Rare Side Effect Research Articles

NCOG-40. RARE ADVERSE EFFECT OF TEMOZOLOMIDE IN A 65-YEAR-OLD FEMALE WITH GLIOBLASTOMA MULTIFORME: A CASE REPORT

Abstract BACKGROUND Temozolomide, an antineoplastic agent is primarily used to treat certain brain tumors, including glioblastoma multiforme (GBM). Common side effects include nausea, vomiting, constipation, loss of appetite, alopecia (hair loss), headache, fatigue, convulsions and rash. A rare (less than 1%) adverse effect includes aplastic anemia refractory to treatment. Herein we present a case of Temozolomide induced severe bone marrow suppression in a 65-year-old woman with GBM refractory to any treatment CASE PRESENTATION A 65-year-old female presented with dizziness and left-hand numbness. Imaging revealed a right hemisphere mass and she underwent partial resection with pathology showing GBM, IDH wildtype, with CDKN2A/B deletion. She was started on radiation therapy with concurrent temozolomide. After nearly 5 weeks of temozolomide/RT, she developed severe thrombocytopenia/neutropenia with onset of neutropenic fever and severe CMV infection, leading to her demise within a week. DISCUSSION Life threatening refractory cytopenias is a very rare side effect of Temozolomide with a high rate of morbidity/mortality. In the case of our patient, she initially had weekly CBC’s which were stable and hence was switched to a monthly schedule. The patient’s ANC and platelets showed a precipitous drop within a month and ended up with aplastic anemia. The development of this rare complication underscores the importance of increased awareness about this often-fatal adverse event and possibly more frequent monitoring to recognize it early, especially in these patients with an already limited life expectancy. A more tailored approach to monitoring blood work may be needed depending on patient factors. CONCLUSIONS Aplastic anemia refractory to treatment is a rare and life threating adverse effect of temozolomide. The frequency of checking blood work for patients on Temodar has not been definitively established with protocols ranging from once weekly to monthly. Given the potential for this fatal adverse event, it is important to develop better tools to help identify patients in whom more frequent monitoring may be necessary.

Valproate-induced hyperammonemic encephalopathy in neurosurgical patients: Our experience and systematic literature review.

Sodium valproate is used for the management of seizures, status epilepticus, chronic pain syndrome, bipolar, and other affective disorders. Even with an acceptable safety profile, severe idiosyncratic reactions can occur with valproate use. A rare, serious, and life-threatening side effect of valproate is valproate-induced hyperammonemic encephalopathy (VHE). We intend to analyze the clinical presentation, diagnosis, treatment options, and outcome of VHE in neurosurgical patients and review the pertinent literature on this rare sequelae. We retrospectively reviewed patients who developed VHE following valproate use, either for the treatment of epilepsy or for seizure prophylaxis in our centre. We analyzed the demographic details, clinical presentation, diagnosis, management, and outcomes. A total of four patients with a mean age of 26.3 ± 5.1 (range 19 - 32years). Valproate was prescribed for primary seizure prophylaxis in 2 patients (50%). The commonest etiology for valproate prescription was for brain tumors (3, 75%) followed by drug-refractory epilepsy (DRE) (1, 25%). None of the patients were documented to have urea cycle disorder. The mean daily prescribed dosage of valproate was 1250 ± 559mg and the mean duration of administration was 13 ± 13.3months (range 4months - 36months). The mean serum NH3 level was 136,5 ± 44.2µmol/L (range 107 - 212.8) and all patients (4, 100%) had hyperammonemia with a mortality rate of 50% (2 patients). The hyperammonemia was treated by stopping the valproate use (4, 100%) and dialysis (2, 50%). Normalization of ammonia levels led to clinical improvement in 50% (2 patients). Neurological deterioration in the postoperative period is a diagnostic challenge. VHE is a rare and life-threatening sequelae of Valproate-associated Hyperammonemia (VAH) in neurosurgical patients. A high index of suspicion is required due to its ambiguous presentation. Early diagnosis and prompt treatment can change the course of this life-threatening sequelae.

