scholarly journals Chest Pain in a Psychiatric Patient Due to Clozapine-Induced Myopericarditis

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
James L. Laws ◽  
Esther Kim ◽  
Rebecca Hung ◽  
JoAnn Lindenfeld ◽  
Richa Gupta
Keyword(s):  
Chest Pain ◽  
Cardiac Function ◽  
Psychiatric Patient ◽  
Drug Induced ◽  
Clozapine Therapy ◽  
Variable Presentation ◽  
Drug Cessation

Drug-induced myocarditis is a rare, but underrecognized complication of clozapine therapy for schizophrenia. We present a case of clozapine-induced myocarditis with recovery of cardiac function after drug cessation and summarize the literature to highlight the variable presentation of this condition.

scholarly journals Clinical and laboratory characteristics of clozapine-treated patients with schizophrenia referred to a national immunodeficiency clinic reveals a B-cell signature resembling common variable immunodeficiency (CVID)

2020 ◽  
Vol 73 (9) ◽  
pp. 587-592 ◽  
Author(s):  
Mark James Ponsford ◽  
Rachael Steven ◽  
Kathyrn Bramhall ◽  
Mathew Burgess ◽  
Sonali Wijetilleka ◽  
...  
Keyword(s):  
Common Variable Immunodeficiency ◽  
Antibody Deficiency ◽  
Case Note ◽  
Retrospective Case ◽  
Clozapine Therapy ◽  
Clozapine Treatment ◽  
Immunoglobulin Replacement ◽  
Common Variable ◽  
Case Note Review ◽  
Drug Cessation

AimsAn association between antibody deficiency and clozapine use in individuals with schizophrenia has recently been reported. We hypothesised that if clozapine-associated hypogammaglobulinaemia was clinically relevant this would manifest in referral patterns.MethodsRetrospective case note review of patients referred and assessed by Immunology Centre for Wales (ICW) between January 2005 and July 2018 with extraction of clinical and immunological features for individuals with diagnosis of schizophrenia-like illness.Results1791 adult patients were assessed at ICW during this period; 23 patients had a psychiatric diagnosis of schizophrenia or schizoaffective disorder. Principal indications for referral were findings of low calculated globulin and immunoglobulins. Clozapine was the single most commonly prescribed antipsychotic (17/23), disproportionately increased relative to reported use in the general schizophrenia population (OR 6.48, 95% CI: 1.79 to 23.5). Clozapine therapy was noted in 6/7 (86%) of patients subsequently requiring immunoglobulin replacement therapy (IgRT). Marked reduction of class-switched memory B cells (CSMB) and plasmablasts were observed in clozapine-treated individuals relative to healthy age-matched controls. Clozapine duration is associated with CSMB decline. One patient discontinued clozapine, with gradual recovery of IgG levels without use of IgRT.ConclusionsOur findings are consistent with enrichment of clozapine-treatment within schizophrenic individuals referred for ICW assessment over the last 13 years. These individuals displayed clinical patterns closely resembling the primary immunodeficiency common variable immunodeficiency, however appears reversible on drug cessation. This has diagnostic, monitoring and treatment implications for psychiatry and immunology teams and directs prospective studies to address causality and the wider implications for this patient group.

scholarly journals Antifungals in a case of basidiobolomycosis: role and limitations

2019 ◽  
Vol 12 (9) ◽  
pp. e230206 ◽  
Author(s):  
Anjum Saeed ◽  
Asaad M Assiri ◽  
Ishfaq A Bukhari ◽  
Rasha Assiri
Keyword(s):  
Chest Pain ◽  
Antifungal Activity ◽  
Drug Induced ◽  
Severe Chest Pain ◽  
Oral Itraconazole

