Mechanisms for Linezolid-Induced Anemia and Thrombocytopenia

2003 ◽  
Vol 37 (4) ◽  
pp. 517-520 ◽  
Author(s):  
Wendy B Bernstein ◽  
Richard F Trotta ◽  
James T Rector ◽  
Jeffery A Tjaden ◽  
Anthony J Barile
Keyword(s):  
Heart Failure ◽  
Staphylococcus Epidermidis ◽  
White Woman ◽  
Causality Assessment ◽  
Drug Event ◽  
Ringed Sideroblasts ◽  
Case Summary ◽  
Immune Mediated ◽  
Linezolid Therapy ◽  
Rate Of Decline

BACKGROUND: Linezolid has been associated with anemia and thrombocytopenia. Mechanisms for neither have been elucidated. OBJECTIVE: To propose mechanisms for linezolid-induced anemia and thrombocytopenia. CASE SUMMARY: A 78-year-old white woman with Staphylococcus epidermidis endocarditis was treated with linezolid after developing resistance to multiple antibiotic regimens. After 7 days of linezolid therapy, she developed thrombocytopenia, while an anemia present since admission remained unchanged. A bone marrow biopsy was performed, primarily looking for a mechanism for the thrombocytopenia. Histopathology revealed adequate megakaryocytes, ringed sideroblasts, and vacuolated pronormoblasts. A course of immune globulin (IVIG) was administered, with slowing in the rate of decline in platelets. She died 24 hours after her last dose of IVIG of congestive heart failure. DISCUSSION: The presence of ringed sideroblasts and vacuolated pronormoblasts suggests that linezolid-induced anemia is secondary to a chloramphenicol-like suppression of erythropoiesis. The presence of adequate, normal-appearing megakaryocytes suggests immune-mediated thrombocytopenia, not marrow suppression. Although the response to IVIG is difficult to interpret because of the patient's death, there was a slowing in the rate of decline of the platelet count, further supporting immune-mediated thrombocytopenia. An objective causality assessment indicated that the adverse drug event was probably due to linezolid. CONCLUSIONS: There appear to be 2 distinct mechanisms for linezolid-induced cytopenias. While anemia is reversible and manageable with transfusions, thrombocytopenia can be a treatment-limiting toxicity. The ability to treat through an immune-mediated cytopenia with IVIG may be beneficial for critically ill patients with few therapeutic options.

Carbimazole-Related Gastroschisis

2003 ◽  
Vol 37 (6) ◽  
pp. 829-831 ◽  
Author(s):  
Anne-Maëlle Guignon ◽  
Michel P Mallaret ◽  
Pierre Simon Jouk
Keyword(s):  
Abdominal Wall ◽  
White Woman ◽  
Surgical Repair ◽  
Causality Assessment ◽  
In Utero ◽  
Abdominal Wall Defects ◽  
Rare Occurrence ◽  
Case Summary ◽  
The Relationship ◽  
Malformative Syndrome

OBJECTIVE: To report a case of gastroschisis in a newborn secondary to carbimazole exposure in utero. CASE SUMMARY: A 25-year-old white woman was treated for Graves disease with carbimazole throughout pregnancy. A boy was born prematurely by vaginal delivery, with a gastroschisis without associated malformative syndrome. Death occurred in the 25th hour of life after surgical repair. DISCUSSION: Carbimazole is completely metabolized to methimazole after absorption. Carbimazole or methimazole intake during pregnancy has been associated with an increased incidence of scalp aplasia. Abdominal wall defects secondary to carbimazole or methimazole exposure in utero seem to be a rare occurrence. However, other cases of abdominal wall defects have been reported in 4 newborns, 2 of them associated with scalp aplasia. An objective causality assessment revealed that the relationship between the gastroschisis and the exposure to carbimazole in utero was possible. CONCLUSIONS: It is important to emphasize the possible risk of abdominal wall defects in newborns to pregnant women taking carbimazole or methimazole.