Analysis of immunological and biochemical parameters after booster dose vaccination using protein-based and inactivated virus vaccine for safety

IntroductionHeterologous vaccines enhance the immune response to new variants and allow flexibility in booster administration when the original vaccine is unavailable. Studies show that heterologous boosters can generate comparable or superior antibody responses compared to homologous boosters. Considering rare side effects is essential in evaluating COVID-19 vaccines, especially those associated with ChAdOx1-S (AstraZeneca) and Ad26.COV2.S (Janssen), including blood clotting and idiopathic thrombocytopenia. Severe side effects, such as myocarditis and pericarditis, may occur after Pfizer or Moderna boosters but are rare. MethodsThis study administered two vaccines: the Sinopharm inactivated virus vaccine and the Razi-CoV-Pars (RCP) booster. Various evaluations included biochemical markers, coagulation factors, autoimmune antibodies, and antibodies against concerning variants. ResultsAll 90 participants exhibited a notable rise in antibody levels against the variant of concern (VOC). Participants receiving the Razi-CoV-Pars booster after Sinopharm/BBIBP-CorV showed significantly higher antibody levels (Wuhan ∼ 3.25 times, Delta ∼4 times, Omicron ∼ 14 times) compared to those receiving Sinopharm's homologous vaccine. No significant changes (P: <0.05) were found in LDH, CPK, CK-MB, ANA, and Anti-CCP levels. However, individuals receiving Sinopharm's booster after two doses showed a significant increase (4 cases) in D-Dimer levels. ConclusionThe Razi-CoV-Pars vaccine demonstrates a favorable safety profile and promising potential as an effective booster against current variants, particularly due to its significant protective titer against Omicron.

Isotretinoin-associated chronic diarrhea as a complication of systemic isotretinoin therapy

Objective: Isotretinoin is a synthetic derivative of vitamin A that is highly effective in treating acne vulgaris. Although its common side effects include skin dryness, photosensitivity, epistaxis, and depressive disorders, gastrointestinal side effects should also be considered, though they are less frequently highlighted. Case: We aim to present a 28-year-old female patient who developed chronic diarrhea and associated hypokalemic paralysis during isotretinoin treatment, prescribed for acne management. This case underlines the importance of recognizing gastrointestinal side effects, alongside the more commonly known adverse effects of isotretinoin. Conclusion: Chronic diarrhea is a rare but significant side effect of isotretinoin that may lead to serious complications such as hypokalemic paralysis. In this case, we demonstrated how isotretinoin can cause metabolic imbalances, even in relatively healthy young adults, by inducing diarrhea. While the association between isotretinoin and inflammatory bowel disease remains inconclusive, clinicians should remain vigilant regarding the gastrointestinal side effects of isotretinoin. Early recognition and discontinuation of the drug, combined with appropriate supportive treatments, are essential in preventing further complications. Dermatologists and gastroenterologists should collaborate in identifying patients at higher risk, such as those with pre-existing gastrointestinal conditions, and closely monitor for any adverse effects during isotretinoin treatment. Future studies, particularly large-scale randomized controlled trials, are needed to better understand the relationship between isotretinoin and gastrointestinal side effects.

Up-titration of Guideline Directed Medical Therapy (GDMT) and the occurrence of side effects in Heart Failure with reduced Ejection Fraction (HFrEF)

Abstract Background The ESC Guidelines recommend early, full-dose use of heart failure (HF) medications to enhance survival, but real-world application often faces delays and inconsistencies. Clinicians often fear side effects during up-titration to the recommended target dose (TD), i.e. hypotension, bradycardia, renal impairment, and hyperkalemia (HK). The dependency of side effects during dose escalation from the severity of HF remains unclear. Purpose This study aimed to evaluate the relationship between the occurrence of side effects during up-titration of HF medication and HF severity reflected by N-terminal pro B-type natriuretic peptide (NT-proBNP). Methods 425 patients with HFrEF and a complete data set of patient characteristics, medications and laboratory values at baseline (BL), 2 months (2M), and 6 months (6M) were included from our outpatient HF unit's prospective registry. Significant side effects were defined as: systolic blood pressure (SBP) &amp;lt;90mmHg, heart rate (HR) &amp;lt;50 beats per minute (bpm), potassium (K) &amp;gt;5.0mmol/l or K &amp;gt;5,5mmol/l and estimated glomerular filtration rate (eGFR) &amp;lt;30ml/min/1.73m2. Patients were categorized into three risk groups based on their NT-proBNP levels, i.e. low-risk with NT-proBNP &amp;lt;1000pg/ml, medium-risk with NT-proBNP 1000-2000pg/ml or high-risk with NT-proBNP &amp;gt;2000pg/ml. The occurrence of side effects was recorded and the development compared among the HF risk groups. Results Figure 1 shows up-titration of HF medication. Mean daily dosages of betablockers (BB), mineralocorticoid receptor antagonists (MRA) and renin-angiotensin-system inhibitors (RASi) increased significantly during follow-up (BL vs 2M and BL vs 6M, p&amp;lt;0.001 for all). The majority of patients received ≥50% of the recommended TDs at 6M (89% for BB, 83% for MRA, 88% for RASi and 91% for total mean TDs ≥50%), and the achieved daily dosages at 6M were largely comparable across the HF risk groups at 6M, except for RASi (p=0.030). Figure 2 depicts the side effects. Side effects developed almost exclusively at short-term within 2M except for lower SBP (Figure 2A). Newly developed side effects occurring after up-titration (2B) were even more rare and predominantly occurred within the highest NT-proBNP group. The occurrence of hypotension and bradycardia was infrequent and comparable within the HF risk groups. Renal dysfunction (at 6M p=0,041) and HK occurred predominantly in higher risk patients (HK at 2M p=0,001 and at 6M p&amp;lt;0,001). Conclusions Up-titration of HF medications is highly feasible, particularly in low- and medium-risk patients. Despite rare side effects such as hyperkalemia and renal impairment, up-titration remains unimpeded, especially in patients with NT-proBNP levels below 2000pg/ml. These findings emphasize the safety of up-titration in HF.

