (0.52) D, - 0.93 (0.59) D and - 1.33 (0.72) D and the AL changes were 0.62 (0.29) mm, 0.72 (0.31) mm and 0.88 (0.35) mm in the 0.02% and 0.01% atropine groups and control group, respectively. There were significant differences between changes in SER and AL in the three groups (all P < 0.001). The changes in SER and AL in the 2nd year were similar to the changes in the 1st year in the three groups (all P > 0.05). From baseline to 2 years, the overall decrease in AMP and increase in PD were not significantly different in the two atropine groups, whereas the AMP and PD in the control group remained stable (all P > 0.05). 0.02% atropine had a better effect on myopia control than 0.01% atropine, and its effects on PD and AMP were similar to 0.01% atropine. 0.02% or 0.01% atropine controlled myopia progression and AL elongation synchronously and had similar effects on myopia control each year.

The clinical efficacy and safety of atropine combined with omeprazole in the treatment of patients with acute gastritis: a systematic review and meta-analysis.

BACKGROUND: To date, guidelines on the impact and value of atropine combined with omeprazole in the treatment of acute gastritis have not been well established or well defined. This study aimed to clarify the efficacy and safety of combined atropine and omeprazole therapy for the management of patients with acute gastritis. METHODS: Through searching the electronic database, the related literature of the combination of atropine with omeprazole in the treatment of acute gastritis were reviewed. A meta-analysis was performed after literature selection according to inclusion criteria. The treatment efficiency and the incidence of adverse reactions were used as the main outcome indicators. The odds ratios (ORs), standardized mean differences (SMDs), and 95% confidence intervals (CIs) of the two treatment regimens were analyzed. RESULTS: This study analyzed 11 articles from the literature with a total of 1,053 subjects. The combination of atropine and omeprazole significantly improved the clinical outcomes of patients with acute gastritis compared to patients treated with combined anisodamine and omeprazole (control group). The effective rate of combined atropine and omeprazole treatment was 1.21 times higher than that observed with the control group, and the incidence of adverse reactions was 0.41 times that of the control group. Atropine combined with omeprazole significantly alleviated the clinical symptoms of the patients. The total treatment time was shortened by 0.57 days, duration of abdominal pain was shortened by 2.82 days, duration of diarrhea was reduced by 1.99 days, and the duration of nausea and vomiting was shortened by 2.68 days compared to the control group. DISCUSSION: The combination of atropine with omeprazole in the treatment of acute gastritis demonstrated a high effective rate with few adverse reactions than. It was effective at alleviating the clinical symptoms associated with acute gastritis. The results of this study provide support for the clinical implementation of combined atropine and omeprazole in the treatment of patients with acute gastritis.

Risk factors for rapid axial length elongation with low concentration atropine for myopia control.

Three hundred and twenty-eight myopic children, randomized to use either 0.01% (N = 166) or 0.02% (N = 162) atropine were enrolled in this study. Gender, age, body mass index(BMI), parental myopia status, atropine concentration used, pupil diameter, amplitude of accommodation, spherical equivalent refractive error (SER), anterior chamber depth (ACD) and axial length (AL) were collected at baseline and 1 year after using atropine. Rapid AL elongation was defined as > 0.36 mm growth per year. Univariate analyses showed that children with rapid AL elongation tend to be younger, have a smaller BMI, use of 0.01% atropine, narrow ACD, lower SER, shorter AL, smaller change in pupil diameter between 1 year and baseline (all P < 0.05). Multivariate logistic regression analyses confirmed that rapid AL elongation was associated with children that were younger at baseline (P < 0.0001), use of 0.01% atropine (P = 0.04), a shorter baseline AL (P = 0.03) and a smaller change in pupil diameter between 1 year and baseline (P = 0.04). Younger children with shorter AL at baseline, less change in their pupil diameter with atropine treatment and using the lower of the two atropine concentrations may undergo rapid AL elongation over a 12 months myopia control treatment period.

[The safety of atropine for myopia prevention and control].

Atropine is a classical drug with a wide use in clinical practice. In ophthalmology, atropine can be used for cycloplegia before optometry, and the treatment of amblyopia, iridocyclitis, malignant glaucoma, etc. In recent years, the "old drugs with new application " research and application of atropine for myopia prevention and control has become a hotspot and the efficacy of atropine has been preliminarily recognized. However, before the widely used in clinical, the safety of atropine draws attention. Researches concerning side effects of atropine were searched. The most common problem is photophobia due to dilated pupils, followed by poor near visual acuity, allergy and inflammation, local irritation. Other side effects include withdraw rebound, dry eyes, elevation of intraocular pressure, system reactions, photic damage and toxicity. Among them, some side effects are theoretical yet, and the long-term effects of some side reactions are not clear. Further research and exploration is needed to serve clinical evidence. At present, investigational usage for myopia prevention and control in clinical trials of atropine can be beneficial. Safety observation and efficacy evaluation are equally important in the course of application. (Chin J Ophthalmol, 2021, 57: 299-304).

Atropine-induced toxicity after off-label sublingual administration of eyedrop for sialorrhoea treatment in neurological disabled patients.

Sialorrhea is a troublesome and disabling symptom defined by the unintentional loss of saliva from the mouth, usually associated with swallowing disorders. Today there is no consensus about the management of sialorrhoea, but off-label use of ophthalmic atropine eyedrop administered sublingually may offer benefits, despite limited safety data. We report 2 cases of atropine overdose after sublingual administration illustrating that atropine can expose to severe adverse effects when administered sublingually. The noncompartmental pharmacokinetic study of atropine performed in 1 patient highlighted that systemic absorption of sublingual atropine was effective (Cmax [1 h] = 2.2 ng mL-1 ; approximately) after a single dose of 1 mg.

Organophosphorus compounds and oximes: a critical review.

Organophosphorus (OP) pesticides and nerve agents still pose a threat to the population. Treatment of OP poisoning is an ongoing challenge and burden for medical services. Standard drug treatment consists of atropine and an oxime as reactivator of OP-inhibited acetylcholinesterase and is virtually unchanged since more than six decades. Established oximes, i.e. pralidoxime, obidoxime, TMB-4, HI-6 and MMB-4, are of insufficient effectiveness in some poisonings and often cover only a limited spectrum of the different nerve agents and pesticides. Moreover, the value of oximes in human OP pesticide poisoning is still disputed. Long-lasting research efforts resulted in the preparation of countless experimental oximes, and more recently non-oxime reactivators, intended to replace or supplement the established and licensed oximes. The progress of this development is slow and none of the novel compounds appears to be suitable for transfer into advanced development or into clinical use. This situation calls for a critical analysis of the value of oximes as mainstay of treatment as well as the potential and limitations of established and novel reactivators. Requirements for a straightforward identification of superior reactivators and their development to licensed drugs need to be addressed as well as options for interim solutions as a chance to improve the therapy of OP poisoning in a foreseeable time frame.

Atropine Eye Drops Inappropriately Used for Diplopia Following Cosmetic Botulinum A Toxin Injections.

This is a first case report of atropine eye drops used inappropriately to treat diplopia that followed botulinum A toxin injections for a cosmetic indication. Also presented is a review of precautions on use of atropine eye drops by non-ophthalmic physicians.