Levofloxacin-Induced Autoimmune Hemolytic Anemia

2003 ◽  
Vol 37 (7-8) ◽  
pp. 1010-1013 ◽  
Author(s):  
Young R Oh ◽  
Sian M Carr-Lopez ◽  
James M Probasco ◽  
Peter G Crawley
Keyword(s):  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Case Reports ◽  
Stable Condition ◽  
Drug Event ◽  
Packed Red Blood Cells ◽  
Case Summary ◽  
Immune Mediated ◽  
Severe Jaundice

OBJECTIVE: To report a case of autoimmune hemolytic anemia (AIHA) secondary to levofloxacin. CASE SUMMARY: An 82-year-old white man was treated with levofloxacin 500 mg/d for cellulitis. Three days following completion of levofloxacin therapy, the patient presented to the emergency department with severe jaundice, dizziness, and loss of vision. He received packed red blood cells (PRBCs) and was discharged home. Two days later at the follow-up visit, he was diagnosed with AIHA secondary to levofloxacin. The patient was hospitalized and treated with a tapering dose of prednisone and additional PRBC infusion. He was discharged from the hospital in stable condition after 3 days. Repeated hematologic laboratory studies following discharge demonstrated that the hemolytic anemia had resolved. DISCUSSION: Hemolytic anemia due to levofloxacin is an extremely rare, but potentially fatal, adverse drug event. An objective causality assessment revealed that the adverse reaction was probable. To our knowledge, this is the first published case of levofloxacin-induced AIHA. However, there are published case reports of hemolytic anemia with other fluoroquinolones including ciprofloxacin (n = 12) and temafloxacin (n = 95). Temafloxacin was withdrawn from the market in 1992 due to this adverse effect. The mechanism by which levofloxacin triggers hemolytic anemia is unknown. We believe that an immune-mediated reaction is most likely. CONCLUSIONS: Levofloxacin-induced AIHA is a rare but serious complication of therapy. Immediate discontinuation of the offending medication and treatment of the hemolytic anemia are essential. Until more information is available, levofloxacin should not be prescribed for patients with previous reactions to any fluoroquinolone.

Dapsone-Induced Sulfone Syndrome

2003 ◽  
Vol 37 (7-8) ◽  
pp. 1044-1046 ◽  
Author(s):  
Kimberly B Lee ◽  
Trisha B Nashed
Keyword(s):  
African American ◽  
Complete Resolution ◽  
Temporal Relationship ◽  
Hepatic Injury ◽  
Causality Assessment ◽  
Clinical Symptoms ◽  
Drug Event ◽  
Objective Data ◽  
Exfoliative Dermatitis ◽  
Case Summary

OBJECTIVE: To report a patient with dapsone-induced sulfone syndrome. CASE SUMMARY: A 42-year-old HIV-infected African American man developed fever, lymphadenopathy, exfoliative dermatitis, hepatitis, and methemoglobinemia 4 weeks after starting dapsone. Complete resolution of symptoms and laboratory abnormalities occurred with cessation of dapsone therapy. DISCUSSION: Sulfone syndrome is not a well-known sequela of dapsone therapy. It is not dose-related, usually occurs in doses of 50–300 mg/d, all cases occur within 2 months of starting dapsone, all patients have fever, and most patients will develop rash and evidence of hepatic injury. The temporal relationship between dapsone therapy and onset of clinical symptoms and objective data led us to believe that dapsone caused sulfone syndrome in our patient. An objective causality assessment revealed that the adverse drug event was probable. CONCLUSIONS: Although sulfone syndrome appears to be relatively uncommon, healthcare practitioners must be aware of the potentially fatal syndrome associated with dapsone use.

Warfarin and Celecoxib Interaction

2000 ◽  
Vol 34 (3) ◽  
pp. 325-327 ◽  
Author(s):  
Tracey L Mersfelder ◽  
Lisa R Stewart
Keyword(s):  
Heart Failure ◽  
White Woman ◽  
International Normalized Ratio ◽  
Fresh Frozen Plasma ◽  
Laboratory Evaluation ◽  
Medication Regimen ◽  
Disease States ◽  
Case Summary ◽  
Fresh Frozen ◽  
Frozen Plasma

OBJECTIVE: To report a case of increased international normalized ratio (INR) in a patient receiving warfarin and celecoxib. CASE SUMMARY: A 73-year-old white woman with hypothyroidism and heart failure was admitted to the hospital with increased orthopnea, dyspnea on exertion, and hemoptysis. On laboratory evaluation, she was noted to have an increased INR. The only reported change in her medications was the addition of celecoxib approximately five weeks before admission. Her INR had previously been stable. After discontinuation of warfarin and celecoxib, fresh frozen plasma and vitamin K were administered to normalize INR. The patient was not rechallenged. DISCUSSION: Warfarin is an oral anticoagulant with numerous reports of drug interactions. It is possible that other drug therapies or disease states may have contributed to the elevation in INR; however, the observed increase in INR occurred five weeks after beginning celecoxib therapy. The Food and Drug Administration has issued a notice about the possibility of interactions between these two medications. CONCLUSIONS: Celecoxib may potentiate the anticoagulant effects of warfarin. Patients receiving warfarin should be carefully monitored when adding, changing, or removing celecoxib from their medication regimen.