Valacyclovir Induced Neurotoxicity, with Therapeutic Drug Monitoring, in a Hospital-Based Setting in the Netherlands.

Valacyclovir-induced neurotoxicity is a rare side effect. The aim of this study was to perform a retrospective analysis of patients with valacyclovir-induced neurotoxicity and establish valacyclovir plasma concentrations in a tertiary hospital between January 2018 and November 2022. In total 208 patients were identified with measured acyclovir concentrations, and the electronic health records of these patients were analysed. Based on the in- and exclusion criteria, 4 patents were identified in whom high plasma concentrations were linked to neurotoxicity. The first patient experienced balance and coordination problems, visual hallucinations, speaking difficulties and headaches. The second patient experienced a progressive decline of consciousness, resulting in coma. The third patient also experienced reduced consciousness and was found unconscious on the floor during the night. The fourth patient experienced vertigo after administration of acyclovir. Based on this study, neurotoxicity appears to be an underreported adverse effect of valacyclovir therapy in a hospital setting. This side effect may have a high impact on individuals as well as on the duration of hospitalization. In order to exclude valacyclovir as the cause, clinicians should consider requesting an acyclovir plasma concentration as standard hospital-based intervention whenever a patient experiences neurotoxic symptoms. Moreover, pharmacists and clinicians should be made better aware of the interaction between valacyclovir and cyclosporine and/or mycophenolic acid, in particular in elderly patients with impaired kidney function. Valaciclovir-induced neurotoxicity diagnosis is underreported.Accessible and frequent therapeutic drug monitoring (TDM) of valacyclovir is recommended.Interactions between valaciclovir and ciclosporin and/or mycophenolic acid, in particular in elderly patients with impaired kidney function, need a follow-up during hospitalization.

Polymyxin-B induced bartter-like syndrome: an unusual adverse effect

Introduction and Importance: Bartter syndrome is a rare autosomal recessive disorder affecting renal tubular function, leading to electrolyte and volume homeostasis disturbances. It can also manifest as Bartter-like syndrome, a rare side effect of certain medications. Polymyxin-B, used to treat multidrug-resistant infections, is infrequently associated with BLS, making early recognition crucial to prevent severe electrolyte imbalances. Case Presentation: A 73-year-old female with coronary artery disease, COPD, hyperlipidemia, and other comorbidities presented with fever, respiratory distress, and hypoxia on mechanical ventilation. Initial labs showed leukocytosis, anemia, and normal potassium. Despite broad-spectrum antibiotics, sputum cultures revealed pandrug-resistant Acinetobacter baumannii, sensitive only to Polymyxin-B. After six days of Polymyxin-B, the patient developed fever, hypotension, hypokalemia, hypomagnesemia, and polyuria. Urine studies indicated increased potassium excretion. A diagnosis of Bartter like syndrome was made. Polymyxin-B was discontinued, and the patient’s electrolytes normalized, resolving the polyuria. She was discharged with daily potassium and magnesium supplements. Clinical Discussion: Bartter-like syndrome can result from Polymyxin-B-induced tubular dysfunction, characterized by hypokalemia and hypomagnesemia. Close electrolyte monitoring is essential for patients receiving this antibiotic, particularly in those with complex medical conditions. Early recognition allowed for timely discontinuation of Polymyxin-B, which rapidly reversed the electrolyte disturbances. Conclusion: This case underscores the importance of recognizing Polymyxin-B-induced Bartter-like syndrome. Clinicians should be vigilant for electrolyte disturbances in patients undergoing treatment with Polymyxin-B, ensuring timely interventions to mitigate adverse outcomes.