A 10-year-old Saudi boy was diagnosed to have basidiobolomycosis after a stormy course of his ailment. Therapy was initiated with intravenous antifungal, voriconazole, which was well tolerated for 6 weeks except for local excoriation at the site of ileostomy. He developed drug-induced hepatitis on oral voriconazole, therefore, switched to oral itraconazole following which he experienced severe chest pain. Alternatively, co-trimoxazole (bactrim) an antibacterial with antifungal activity was prescribed but he had the intolerance to it as well. Unfortunately, posaconazole as an alternative antifungal was not available in our centre. We report here a Saudi boy who developed an intolerance to most common antifungals used clinically 6 weeks after the therapy was initiated.

scholarly journals Drug induced chest pain---rare but important

2000 ◽  
Vol 76 (897) ◽  
pp. 420-422 ◽  
Author(s):  
P. Davey
Keyword(s):  
Chest Pain ◽  
Drug Induced

scholarly journals ELECTROCARDIOGRAM CHANGES IN ADDISON DISEASE: POTENTIAL CLINICAL MARKER FOR ADRENAL CRISIS

2019 ◽  
Vol 5 (5) ◽  
pp. e307-e310
Author(s):  
Pedro E. Perez ◽  
Wilson Sze ◽  
Joshua Miller
Keyword(s):  
Chest Pain ◽  
Cardiac Function ◽  
Adrenal Crisis ◽  
High Dose ◽  
Addison Disease ◽  
Cardiac Evaluation ◽  
History Of ◽  
Glucocorticoid Deficiency ◽  
Underlying Mechanisms ◽  
Ischemic Attack

Objective: To present a unique phenomenon of a patient in addisonian crisis with electrocardiogram (ECG) anomalies that resolved following glucocorticoid therapy. Methods: We present the case report followed by discussion with literature review. Results: A 25-year-old male with Addison disease (AD) presented with a 1-week history of lightheadedness, shortness of breath, chest pain, abdominal pain, postural hypotension, and tachycardia. The patient was diagnosed with addisonian crisis and started on intravenous, high-dose glucocorticoids. An ECG showed right-heart axis deviation and T-wave inversions. In the context of ongoing chest pain, there was concern for myocardial ischemic attack and the patient underwent an extensive cardiac evaluation. Cardiac workup was negative and an echocardiogram showed an ejection fraction of 50 to 55%. The ECG abnormalities resolved 1 day into his hospital admission and his other symptoms resolved 2 days following treatment with steroids. Conclusion: AD is a rare, potentially lethal, and commonly misdiagnosed disease often first encountered clinically amidst an incident episode of adrenal crisis. Our AD patient was undergoing an adrenal crisis with ECG changes positive for probable cardiac ischemia. Glucocorticoid deficiency has been previously linked with decreased cardiac function and myocardial ischemia, though the underlying mechanisms are not fully clear. This patient recovered within 2 days after receiving corticosteroid supplementation. There have been similar cases previously reported. In each of these, patients underwent extensive and costly workup to evaluate cardiac function, yet all patients fully recovered with corticosteroids. Understanding the physiology and clinical presentation of adrenal crisis will be useful in establishing an earlier diagnosis, thus preventing mortality and avoiding unnecessary, expensive evaluations.

scholarly journals Risk Compounds, Preclinical Toxicity Evaluation, and Potential Mechanisms of Chinese Materia Medica–Induced Cardiotoxicity

2021 ◽  
Vol 12 ◽  
Author(s):  
Jie Zhou ◽  
Fu Peng ◽  
Xiaoyu Cao ◽  
Xiaofang Xie ◽  
Dayi Chen ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ion Homeostasis ◽  
Drug Dosage ◽  
Toxicity Evaluation ◽  
China National Knowledge Infrastructure ◽  
Drug Induced ◽  
Chinese Materia Medica ◽  
Materia Medica ◽  
Knowledge Infrastructure ◽  
Specificity And Sensitivity

