Amoxicillin induced toxic epidermal necrolysis (TEN): a case report

Each year many patients are hospitalized due to adverse drug reactions. Adverse reactions are the recognized hazards of drug therapy and they can occur with any class of drugs and many studies revealed that the incidence is more in case of antibiotics. Amoxicillin is a broad spectrum, bactericidal, beta lactam antibiotic, commonly used to combat various infections. Penicillin group of drugs are known to cause cutaneous drug eruptions especially in pediatric population. Most of the time, these eruptions are mild in nature, however, sometimes they represent the early manifestation of rare, severe drug-induced cutaneous reactions, such as Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN). Toxic Epidermal Necrolysis (TEN) is a rare, life threatening dermatological disorder that is usually induced by medications. Seventy percent of the cases of TEN are drug induced, most commonly implicated drugs being anticonvulsants, antibiotics and Non-Steroidal Anti-Inflammatory Drugs (NSAIDS). Here, we report a case of toxic epidermal necrolysis induced by amoxicillin in a 16 year old female patient. Rigorous treatment with systemic corticosteroids and immunoglobulins helped in recovery of the patient. The case is being reported to emphasize the need for efficient pharmacovigilance in order to motivate adverse drug reaction reporting so as to gather more and more data regarding adverse drug reactions. Through this report, we also seek the support of everyone concerned to detect and, if possible, prevent adverse reactions to drugs

Infiltrative and drug-resistant slow-cycling cells support metabolic heterogeneity in glioblastoma

Metabolic reprogramming has been described in rapidly growing tumors, which are thought to mostly contain fast‐cycling cells (FCCs) that have impaired mitochondrial function and rely on aerobic glycolysis. Here, we characterize the metabolic landscape of glioblastoma (GBM) and explore metabolic specificities as targetable vulnerabilities. Our studies highlight the metabolic heterogeneity in GBM, in which FCCs harness aerobic glycolysis, and slow‐cycling cells (SCCs) preferentially utilize mitochondrial oxidative phosphorylation for their functions. SCCs display enhanced invasion and chemoresistance, suggesting their important role in tumor recurrence. SCCs also demonstrate increased lipid contents that are specifically metabolized under glucose‐deprived conditions. Fatty acid transport in SCCs is targetable by pharmacological inhibition or genomic deletion of FABP7, both of which sensitize SCCs to metabolic stress. Furthermore, FABP7 inhibition, whether alone or in combination with glycolysis inhibition, leads to overall increased survival. Our studies reveal the existence of GBM cell subpopulations with distinct metabolic requirements and suggest that FABP7 is central to lipid metabolism in SCCs and that targeting FABP7‐related metabolic pathways is a viable therapeutic strategy

Relation of antifactor-Xa peak levels and venous thromboembolism after trauma

No previous studies have established the optimal antifactor Xa (anti-Xa) level to guide thromboprophylaxis (TPX) dosing with enoxaparin in trauma patients. We hypothesize that achieving 0.2-0.4 IU/mL anti-Xa will decrease venous thromboembolism (VTE) rates after trauma. This was a retrospective review of 194 intensive care unit patients sustaining blunt or penetrating trauma from January 2015 to March 2017. All received initial enoxaparin (30 mg BID subcutaneous) and mechanical devices for TPX. Peak anti-Xa levels were drawn after each third dose. The enoxaparin dose was adjusted up to a maximum of 60 mg BID subcutaneous until a peak level of 0.2-0.4 IU/mL was achieved. Data are expressed as mean ± SD if parametric or median (IQR) if not. The Greenfield Risk Assessment Profile score was 9 ± 4, Injury Severity Score 23 ± 14, and hospital length of stay 19 (11-38) days. The overall VTE rate was 7.2% (n = 14), with 10 deep venous thromboses (DVT) and 5 pulmonary emboli (PE). One patient had both a DVT and PE. The median time to VTE diagnosis was 14 (7-17) days. In those diagnosed with a VTE, 50.0% (n = 7) never reached 0.2-0.4 IU/mL anti-Xa and 42.8% (n = 6) were diagnosed with a VTE after achieving these levels. Prophylactic levels were achieved initially in 64 (33.0%) patients, and achieved later in 38 (19.6%) additional patients, giving an overall prophylactic rate of 52.6% (n = 102). There were no differences in VTE (6.9% vs. 7.6%, p = 0.841), DVT (3.9% vs. 6.5%, p = 0.413), or PE (3.9% vs. 1.1%, p = 0.213) rates between those who became prophylactic and those who did not. There was no difference in VTE incidence between those achieving anti-Xa peak levels of 0.2-0.4 IU/mL and those who did not. Furthermore, these levels were never achieved in some trauma patients despite repeated dosing over a >10-day period. Therapeutic study, level IV

Association of Anti–Factor Xa–Guided Dosing of Enoxaparin With Venous Thromboembolism After Trauma

This study assesses whether anti–factor Xa–guided dosing, compared with standard dosing, reduces the rate of venous thromboembolism in adults admitted to a level I trauma intensive care unit