DESAFIOS DO MANEJO DO LÍTIO NO PACIENTE PSIQUIÁTRICO: ESTRATÉGIAS PARA GARANTIR A SEGURANÇA E EFICÁCIA DO TRATAMENTO

Although lithium has been used for decades, its management remains a clinical challenge, since it is a drug with narrow therapeutic indices and with possible adverse effects. Therefore, this study aims to present evidence and clinical challenges of lithium management in psychiatry, in order to contribute to a better understanding of the use of this drug and the conscious management of patients who use this medication. This is a retrospective, documental Integrative Literature Review about the challenges of lithium management in psychiatric patients. For the development of this work, the following steps were followed: 1) Construction of the theme and the guiding question; 2) Establishment of inclusion and exclusion criteria; 3) Collection of studies in the scientific bases; 4) Evaluation of the selected abstracts; 5) Evaluation and categorization of studies in full; 6) Analysis and interpretation of the results. Lithium, as a mood stabilizer, was a great historical discovery and its importance lies in its effectiveness in controlling the symptoms of bipolarity, being considered a first-line mood stabilizer for the treatment of bipolar disorder and other psychopathologies. It is concluded, therefore, that the management of lithium in the treatment of psychiatric disorders requires a careful and individualized approach, taking into account the efficacy of the drug, patient safety and possible drug interactions and clinical conditions. Knowledge of the common and rare side effects of lithium is essential to ensure successful and safe treatment.

Intestinal obstruction following antituberculosis therapy in a patient with pancreatic carcinoma and pulmonary tuberculosis: a case report

IntroductionIntestinal obstruction is a common complication in patients with advanced malignancies, often attributed to the disease itself or as a side effect of opioid analgesics used for pain management. However, the occurrence of intestinal obstruction following antituberculosis therapy is rare.Case presentationWe report a unique case of a 58-year-old Asian male diagnosed with stage IV pancreatic carcinoma and pulmonary tuberculosis. The patient was initiated on a regimen of ethambutol hydrochloride, pyrazinamide, rifampicin, and isoniazid tablets (II) for tuberculosis, alongside morphine for the management of severe cancer-related pain. Subsequently, he developed symptoms indicative of intestinal obstruction. Despite discontinuation of morphine, the patient’s symptoms persisted until he autonomously ceased all medications, leading to a rapid improvement in his condition. This unexpected resolution highlighted the antituberculosis drugs as the probable cause of his intestinal obstruction.ConclusionsThis case underscores the importance of considering antituberculosis drugs as a potential cause of intestinal obstruction, especially in patients who do not respond to conventional management strategies for drug-induced gastrointestinal side effects. It also emphasizes the need for heightened vigilance and monitoring when prescribing these medications to patients with advanced malignancies, to promptly identify and address rare but significant side effects.

Evaluation of akathisia in patients receiving selective serotonin reuptake inhibitors/serotonin and noradrenaline reuptake inhibitors.

Akathisia is an underestimated but disturbing extrapyramidal side effect of antidepressants, which could reduce treatment compliance in mood disorders. This study aimed to investigate the frequency and risk factors in patients treated with selective serotonin reuptake inhibitors/serotonin and noradrenaline reuptake inhibitors (SSRI/SNRI). In addition, we assessed the impact of akathisia on the quality of life (QoL). Patients were aged between 18 and 75 years, receiving an SSRI/SNRI for 4-8 weeks, and were diagnosed with anxiety, depression, or obsessive-compulsive disorder. The Barnes Akathisia Rating Scale was used to assess the severity of the akathisia. QoL was evaluated using the Short Form 36 (SF-36) questionnaire. Akathisia was observed in 25% (50/198) of patients. Smokers and younger patients were more frequent among patients with akathisia. Physical functioning, physical role, vitality, and mental health domains of the SF-36 were reduced in the presence of akathisia. In conclusion, our results suggest that akathisia is not a rare side effect of SSRI/SNRI in patients with mood disorders, especially in smokers and younger patients. In addition, akathisia may reduce treatment compliance owing to a reduction in QoL. Further investigations are needed to confirm the risk factors, frequency, and consequences of treatment compliance for SSRI/SNRI-induced akathisia in patients with mood disorders.