Chinese materia medica (CMM) has been applied for the prevention and treatment of diseases for thousands of years. However, arrhythmia, myocardial ischemia, heart failure, and other cardiac adverse reactions during CMM application were gradually reported. CMM-induced cardiotoxicity has aroused widespread attention. Our review aimed to summarize the risk compounds, preclinical toxicity evaluation, and potential mechanisms of CMM-induced cardiotoxicity. All relevant articles published on the PubMed, Embase, and China National Knowledge Infrastructure (CNKI) databases for the latest twenty years were searched and manually extracted. The risk substances of CMM-induced cardiotoxicity are relatively complex. A single CMM usually contains various risk compounds, and the same risk substance may exist in various CMM. The active and risk substances in CMM may be transformed into each other under different conditions, such as drug dosage, medication methods, and body status. Generally, the risk compounds of CMM-induced cardiotoxicity can be classified into alkaloids, terpenoids, steroids, heavy metals, organic acids, toxic proteins, and peptides. Traditional evaluation methods of chemical drug-induced cardiotoxicity primarily include cardiac function monitoring, endomyocardial biopsy, myocardial zymogram, and biomarker determination. In the preclinical stage, CMM-induced cardiotoxicity should be systematically evaluated at the overall, tissue, cellular, and molecular levels, including cardiac function, histopathology, cytology, myocardial zymogram, and biomarkers. Thanks to the development of systematic biology, the higher specificity and sensitivity of biomarkers, such as genes, proteins, and metabolic small molecules, are gradually applied for evaluating CMM-induced cardiotoxicity. Previous studies on the mechanisms of CMM-induced cardiotoxicity focused on a single drug, monomer or components of CMM. The interaction among ion homeostasis (sodium, potassium, and calcium ions), oxidative damage, mitochondrial injury, apoptosis and autophagy, and metabolic disturbance is involved in CMM-induced cardiotoxicity. Clarification on the risk compounds, preclinical toxicity evaluation, and potential mechanisms of CMM-induced cardiotoxicity must be beneficial to guide new CMM development and post-marketed CMM reevaluation.

Exercise capacity and cardiac function of rats with drug-induced cardiac enlargement

1982 ◽  
Vol 52 (3) ◽  
pp. 591-595 ◽  
Author(s):  
K. M. Baldwin ◽  
S. B. Ernst ◽  
W. J. Mullin ◽  
L. F. Schrader ◽  
R. E. Herrick
Keyword(s):  
Cardiac Function ◽  
Exercise Capacity ◽  
Maximal Exercise ◽  
Muscle Protein ◽  
Treated Group ◽  
Control Group ◽  
Drug Induced ◽  
Wet Weight ◽  
Cardiac Enlargement

A study was undertaken to determine if sustained administration of isoproterenol (ISO) alters biochemical and functional properties of hearts and the submaximal and maximal exercise capacity of rodents. Compared with sham-treated controls of the same age, sex, and body weight, 4 wk of ISO (0.2--0.4 mg/kg sc) produced an approximate 30% increase in combined ventricle wet weight (P less than 0.001). Respiratory capacity of homogenates, total muscle protein concentration, and actomyosin and myofibril ATPase of heart muscle of the ISO-treated group were the same as in the control group. Various cardiac function parameters in situ, obtained under control conditions and in response to tyramine-induced norepinephrine release, were similar for the two groups. ISO-treated rats had slightly greater endurance for running submaximally on a treadmill than the control rats (P less than 0.10), but their maximal capacity to utilize oxygen (VO2max) was not different from controls. These findings suggest that rodent hearts moderately enlarged by relatively low doses of isoproterenol possess normal metabolic and functional capacity. However, this cardiac enlargement had no apparent effect on maximal exercise performance of the whole animal.