Fulminant Liver Failure Associated with Clarithromycin

2003 ◽  
Vol 37 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Andreas Tietz ◽  
Markus H Heim ◽  
Urs Eriksson ◽  
Stephan Marsch ◽  
Luigi Terracciano ◽  
...  
Keyword(s):  
Heart Failure ◽  
Liver Transplantation ◽  
Liver Failure ◽  
White Woman ◽  
Macrolide Antibiotic ◽  
Hepatic Metabolism ◽  
Hepatic Toxicity ◽  
Fulminant Liver Failure ◽  
Hepatocellular Injury ◽  
Case Summary

OBJECTIVE To report a patient developing fulminant liver failure while being treated with clarithromycin for pneumonia. CASE SUMMARY A 58-year-old white woman developed fulminant liver failure while being treated with the macrolide antibiotic clarithromycin for pneumonia. Comedication included N-acetylcysteine, atenolol, and isradipine. Other causes of liver failure, such as viral hepatitis, autoimmune hepatitis, toxins, and heart failure, were excluded by appropriate diagnostic means. All drugs were stopped, and the patient was transferred to another hospital for liver transplantation. She recovered spontaneously within several days, making transplantation unnecessary. A liver biopsy obtained 10 days after the initial presentation revealed centroacinar necrosis and beginning fibrous reorganization, compatible with recent centroacinar damage. DISCUSSION Since no other cause could be identified, liver injury was considered to be drug related. Fulminant liver failure has not previously been described with concomitant use of atenolol and N-acetylcysteine. Although isradipine has been associated with hepatocellular injury, there are no reports of fulminant liver failure with this agent, and our patient had been treated for >2 years without signs of toxicity. The most likely cause of liver failure in this patient was, therefore, clarithromycin, which undergoes hepatic metabolism and has been reported to cause fulminant hepatic failure. A second possibility is an interaction between clarithromycin and isradipine, potentially increasing the hepatic toxicity of isradipine. CONCLUSIONS Clarithromycin may be a cause of fulminant liver failure either alone or by inhibiting the metabolism of other drugs.

scholarly journals Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

2019 ◽  
Vol 12 (9) ◽  
pp. 1491-1498 ◽  
Author(s):  
Yu Vatnikov ◽  
A. Rudenko ◽  
P. Rudenko ◽  
Ev Kulikov ◽  
A. Karamyan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Dilated Cardiomyopathy ◽  
Internal Organs ◽  
Clinically Normal ◽  
Progressive Loss ◽  
Intestinal Dysbiosis ◽  
Immune Mediated ◽  
Functional Classes ◽  
Neurohumoral System

Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.

scholarly journals Classification and applying pharmacovigilance principles to study adverse drug reaction and its management

2017 ◽  
Vol 6 (11) ◽  
pp. 2537
Author(s):  
Srihitha Pendota ◽  
Sre Akshaya Kalyani Surabhineni ◽  
Abhinay Sharma Katnapally ◽  
Dharanija Porandla ◽  
Sandeep Kumar Beemreddy
Keyword(s):  
Adverse Drug Reaction ◽  
Drug Reaction ◽  
Causality Assessment ◽  
Causal Relation ◽  
Drug Event ◽  
Multiple Drug ◽  
Different Types ◽  
Multiple Drug Therapy ◽  
Assessment Scales ◽  
Reason For Admission

Adverse drug reaction (ADR) is an unwanted, undesirable effect of medication resulting in mild to severe effect on the patient. This review explains definitions of ADR and it differentiation with adverse drug event, medication error. ADRs may cause increased length of stay or initial reason for admission and are major cause of morbidity and mortality worldwide. Risk factors for ADR occurrence include age, gender, patients with multiple diseases and multiple drug therapy (polypharmacy). ADRs are classified into different types based on the mechanism and onset of reaction. The causal relation between suspected drug and reaction can be assessed by using causality assessment scales. The severity and preventability of ADR can be assessed by severity assessment scale and preventability scale respectively. Clinical Pharmacists play an important role in monitoring and management of ADRs.

scholarly journals Presumed immune-mediated haemolytic anaemia associated with pregnancy in a cat

