Early damage to transplanted organs initiates excess inflammation that can cause ongoing injury, a leading cause for late graft loss. The endothelial glycocalyx modulates immune reactions and chemokine-mediated haptotaxis, potentially driving graft loss. In prior work, conditional deficiency of the glycocalyx-modifying enzyme N-deacetylase-N-sulfotransferase-1 (Ndst1f/f TekCre+) reduced aortic allograft inflammation. Here we investigated modification of heparan sulfate (HS) and chemokine interactions in whole-organ renal allografts. Conditional donor allograft Ndst1 deficiency (Ndst1−/−; C57Bl/6 background) was compared to systemic treatment with M-T7, a broad-spectrum chemokine-glycosaminoglycan (GAG) inhibitor. Early rejection was significantly reduced in Ndst1−/− kidneys engrafted into wildtype BALB/c mice (Ndst1+/+) and comparable to M-T7 treatment in C57Bl/6 allografts (P < 0.0081). M-T7 lost activity in Ndst1−/− allografts, while M-T7 point mutants with modified GAG-chemokine binding displayed a range of anti-rejection activity. CD3+ T cells (P < 0.0001), HS (P < 0.005) and CXC chemokine staining (P < 0.012), gene expression in NFκB and JAK/STAT pathways, and HS and CS disaccharide content were significantly altered with reduced rejection. Transplant of donor allografts with conditional Ndst1 deficiency exhibit significantly reduced acute rejection, comparable to systemic chemokine-GAG inhibition. Modified disaccharides in engrafted organs correlate with reduced rejection. Altered disaccharides in engrafted organs provide markers for rejection with potential to guide new therapeutic approaches in allograft rejection.

Following an elective transphenoidal resection of a pituitary tumor, a 66-year-old Hispanic male acutely developed fulminant hepatic failure and severe coagulopathy. He received parenteral corticosteroids the day prior to surgery, and was first noted to have significant coagulopathy intraoperatively. Despite aggressive workup and treatment for fulminant hepatic failure, the patient developed multiorgan failure by post-operative day 2, and expired on post-operative day 3. On post-mortem examination, hemorrhagic necrosis of the liver was noted and microscopic examination revealed Cowdry type A inclusions, consistent with Herpes Simplex Virus (HSV) infection. This diagnosis was subsequently confirmed by immunehistochemistry. Fulminant hepatic failure due to HSV is a rare but highly fatal disease if untreated. Most case reports include only immunocompromised or pregnant patients. However, the lack of clinical suspicion in this previously healthy patient may have delayed prompt treatment with antiviral agents. It is important to raise the awareness of this rare and life-threatening, but potentially treatable, etiology when clinicians are faced with acute idiopathic fulminant hepatic failure.

Background: Coronary vasospasm leading to variant angina is uncommon, and the condition is rare in pregnant patients. Many physiologic changes occur during pregnancy, but how these changes affect the spasticity of coronary arteries in patients predisposed to vasospasm is unknown. Vasospasm causing unstable arrhythmia from multiple foci can be difficult to treat.Case Report: A 22-year-old gravida 1 para 0 female at 17 weeks’ gestation with twins presented with chest pain refractory to sublingual nitroglycerin, ST segment elevation on electrocardiogram, and subsequent ventricular tachycardia requiring a shock by her implantable cardioverter defibrillator (ICD). The patient had a history of coronary vasospasm with ventricular arrhythmia that required placement of the ICD 5 years prior. Because of refractory symptoms, she required prolonged admission in the intensive care unit with high-dose intravenous nitroglycerin, calcium channel blockers, benzodiazepines, beta blockers, chemical sympathectomy, and intubation and sedation. Despite these measures, the patient continued to have vasospasm and ventricular tachycardia, so cesarean delivery and tubal ligation were performed. After delivery, she was rapidly weaned from all invasive treatment modalities and was discharged on oral nitrates and calcium channel blockers.Conclusion: To our knowledge, this case is the first report of severe drug-refractory vasospastic angina triggered by pregnancy. The hormonal and nervous system changes that occur during pregnancy appear to be a trigger for vasospasm, further highlighted by the quick resolution of the patient's symptoms postdelivery. A multidisciplinary approach for treatment of both mother and baby was necessary. Our case provides a cautionary tale that patients with refractory vasospastic angina may want to pursue definitive contraception.

Influenza causes cardiac and pulmonary complications that can lead to death. Its effect on the conduction system, first described a century ago, has long been thought to be fairly benign. We report 2 cases of high-grade atrioventricular block associated with acute influenza infection. Both patients—a 50-year-old woman with no history of cardiac disease or conduction abnormalities and a 20-year-old man with a history of complex congenital heart disease and conduction abnormalities—received a permanent pacemaker. In the first case, pacemaker interrogation at 4 months revealed persistent atrioventricular block. In the second case, pacemaker interrogation at 3 months suggested resolution. Whether such influenza-associated changes are transient or permanent remains unknown. We recommend keeping a careful watch on influenza patients with cardiac rhythm abnormalities and monitoring them closely to see if the problem resolves.

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