scholarly journals Antitumor Necrosis Factor-Alpha (TNF-α) Infliximab-Induced Pleural Effusion and Pericarditis in Crohn’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Ashley Fonseca ◽  
Julee Sunny ◽  
Lina M. Felipez
Keyword(s):  
Crohn’S Disease ◽  
Chest Pain ◽  
Pleural Effusion ◽  
Crohn's Disease ◽  
Pleural Effusions ◽  
Drug Induced ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Crohn’s disease (CD) is a chronic inflammatory disease that can be associated with intestinal and extraintestinal manifestations. Some patients are treated with infliximab, an antitumor necrosis factor-alpha (TNF-α) agent, to help them achieve and maintain clinical and biochemical remission. However, some patients with CD can present severe adverse effects such as drug-induced lupus and rarely present with pleural space and pericardium involvement. We report a case of an 18-year-old Hispanic male with CD who acquired anti-TNF-α-induced lupus after infliximab therapy presenting with pleural effusion and pericarditis. The patient presented with a 2-week history of pleuritic chest pain. Initial laboratory workup was remarkable for leukocytosis and increased inflammatory markers. Imaging and cardiovascular studies were consistent with pericarditis and pleural effusions. Serositis was initially thought to be reactive secondary to the current Mycoplasma pneumoniae infection. He was treated with colchicine 0.6 mg PO TID for six weeks and azithromycin 500 mg PO for seven days. Pain improved after discharge but resurfaced on the day of infliximab infusion. Imaging and cardiovascular studies demonstrated the persistence of pleural effusions and pericarditis. Ultrasound-guided thoracentesis was consistent with exudative pleural effusions. Rheumatological workup was remarkable for increased antihistone antibodies, consistent with drug-induced lupus. Infliximab-induced pericarditis and pleural effusions are rarely reported in the literature. It is thought that infliximab may have a proinflammatory activity or have a delayed type III hypersensitivity reaction. The first line of therapy of anti-TNF-α-induced lupus is the withdrawal of the offending drug. Our patient is unique as few cases of anti-TNF-α-induced pleural effusion and pericarditis in CD are reported. After discontinuing the offending drug, ustekinumab was started, and maintaining a steroid and colchicine regimen, the patient’s chest pain improved. Antihistone antibodies have returned to normal one month after starting ustekinumab.

scholarly journals Drug-induced esophageal injuries with an atypical presentation mimicking acute coronary syndrome

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guda Merdassa Roro ◽  
Geir Folvik ◽  
Liu Louis ◽  
Abate Bane
Keyword(s):  
Acute Coronary Syndrome ◽  
Chest Pain ◽  
Acute Chest Pain ◽  
Febrile Illness ◽  
Esophageal Injury ◽  
Drug Induced ◽  
Delay In Diagnosis ◽  
Atypical Symptoms ◽  
Coronary Syndrome ◽  
History Of

Abstract Background Pill-induced esophageal injury may cause severe complications if not diagnosed in a timely fashion. The condition is under-recognized and under-reported, and some patients present with atypical clinical or endoscopic features mimicking other common conditions. If the diagnosis is missed the patient will continue to take the offending drug, potentially worsening the illness. We present a case in which acute coronary syndrome was the initial working diagnosis leading to a delay in diagnosis of doxycycline-induced esophageal injury. The patient developed multiple esophageal ulcers and hemorrhage. Case presentation A 50-year-old male driver with a history of hypertension and dyslipidemia was brought to the emergency department with complaints of severe retrosternal chest pain, vomiting, diaphoresis and syncope. On initial evaluation, acute coronary syndrome was considered due to the clinical presentation and history of cardiovascular risk factors. Electrocardiogram and serum troponins were normal. On the second day of his admission, the patient developed odynophagia and bloody vomitus. Esophagogastroduodenoscopy revealed extensive esophageal ulcerations with hemorrhage. The patient was taking Doxycycline capsules for an acute febrile illness. Doxycycline is the oral medication most commonly reported to cause esophageal injury. Doxycycline was discontinued, and the patient was treated with intravenous omeprazole and oral antacid suspension. The patient improved, was discharged after 6 days of hospitalization, and reported resolution of all symptoms at an outpatient follow-up visit 3 weeks later. Conclusion Medication-induced esophageal injury can present with atypical symptoms mimicking acute coronary syndrome. This condition should be included in the initial differential diagnosis of patients presenting with acute chest pain, especially those taking oral medications known to cause esophageal injury.

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