Resolution of severe gastroparesis induced by parasympathetic surge following facial trauma: a case report.

BACKGROUND: Gastroparesis is a condition that affects the motility of the gastrointestinal (GI) tract, causing a delay in the emptying process and leading to nausea, vomiting, bloating, and upper abdominal pain. Motility treatment along with symptom management can be done using antiemetics or prokinetics. This study highlights the diagnostic and therapeutic challenges of gastroparesis and suggests a potential link between facial trauma and symptom remission, indicating the need for further investigation. CASE PRESENTATION: A 46-year-old Hispanic man with hypertension, type 2 diabetes (T2D), and hyperlipidemia on amlodipine 10 mg, lisinopril 5 mg, empagliflozin 25 mg, and insulin glargine presented with a diabetic foot ulcer with probable osteomyelitis. During hospitalization, the patient developed severe nausea and vomiting. The gastroenterology team advised continuing antiemetic medicine and trying very small sips of clear liquids. However, the patient didn't improve. Therefore, the gastroenterology team was contacted again. They advised having stomach emptying tests to rule out gastroparesis as the source of emesis. In addition, they recommended continuing metoclopramide, and starting erythromycin due to inadequate improvement. Studies found a 748-min stomach emptying time. Normal is 45-90 min. An uneventful upper GI scope was done. Severe gastroparesis was verified, and the gastroenterology team advised a percutaneous jejunostomy or gastric pacemaker for gastroparesis. Unfortunately, the patient suffered a mechanical fall resulting in facial trauma. After the fall, the patient's nausea eased, and emesis stopped. He passed an oral liquids trial after discontinuation of erythromycin and metoclopramide. CONCLUSION: This case exemplifies the difficulties in diagnosing and treating gastroparesis. An interesting correlation between parasympathetic surges and recovery in gastroparesis may be suggested by the surprising remission of symptoms following face injuries.

Candida lusitaniae, an Emerging Opportunistic Pathogen in Immunocompetent Populations: A Case Report.

Candida lusitaniae is an emerging opportunistic pathogen in immunocompromised hosts and hospitalized patients. However, the incidence is low in immunocompetent hosts. Because of their characteristic similarities, C. lusitaniae may be confused with other fungal species, such as Candida tropicalis, Candida parapsilosis, and even Saccharomyces cerevisiae. Recently reported cases of serious infections caused by C. lusitaniae have proven detrimental, and some cases reported amphotericin resistance. Here, we present a case report of empyema caused by C. lusitaniae in an immunocompetent patient who was admitted to the intensive care unit and intubated for acute hypoxic respiratory failure. This case demonstrates the importance of recognizing this organism and initiating early treatment for the prevention of fatal complications.

Sinus of Valsalva Aneurysm: An Atypical Etiology of Recurrent Syncope.

The sinus of Valsalva presents the initial segment of the aorta from where the coronary vessels arise. Sinus of Valsalva aneurysms (SOVAs) present as progressive dilatation of the aortic sinus. SOVA arises both from the congenital and acquired weakness of the elastic lamina of the aortic media. Though most of the SOVAs are asymptomatic and diagnosed on screening for other pathologies, patients can present with symptoms of arrhythmia, aortic insufficiency, aorto-cardiac fistulas, and, in a few cases, with rupture. We describe a patient who presented with recurrent syncope and was found to have a 6 cm dilated SOVA with an ectatic ascending aorta. Further assessment revealed a left anterior fascicular block, aortic regurgitation, and mitral regurgitation. On further assessment, no other cause of syncope was found. There was no family history of aneurysm or sudden cardiac death. The patient was eventually discharged with outpatient follow-up with cardiothoracic surgery. In patients presenting with asymptomatic SOVA, a dilatation with a maximum diameter of 6.0 cm requires stringent monitoring and should be considered for surgery.

Wnt7a deficit is associated with dysfunctional angiogenesis in pulmonary arterial hypertension.

INTRODUCTION: Pulmonary arterial hypertension (PAH) is characterised by loss of microvessels. The Wnt pathways control pulmonary angiogenesis but their role in PAH is incompletely understood. We hypothesised that Wnt activation in pulmonary microvascular endothelial cells (PMVECs) is required for pulmonary angiogenesis, and its loss contributes to PAH. METHODS: Lung tissue and PMVECs from healthy and PAH patients were screened for Wnt production. Global and endothelial-specific Wnt7a -/- mice were generated and exposed to chronic hypoxia and Sugen-hypoxia (SuHx). RESULTS: Healthy PMVECs demonstrated >6-fold Wnt7a expression during angiogenesis that was absent in PAH PMVECs and lungs. Wnt7a expression correlated with the formation of tip cells, a migratory endothelial phenotype critical for angiogenesis. PAH PMVECs demonstrated reduced vascular endothelial growth factor (VEGF)-induced tip cell formation as evidenced by reduced filopodia formation and motility, which was partially rescued by recombinant Wnt7a. We discovered that Wnt7a promotes VEGF signalling by facilitating Y1175 tyrosine phosphorylation in vascular endothelial growth factor receptor 2 (VEGFR2) through receptor tyrosine kinase-like orphan receptor 2 (ROR2), a Wnt-specific receptor. We found that ROR2 knockdown mimics Wnt7a insufficiency and prevents recovery of tip cell formation with Wnt7a stimulation. While there was no difference between wild-type and endothelial-specific Wnt7a -/- mice under either chronic hypoxia or SuHx, global Wnt7a +/- mice in hypoxia demonstrated higher pulmonary pressures and severe right ventricular and lung vascular remodelling. Similar to PAH, Wnt7a +/- PMVECs exhibited an insufficient angiogenic response to VEGF-A that improved with Wnt7a. CONCLUSIONS: Wnt7a promotes VEGF signalling in lung PMVECs and its loss is associated with an insufficient VEGF-A angiogenic response. We propose that Wnt7a deficiency contributes to progressive small vessel loss in PAH.