A Potential Pneumothorax Induced by Immune Checkpoint Inhibitors: A Case Report and Literature Review

Background and Objectives: Immune checkpoint inhibitors (ICIs), which target immune checkpoints in cancer cells, are increasingly used as a mainstay in anticancer treatment. The combination of atezolizumab and bevacizumab is also a first-line treatment for hepatocellular carcinoma (HCC). However, ICIs can cause immune-related adverse events (IrAEs) which range from mild to severe, potentially leading to the need for discontinuing immunotherapy. We report a case of a pneumothorax, a rare side effect caused by IrAEs. Materials and Methods: This paper reports a case of a 78-year-old male HCC patient who developed a recurrent pneumothorax, suspected to be an adverse effect of ICIs. Results: The patient was a current smoker with a 30 pack-year smoking history. Prior to initiating ICIs, a chest CT scan showed mild emphysema and fibrosis attributable to smoking. Following ICI treatment, the patient developed a recurrent pneumothorax. Further tests revealed no underlying cause for the pneumothorax other than the ICIs and smoking, and there were no signs of intrapulmonary metastasis or pneumonitis. Conclusions: When a pneumothorax occurs in a patient undergoing immunotherapy, it is important to consider it as a potential adverse effect of the treatment. Special attention should be given to the possibility that immunotherapy may exacerbate underlying lung conditions. Patients should be advised on the importance of smoking cessation. As there are currently no guidelines for resuming immunotherapy after a pneumothorax, it is crucial to weigh the risks and benefits and consider dose reduction or discontinuation of the medication.

12564 A Rare Case Of Pembrolizumab Induced Secondary Adrenal Insufficiency

Abstract Disclosure: L. Escano Volquez: None. P. Desai: None. Pembrolizumab is an immune check-point inhibitor that blocks the PD1 receptor and is currently used in the treatment of a vast variety of malignancies. Despite adrenal insufficiency (AI) already being documented as a rare but potential side effect, its diagnosis is usually delayed due to vague presentation, increasing the risk of deleterious outcomes. We present a case of secondary AI while on pembrolizumab in which diagnosis was delayed due to unspecific clinical picture.This is a 66-year-old male who presented to the hospital with decreased appetite, nausea and generalized weakness. Patient was seen a month prior with similar symptoms which were thought to be secondary to poor oral intake in the setting of underlying malignancy. Medical history remarkable for squamous cell carcinoma of the skin with recent lung metastasis for which he was started on pembrolizumab a year ago. On arrival to the emergency department, patient was hypertensive with BP 144/68 mmHg, HR 88, and RR 15. Orthostatic vitals were positive. Physical examination otherwise unremarkable. Laboratory tests revealed mild hypernatremia of 147, potassium of 4.7, chloride 108, HCO3 18, anion gap 21, BUN 33, elevated creatinine 1.62 and elevated beta-hydroxybutyrate 5.4. EKG revealed sinus rhythm. Patient was admitted for further evaluation of orthostasis and starvation ketosis. Initial management included IV fluids and Midodrine. However, patient continued to have episodes of orthostatic hypotension. Lack of improvement of symptoms led to further workup which revealed low AM cortisol of 1.0 and a low ACTH level &amp;lt;3.0 pg/ml, concerning for secondary adrenal insufficiency. Patient was administered Solu-Medrol 40 mg IV before being transitioned to a daily hydrocortisone regimen with subsequent improvement of symptoms. Pembrolizumab induced AI is a very rare event. It is estimated that the incidence approaches 1% and symptoms can develop at any time throughout treatment. Despite its low incidence, it can be life-threatening if not diagnosed and treated promptly. However, given its very heterogeneous and vague clinical presentation, a prompt diagnosis can be difficult. The clinical course of our patient and subsequent resolution of symptoms after appropriate treatment was started, supports the diagnosis of pembrolizumab induced adrenal insufficiency after a year of initiating treatment. This patient had prior hospitalizations and office visits with symptoms that are usually already present in individuals with underlying malignancy, which resulted in underestimation of his symptoms. This case highlights the importance of always considering AI as a potential adverse effect of immune check-point inhibitors. This will ensure a prompt diagnosis and treatment of an endocrine disorder that could otherwise lead to deleterious outcomes if left untreated. Presentation: 6/1/2024

8439 Targeting Interferon Gamma-Mediated CXCL16-CXCR6 Chemokine-Receptor Interactions As A Strategy To Prevent Immune Checkpoint Inhibitor Autoimmune Diabetes

