ABSTRACT
Introduction: Dysphagia in post COVID-19 patients could be caused by several factors, including reduced pharyngolaryngeal coordination due to SARS-CoV-2 tropism to the central and/or peripheral nervous system. To our knowledge, this is the first reported case of COVID-19-related dysphagia successfully treated with botulinum toxin type A injection. Case description: We report the case of a patient with severe oropharyngeal dysphagia due to COVID-19 confirmed by fibre endoscopy. As a result, the patient required an enteral feeding tube. After two months of traditional swallowing therapies, there was only limited improvement. An electrophysiologic evaluation of the cricopharyngeal muscle was performed and showed a normal inhibition of the cricopharyngeal muscle, followed by a hypertonic rebound. Based on this result, we decided to perform a unilateral laryngeal injection of botulinum toxin type A. After the injection, the patient's swallowing function improved significantly, allowing him to return to oral feeding. Discussion: Newly diagnosed oropharyngeal dysphagia was found in 35.3% of hospitalised patients with COVID-19. There are several possible causes of COVID-19-associated dysphagia, including stroke, encephalitis, critical illness neuropathy, Guillain-Barré syndrome and skeletal muscle injury. In our case, since stroke was excluded by brain MRI, cranial nerve injury was a possible explanation for the difficult recovery of swallowing despite daily swallowing therapy. Conclusion: We suggest that electrophysiology is a valid tool for the diagnosis and follow-up of patients with oropharyngeal dysphagia. LEARNING POINTS: SARS-CoV-2 tropism to the central and/or peripheral nervous system can cause dysphagia in post COVID-19 patients.An electrophysiologic approach is useful for the diagnosis and follow-up of patients with oropharyngeal dysphagia.A single botulinum toxin type A injection is a valid treatment option to improve the swallowing function in patients with post COVID-19 dysphagia.
ABSTRACT
Partial deficiency of the last enzyme of the heme biosynthetic pathway, namely, ferrochelatase (FECH), is responsible for erythropoietic protoporphyria (EPP) in humans. This disorder is characterized by painful skin photosensitivity, due to excessive protoporphyrin IX (PPIX) production in erythrocytes. Although several papers report the presence of iron deficiency anemia in about 50% of EPP patients, there is still no a conclusive explanation of the why this occurs. In the present work, we explored hematological indices and iron status in 20 unrelated Italian EPP patients in order to propose a new hypothesis. Our data show that microcytosis is present in EPP patients also in the absence of anemia and iron deficiency with a link between PPIX accumulation and reduced MCV, probably indicating an indirect condition of heme deficiency. Patients studied had a downward shift of iron parameters due to increased hepcidin concentrations only in a state of repleted iron stores. Interestingly, hemoglobin synthesis was not limited by iron supply except in cases with further iron loss, in which concomitantly increased soluble transferrin (Tf) receptor (sTfR) levels were detected. The mechanisms involved in the iron uptake downregulation in EPP remain unclear, and the role of PPIX accumulation in microcytosis.