2019 ◽  
Vol 5 (1) ◽  
pp. 205511691984168
Author(s):  
Matthew A Kopke ◽  
Sarah Pemberton ◽  
Craig G Ruaux
Keyword(s):  
Haemolytic Anaemia ◽  
Cardiac Activity ◽  
Abdominal Ultrasound ◽  
Serum Biochemistry ◽  
Acute Onset ◽  
Gram Staining ◽  
Case Summary ◽  
Immune Mediated ◽  
Large Uterus ◽  
Saline Test

Case summary A 7-year-old female entire Birman presented with acute-onset haemorrhagic vulvar discharge. Moderate, normocytic, normochromic, non-/pre-regenerative anaemia, along with a moderate mature neutrophilia, were seen on haematology. Saline test for agglutination was positive. No haemotropic mycoplasmas were identified. Serum biochemistry revealed severe hyperbilirubinaemia. Retroviral testing was negative. Serology for toxoplasmosis revealed a titre of 1:512. Abdominal ultrasound identified a large uterus, containing at least three advanced-stage fetuses, two of which failed to exhibit independent motion or cardiac activity. Ovariohysterectomy was performed. Histology demonstrated mild, multifocal suppurative placentitis, with Gram staining revealing no evidence of bacteria. Complete resolution of the anaemia was seen within 1.5 months of ovariohysterectomy. Relevance and novel information Immune-mediated haemolytic anaemia (IMHA) in association with pregnancy has not been previously reported in cats. This case represents a potential novel cause for IMHA in cats, which resolved following ovariohysterectomy.

scholarly journals It is easy to see, but it is better to foresee: a case report on the favourable alliance between CardioMEMS and levosimendan

2020 ◽  
Vol 4 (4) ◽  
pp. 1-5
Author(s):  
Valeria Visco ◽  
Cristina Esposito ◽  
Paolo Vitillo ◽  
Carmine Vecchione ◽  
Michele Ciccarelli
Keyword(s):  
Heart Failure ◽  
Hospital Admissions ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Optimal Management ◽  
Reduced Ejection Fraction ◽  
The Past ◽  
Case Summary ◽  
Pressure Profiles ◽  
Patients With Heart Failure

Abstract Background In the past years, different devices have been investigated to help in identifying early decompensation events in patients with heart failure (HF) and reduced ejection fraction (EF), reducing hospital admissions. In this report, we present the first patient experience with levosimendan infusion led by CardioMEMS. Case summary A 68-year-old man with HF and reduced EF with more than 20 hospitalizations for exacerbation of HF was enrolled in our HF Clinic from October 2017. Echocardiogram showed a dilated left ventricle with severely reduced EF (29%) and increased pulmonary artery systolic pressure (40 mmHg). From October 2017 to May 2019, the patient went through numerous hospitalizations, despite optimal medical therapy; subsequently, was adopted a strategy of levosimendan infusions guided by CardioMEMS. Levosimendan infusions improved haemodynamic and pressure profiles. The patient was monitored daily by CardioMEMS, and from June to December 2019, he had only two hospitalizations scheduled for levosimendan infusion and none for HF exacerbation. Discussion Our case supports the combination of CardioMEMS and levosimendan for the optimal management of patients with advanced HF. These results further strengthen the development of a randomized clinical trial to demonstrate the clinical usefulness of this device in combination with the levosimendan infusion programme in advanced HF patients.

scholarly journals Pulsed Levosimendan in advanced heart failure due to congenital heart disease: a case series

2020 ◽  
Vol 4 (3) ◽  
pp. 1-6
Author(s):  
James Cranley ◽  
Antonia Hardiman ◽  
Leisa J Freeman
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Congenital Heart ◽  
Case Series ◽  
Advanced Heart Failure ◽  
Good Evidence ◽  
Case Summary ◽  
Acute Decompensation

Abstract Background Levosimendan is a non-adrenergic calcium-sensitizing agent with positive inotropic and vasodilatory effects. Its use in acute decompensation of heart failure is established. Good evidence now exists for repetitive infusions of Levosimendan to improve symptoms and reduce hospitalization in advanced heart failure (AdHF) populations. Its use in heart failure resulting from congenital heart disease is not yet commonplace. Case summary We present three cases in which pulsed Levosimendan was used in the management of AdHF secondary to underlying congenital heart disease. There was symptomatic and biomarker evidence of improvement. Discussion Intermittent Levosimendan may represent a valuable therapy to reduce hospitalization and improve quality of life in adults with congenital heart conditions.

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