Excess Iodine Exposure Acutely Increases Salivary Iodide And Antimicrobial Hypoiodous Acid Concentrations In Humans

The lactoperoxidase (LPO)-hydrogen peroxide-halides reaction (LPO system) converts iodide and thiocyanate (SCN-) into hypoiodous acid (HOI) and hypothiocyanite (OSCN-), respectively. Since this system has been implicated in defense of the airways and oropharynx from microbial invasion, we measured the concentrations of these analytes in human saliva before and after iodine administration to test the hypothesis that an iodide load increases salivary iodide and HOI concentrations. Salivary iodide, SCN-, HOI and OSCN- were measured using standard methodology. Salivary iodide and HOI levels significantly increased after iodinated contrast injection compared with baseline levels, whereas there was no significant change in salivary SCN- and OSCN- levels. The contrast dye iodine load and changes of salivary iodide and HOI levels were positively correlated, suggesting that higher iodide in the circulation increases iodide output and salivary HOI production. Excess iodine exposure in humans increases the salivary output of iodide, increasing salivary HOI concentrations with no effect on SCN-/OSCN- levels. This first of its kind study suggests that a sufficient but safe iodide supplementation may augment the generation of antimicrobial HOI by the salivary LPO system against airborne viral pathogens, including coronaviruses and influenza viruses, a possible inexpensive means of effectively curbing viral pandemics.

Abstract 1122‐000229: Simultaneous Transarterial‐Transvenous Contrast Injection to Reveal Connection Point for Treatment of Carotid Cavernous Fistula

Introduction : Cavernous sinus (CS) via inferior petrosal sinus (IPS) access can present a challenge in the treatment of carotid‐cavernous fistulas (CCF) due to anatomical variations, tortuosity, and/or difficult visualization of IPS given high retrograde flow through the fistulous connection. Methods : A 58‐year‐old male was referred to our academic medical center for three weeks of right eye pain, now complicated by redness, diplopia and blurry vision. Magnetic Resonance Imaging (MRI) brain at the outside hospital revealed hemorrhagic lesion in right parietotemporal region. Computerized tomography‐angiogram (CTA) of the head revealed filling of cavernous sinus during an arterial phase suspicious for CCF. Under general anesthesia, after accessing right common femoral artery, 4 French (F) cook catheter (Cook Medical LLC, Bloomington, IN) was advanced over 0.035 angled glide wire to the proximal right internal carotid artery. Contrast injected through the ICA showed the CS but not the IPS (Fig. 1A). Through the left common femoral vein, access was obtained using an Infinity guide catheter (Stryker Neurovascular, Fremont, CA) and Catalyst 5 (Stryker Neurovascular, Fremont, CA) distal access catheter. A Synchro 2 soft microwire (Stryker Neurovascular, Fremont, CA) was advanced through Echelon 10 (Medtronic, Minneapolis, MN) microcatheter. The venous guide catheter was advanced into right internal jugular vein (IJV) and the distal access catheter was placed into sigmoid jugular junction. Injection of contrast revealed the IPS, but not the CS (Fig. 1B). A subsequent simultaneous hand injection with the microcatheter within the IPS and the diagnostic catheter in the left ICA elucidated the venous‐venous connection (Fig. 1C,) allowing for subsequent navigation and complete treatment of the fistula through IPS using target coils (Fig. 1D). Results : Given the arterial system is a high‐pressure system and the usual direction of flow of contrast would be from the high‐pressure ICA to the low‐pressure CS, injecting a simultaneous contrast bolus from the venous end would oppose the arterial contrast flow. As a result, the fistulous connection that was previously obscured became visible allowing roadmap imaging guiding navigation into the CS. Conclusions : Use of simultaneous trans‐arterial/trans‐venous contrast injection is relatively simple compared to other reported techniques to reveal an obscure connection point. It also shortens the duration of endovascular tools in the bloodstream and thus, reduces the potential complication rate. Further use of this technique on larger study samples is important to validate its general use.

Serum neutrophil-gelatinase associated lipocalin as a predictor of post-contrast acute kidney injury in children

Background Diagnosis of post-contrast acute kidney injury (PC-AKI) by serum creatinine can be delayed because of various factors. A new biomarker neutrophilgelatinase associated lipocalin (NGAL) is postulated to be more sensitive for recognizing patients prone to PC-AKI. Objective To assess serum NGAL changes as an early biomarker of PC-AKI in children with congenital heart disease undergoing cardiac catheterization. Methods This observational study included 30 children with congenital heart disease who underwent cardiac catheterization at the Pediatric Cardiac Catheterization Unit, New Children’s Hospital, Ain Shams University. They had a median age of 30 months and 63% were females. Serum NGAL was measured just before the catheterization, 6hrs and 24hrs after contrast media administration while serum creatinine was measured before and after 24hrs of contrast media administration. Results Significant rise of serum NGAL was noted within 24hrs after contrast administration (p < 0.05) while serum creatinine showed a non-significant rise (p > 0.05). Serum NGAL was positively correlated with age, weight, height, body surface area and rate of contrast injection (p < 0.01). Higher levels of serum NGAL were found among patients who underwent diagnostic cardiac catheterization and those who received Midazolam for initial sedation during induction of anesthesia (p < 0.05). Conclusions Serum NGAL was elevated as early as 6 hours post contrast injection, however its serum level is affected by many factors. It’s important to be aware of other possible risk factors of PC-AKI rather than contrast media as type of cardiac catheterization and the anaesthetic Midazolam.