Abstract Disclosure: S. Wang: None. N. Huang: None. J.G. Ortega: None. J. Lee: None. K. Kimbrell: None. J. Nguyen: None. J. Olay: None. E. McCarthy: None. E. Peluso: None. H. Chen: None. M.G. Lechner: None. Autoimmune diabetes mellitus is a rare but life-threatening side effect of immune checkpoint inhibitor (ICI) cancer therapy. Checkpoint inhibitors increase immune activation by blocking regulatory molecules on T cells, including programmed death protein (PD1). As a result of this heightened immune activation, patients can develop autoimmunity in healthy tissues, known as immune related adverse events (IRAEs). ICI-associated diabetes mellitus (ICI-T1DM) is an IRAE that results in autoimmune destruction of insulin-producing pancreatic beta-cells. Patients with ICI-T1DM require life-long insulin therapy and more than half present initially with diabetic ketoacidosis. Unfortunately, the mechanism of this IRAE is not fully understood. Anti-PD1 antibody treatment (10mg/kg/dose, twice weekly, i.p.) of male and female non-obese diabetic (NOD) mice leads to autoimmune infiltrates in multiple tissues, including accelerated insulitis and DM. Single cell RNA sequencing of islet infiltrating immune cells from ICI-treated mice previously showed a role for CD8+ T cells and cytokine interferon gamma (IFNγ) in the development of ICI-T1DM. Using CellChat to perform receptor-ligand interaction analysis of these data, we identified both CD8+ and CD4+ T cells as the primary source of IFNγ in immune infiltrates and islet myeloid cells as the primary target. Furthermore, CellChat analysis showed increased receptor-ligand interactions between T cell receptor CXCR6 and its chemokine CXCL16, as well as CXCR3 and chemokines CXCL9 and CXCL10. In vitro IFNγ stimulation of myeloid cells induced strong expression of CXCL16, 9, and 10, suggesting a potential mechanism by which effector T cells are recruited to islets during ICI therapy. Immunophenotyping of islet-infiltrating immune cells indeed showed increased IFNγ+CXCR6+ effector CD8+ cells in anti-PD1 treated mice compared to isotype-treated controls. Moreover, these IFNγ+CXCR6+CD8+ T cells stained positively for the NRP-V7 mimotope tetramer, a known antigen for CD8+ T cells in spontaneous autoimmune diabetes in NOD mice, suggesting this as an antigen-specific population contributing to the immunopathogenesis of ICI-T1DM. Finally, genetic deletion of CXCR6 in NOD mice delayed the onset of autoimmune diabetes during anti-PD1 treatment in female (p=0.0162) but not male mice (p=0.3656). In summary, these data further elucidate the cellular mechanisms by which IFNγ and chemokine signaling pathways drive the development of ICI-T1DM and identify the CXCR6-CXCL16 axis as a potential therapeutic target to prevent this IRAE in checkpoint inhibitor-treated cancer patients. Presentation: 6/2/2024

7173 Cabergoline Induced Psychosis in a Patient with no Previous History of Psychiatric Disorder

Abstract Disclosure: B. Aryal: None. K. Kim: None. A. Shafi: None. M. Ganesh: None. Introduction: Cabergoline is a dopamine agonist (DA) used to treat prolactinomas. It is well established that DAs may cause psychotic symptoms. However, very few cases report cabergoline-associated psychosis in patients without personal or family history of psychiatric disorders. We report a rare case of cabergoline-induced psychosis in a patient with a prolactinoma without any underlying psychiatric disorder, which was managed with the addition of olanzapine. Case: A 41 year old male with no history of psychiatric disorder was started on cabergoline 0.5mg twice a week for a newly diagnosed prolactinoma. 4 weeks later, he presented to the emergency room for aggressive behavior and confusion for the past 2 weeks. He endorsed visual and auditory hallucinations. Cabergoline was discontinued. During hospitalization, he attempted suicide and required 1:1 observation. He was started on olanzapine per the inpatient psychiatry team. Surgical resection of the prolactinoma was considered given his acute psychosis associated with cabergoline. However, complete resection of the tumor was deemed impossible given encasement of the internal carotid arteries. After discussion with the patient, he underwent re-challenge with cabergoline 0.25mg weekly while on olanzapine under 1:1 observation in the ICU. He was monitored for 2 weeks and eventually discharged home on cabergoline 0.25mg twice a week and olanzapine with improvement in prolactin levels to 4973.7 ng/mL after 4 weeks. He continued to remain free of psychotic symptoms upon follow up as an outpatient. Discussion: Psychosis is a rare side effect of DA mediated via D2/D3 receptors in the mesocortical and mesolimbic pathways. Several cases report psychosis associated with cabergoline in patients with a history of psychiatric disorders. However only one case reports de novo psychosis. Our patient developed severe psychosis while on low-dose cabergoline for 4 weeks. This rare case of de novo cabergoline-associated psychosis re-emphasizes that psychosis may occur regardless of previous history of psychiatric disorder and independent of the dose or duration of cabergoline. Treatment of a prolactinoma in the setting of cabergoline-associated psychosis requires a multidisciplinary approach. Alternative treatment of surgical resection was considered for our patient. However surgical resection was not plausible given difficult surgical anatomy. Therefore he was monitored closely to re-initiate cabergoline while on olanzapine. Several cases report successful use of clozapine, aripiprazole, and quetiapine for patients with psychiatric symptoms while on cabergoline. Patients who are on cabergoline should be closely monitored for any psychotic symptoms. Further studies are warranted to identify patients at risk of developing psychosis while on cabergoline to tailor an individualized approach to therapy and monitoring. Presentation: 6/2/2024

