Renally Dosed Cefepime Leading to Cefepime-Induced Neurotoxicity: A Case Report.

Cefepime is a broad-spectrum fourth-generation cephalosporin with activity against both gram-positive and gram-negative bacteria, including Pseudomonas aeruginosa. Cefepime is most commonly used for urinary tract infections, soft tissue infections, and febrile neutropenia. Up to 15% of ICU patients on cefepime may experience cefepime-induced neurotoxicity (CIN), with risk factors including renal dysfunction, excessive dosage, elevated serum cefepime concentrations, and history of prior brain injury. The adverse effects of CIN, including encephalopathy, seizures, and coma can be resolved with drug cessation, antiepileptics, or hemodialysis. Here, we present the case of CIN in a 59-year-old female patient with long-term cefepime antibiotic prescription for Pseudomonas bacteremia and endocarditis with multiple risk factors for reduced renal function. We discuss the relevant risk factors and preventive measures that may have prevented her from developing CIN, as well as the importance of early recognition and prevention of CIN in patient care.

Guillain-Barré Syndrome Presenting as Symmetrical Proximal Muscle Weakness: An Atypical Presentation.

Guillain-Barré syndrome occurs via molecular mimicry when a trigger sets off an immune response on peripheral nerve epitopes. Patients typically report an antecedent infection, such as an upper respiratory infection or Campylobacter jejuni gastroenteritis. It is typically characterized by progressive, symmetric muscle weakness with absent/decreased deep tendon reflexes. Most cases in the literature report that the paralysis begins in the legs distally and ascends to the extremities. Patients may have sensory symptoms or dysautonomia as well. Notable variant forms include acute motor axonal neuropathy, acute motor/sensory neuropathy, Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Diagnosis is confirmed if a lumbar puncture shows albuminocytologic dissociation (typically 45 to 200 mg/dL). Nerve conduction studies may also be considered but are not necessary. Management is largely supportive, but intravenous immunoglobulin and/or plasmapheresis for more severe cases may be considered.

A Case of Sudden-Onset Flaccid Paralysis In a Previously Healthy Person.

Flaccid paralysis is a neurological syndrome characterized by weakness and paralysis of the limbs, followed by reduced muscle tone. Common causes of flaccid paralysis include blockage of the anterior spinal artery, trauma to the spinal cord, cancer, arterial disease, or thrombosis. A potential differential diagnosis in a 35-year-old male presenting with sudden-onset flaccid paralysis with no history of trauma is hypokalemic periodic paralysis. Treatment with potassium can alleviate symptoms in affected patients. .

Complex Interplay Among Nuclear Receptor Ligands, Cytosine Methylation, and the Metabolome in Driving Tris(1,3-dichloro-2-propyl)phosphate-Induced Epiboly Defects in Zebrafish.

Tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) is a high-production-volume organophosphate flame retardant (OPFR) that induces epiboly defects during zebrafish embryogenesis, leading to the disruption of dorsoventral patterning. Therefore, the objectives of this study were to (1) identify the potential mechanisms involved in TDCIPP-induced epiboly defects and (2) determine whether coexposure to triphenyl phosphate (TPHP)-an OPFR commonly detected with TDCIPP-enhances or mitigates epiboly defects. Although TDCIPP-induced epiboly defects were not associated with adverse impacts on cytoskeletal protein abundance in situ, the coexposure of embryos to TPHP partially blocked TDCIPP-induced epiboly defects. As nuclear receptors are targets for both TPHP and TDCIPP, we exposed the embryos to TDCIPP in the presence or absence of 69 nuclear receptor ligands and, similar to TPHP, found that ciglitazone (a peroxisome proliferator-activated receptor γ agonist) and 17ß-estradiol (E2; an estrogen receptor α agonist) nearly abolished TDCIPP-induced epiboly defects. Moreover, E2 and ciglitazone mitigated TDCIPP-induced effects on CpG hypomethylation within the target loci prior to epiboly, and ciglitazone altered TDCIPP-induced effects on the abundance of two polar metabolites (acetylcarnitine and cytidine-5-diphosphocholine) during epiboly. Overall, our results point to a complex interplay among nuclear receptor ligands, cytosine methylation, and the metabolome in both the induction and mitigation of epiboly defects induced by TDCIPP.