6609 Central Serous Chorioretinopathy in the Eyes of the Beholder of Testosterone Depot Injection

Abstract Disclosure: H. Ni: None. D. Kankanamge: None. J. Jabbour: None. V.A. Preda: None. Background: Central serous chorioretinopathy (CSC) is a characterised by subretinal fluid accumulation causing detachment of the neurosensory retina and visual disturbance[1]. It has been postulated that increased focal choriocapillaris permeability results in leakage of interstial fluid into the subretinal space[1]. CSC is a rare side effect of testosterone therapy, the exact mechanism is unclear. Case : We present a 32-year-old male gym manager who has been self-administering anabolic steroids with testsoterone ethanoate IM injections every 14 days for body building. He reported left blurred vision for 8 weeks. He was normotensive and reported taking doxycycline and azithromycin for mycoplasma genitalia. There was no history of glucocorticoid exposure, smoking, alcohol use, gastoesophageal reflux disease, hypertension, shift work, sleep apnoea, nor other established risk factors for CSC. The visual acuity was OD 6/6 and OS 6/9 with intraocular pressures of 12mmHg on the right and 15mmg on the left. Fundoscopy revealed a left serous macular elevation involving the left fovea. A macular OCT confirmed the left acute central serous chorioretinopathy and right retinal pigment epithelial changes. The latter were suggestive of right CSC in the past. Discussion: Androgens have been associated with CSC in the literature. It has been hypothesised that exogenous testosterone may cause increased choriodal blood flow and permeability, promote atheroscleorsis, cause sodium retention and potentially interact with retinal pigment epithelium (RPE) via androgen receptors4. Intramuscular testosterone therapy causes fluctuation in plasma testosterone concentration (which is thought to be more relevant than absolute value of testosterone). Most cases (60%) of CSC resolve spontaneously, and appear to coincide with cessation of testosterone therapy5. Conclusion: Clinicans need to be alert to the use of testosterone and other anabolic steroids, prescribed or self administered, particularly in their patients with CSC or who have other risk factors for CSC, such as corticosteroids, smoking and hypertension.

8158 Transient Blindness In Metformin-Associated Lactic Acidosis

Abstract Disclosure: Y. Abouelkheer: None. A. Nasir: None. M. Ibrahem: None. Transient Blindness in Metformin-associated Lactic Acidosis Background: Metformin-associated lactic acidosis (MALA) is a rare side effect of metformin use. MALA can result in acute transient blindness in patients with severe metabolic derangements. Clinical Case: A 62-year-old woman presented with severe diarrhea, poor oral intake, malaise, and vomiting on a background of metformin-treated type 2 diabetes mellitus. Laboratory investigations showed bicarbonate &amp;lt;2 mmol/L, anion gap 48 mmol/L, lactic acid 20.5 mmol/L, serum osmolality 352 mOsm/kg, negative urine toxicology screen, and positive SARS-CoV-2. In the emergency department, the patient developed sudden onset bilateral vision loss. The examination was remarkable for complete vision loss bilaterally in all fields, associated with minimally reactive pupils and spontaneous ocular movements with an otherwise unrevealing neurological examination. Computed Tomography (CT) of the brain with stroke protocol showed no evidence of acute intracranial process. CT angiogram of the brain and neck showed patent intracranial and cervical vasculature without high-grade stenosis, large vessel occlusion, or aneurysm. While receiving medical management with intravenous fluid resuscitation and sodium bicarbonate supplementation, the patient had a spontaneous return of vision with no additional neurological complications or deficits. The severe metabolic derangements were associated with distributive shock, requiring admission to the intensive care unit for urgent hemodialysis, pressor support, empiric antibiotics, and stress-dose steroids. Shortly after the patient’s only hemodialysis session, we noted the resolution of her critical metabolic disturbances, renal failure, and shock state. Laboratory investigations post-dialysis showed bicarbonate 12 mmol/L, anion gap 36 mmol/L, and lactic acid 10.5 mmol/L. Follow-up MRI showed chronic lacunar infarct of the left basal ganglia, and she was discharged home six days later. Conclusion: Transient blindness in MALA can mimic acute neurovascular events. Prompt correction of metabolic derangements can aid in reversing systemic symptoms and blindness. Reference: DeFronzo R, Fleming GA, Chen K, Bicsak TA. Metformin-associated lactic acidosis: Current perspectives on causes and risk. Metabolism. 2016;65(2):20-29. doi:10.1016/j.metabol.2015.10.014 Presentation: 6/2/2024

Cerebral Artery Vasoconstriction After Galcanezumab Loading Dose for Migraine Prevention: A Case Report.

Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies that target CGRP ligands or receptors, may cause a very rare side effect of reversible cerebral vasoconstriction syndrome (RCVS). This study is a case report of a patient who developed cerebral artery vasoconstriction documented on serial brain magnetic resonance angiography (MRA) scans without the typical manifestations of RCVS following galcanezumab loading dose. Case report: A 40-year-old female patient with high-frequency episodic migraine with visual aura on topiramate 100mg/day developed transient numbness of the right upper and lower extremities and right face without headache and a normal neurological examination 10min after a loading dose of galcanezumab, which resolved over the next 2days. Magnetic resonance angiography brain imaging showed segmental arterial constriction of both middle cerebral arteries in the M1-2 segments and both posterior cerebral arteries in the P1-2 segments, which partial resolved in a subsequent study by the end of 6months. There were no other supporting examination data, such as transcranial Doppler, which might provide additional information on the progression and improvement of the vasoconstriction. Her differential diagnosis included prolonged migraine sensory aura without headache, RCVS, or cerebral vasoconstriction secondary to the effect of an anti-CGRP monoclonal antibody. Further research needs to be conducted.

Metoclopramide-induced opsoclonus-myoclonus-ataxia syndrome: A rare side-effect

Opsoclonus-myoclonus-ataxia syndrome (OMAS) is an autoimmune disorder involving the nervous system characterized by rapid involuntary eye movements (opsoclonus), involuntary brief muscle twitching (myoclonus), loss of coordination of movements, imbalance, disturbances of sleep, irritability, slurring of speech, and decreases muscle tone. Hyperemesis gravidarum, intractable vomiting during pregnancy, results in reduction in intravascular volume, can produce ketonemia. We describe a case of primigravida who had hyperemesis gravidarum and suffered metoclopramide-induced OMAS.

Ketorolac Dose Ceiling Effect for Pediatric Headache in the Emergency Department

OBJECTIVE This study sought to demonstrate a non-inferiority analgesic ceiling effect previously ­demonstrated within adults for pediatric patients receiving a maximum ketorolac dose of 15 mg. METHODS We conducted a retrospective cohort study of pediatric ED patients weighing at least 60 kg treated with 30 mg (pre-intervention) or 15 mg (post-intervention) intravenous (IV) ketorolac for headache. The primary outcome included patient-reported pain scores. Additional outcomes included demographic variables, adjunct medication use and adverse effects. Categorical data were evaluated using a χ2 test, and numerical data were evaluated using an ANOVA F test and Welch 2-sample t test. RESULTS The pre- and post-intervention groups included 216 and 62 patients, respectively. Overall demographics were similar between the groups (72.3% female, 49.3% White/Caucasian, mean age 15.5 years, mean weight 79.2 kg, and mean baseline 10-point pain score 7.5). Twelve (5.6%) in the pre-intervention group required rescue analgesic compared with 2 patients (3.2%) in the post-intervention group (p = 0.416). In the pre-intervention group, 198 patients (91.7%) received nausea medication compared with 52 patients (83.9%) in the post-intervention group (p = 0.087). Mean 10-point pain scores following ketorolac administration decreased by 3.9 in the pre-intervention group compared with 5.1 in the post-intervention group (p = &amp;lt; 0.001). Common (0.9%) or rare (0.9%) side effects were infrequent and only seen in the pre-intervention group patients. CONCLUSIONS Truncating the maximum intravenous ketorolac dose in pediatric patients at least 60 kg in weight to 15 mg compared with 30 mg results in effective analgesia in pediatric patients with headache. Future research could explore differences in admission rates, treatment of other indications, or treatment with multiple-dose regimens.

Olanzapine‐Induced Pedal Oedema With Delayed Resolution: A Case Report and Review of Literature

ABSTRACTOlanzapine can have a better impact on negative symptoms of schizophrenia with reduced motor side effects compared to other atypical antipsychotics, according to some literature. Here, the authors describe a case of a woman with a diagnosis of schizophrenia who developed the rare side effect of bilateral pedal oedema while on oral olanzapine. The possible mechanism behind the condition and the clinical management measures taken to resolve the oedema is discussed.