Glucagon-Like Peptide Receptor Agonists Use Before Endoscopy Is Associated With Low Retained Gastric Contents: A Multicenter Cross-Sectional Analysis.

INTRODUCTION: While ubiquity of glucagon-like peptide receptor agonists (GLP1-RAs) is rising, guidance from the gastroenterology societies and American Society of Anesthesiologist (ASA) remains in conflict on recommendations regarding preoperative holding before endoscopy. The aim of this study was to address this by evaluating the effect of GLP1-RAs on gastric retention during upper endoscopy. METHODS: This multicenter cross-sectional study included patients on confirmed GLP1-RAs receiving an endoscopy from 2021 to 2023. Demographics, prescribing practices, and procedure outcomes were captured. GLP1-RA management of preoperative holding was retroactively classified per ASA guidance. Multivariable logistic regression was performed to assess factors influencing retained gastric contents. RESULTS: Of 815 patients, 70 (8.7%) had retained gastric contents on endoscopy of whom 65 (93%) had type 2 diabetes mellitus. Only 1 (1.4%) of these patients required unplanned intubation, and none had aspiration events. Those with GLP1-RA held per ASA guidance (406, 49.8%) were less likely to have retained contents (4.4% vs 12.7%, P < 0.001), but there were no significant differences to intubation (0% vs 2%, P = 0.53) or aborting procedure rates (28% vs 18%, P = 0.40) due to gastric retention. On multivariable analysis, likelihood of food retention increased 36% (95% confidence interval 1.15-1.60) for every 1% increase in hemoglobin A1C after adjusting for GLP1-RA type and preoperative medication hold. DISCUSSION: In this multicenter study, very low rates of retained gastric contents were seen during endoscopy in patients on GLP1-RAs and most were in patients with type 2 diabetes mellitus. Our findings suggest an individualized approach rather than universal preoperative holding of medications before endoscopy.

Human TH1 and TH2 cells targeting rhinovirus and allergen coordinately promote allergic asthma.

BACKGROUND: Allergic asthmatic subjects are uniquely susceptible to acute wheezing episodes provoked by rhinovirus. However, the underlying immune mechanisms and interaction between rhinovirus and allergy remain enigmatic, and current paradigms are controversial. OBJECTIVE: We sought to perform a comprehensive analysis of type 1 and type 2 innate and adaptive responses in allergic asthmatic subjects infected with rhinovirus. METHODS: Circulating virus-specific TH1 cells and allergen-specific TH2 cells were precisely monitored before and after rhinovirus challenge in allergic asthmatic subjects (total IgE, 133-4692 IU/mL; n = 28) and healthy nonallergic controls (n = 12) using peptide/MHCII tetramers. T cells were sampled for up to 11 weeks to capture steady-state and postinfection phases. T-cell responses were analyzed in parallel with 18 cytokines in the nose, upper and lower airway symptoms, and lung function. The influence of in vivo IgE blockade was also examined. RESULTS: In uninfected asthmatic subjects, higher numbers of circulating virus-specific PD-1+ TH1 cells, but not allergen-specific TH2 cells, were linked to worse lung function. Rhinovirus infection induced an amplified antiviral TH1 response in asthmatic subjects versus controls, with synchronized allergen-specific TH2 expansion, and production of type 1 and 2 cytokines in the nose. In contrast, TH2 responses were absent in infected asthmatic subjects who had normal lung function, and in those receiving anti-IgE. Across all subjects, early induction of a minimal set of nasal cytokines that discriminated high responders (G-CSF, IFN-γ, TNF-α) correlated with both egress of circulating virus-specific TH1 cells and worse symptoms. CONCLUSIONS: Rhinovirus induces robust TH1 responses in allergic asthmatic subjects that may promote disease, even after the infection resolves.

Understanding the asthmatic response to an experimental rhinovirus infection: Exploring the effects of blocking IgE.

BACKGROUND: Rhinovirus frequently causes asthma exacerbations among children and young adults who are allergic. The interaction between allergen and rhinovirus-induced symptoms and inflammation over time is unclear. OBJECTIVE: Our aim was to compare the response to an experimental inoculation with rhinovirus-16 in allergic asthmatics with the response in healthy controls and to evaluate the effects of administrating omalizumab before and during the infection. METHODS: Two clinical trials were run in parallel. In one of these trials, the response to an experimental inoculation with rhinovirus-16 among asthmatics with high levels of total IgE was compared to the response in healthy controls. The other trial compared the effects of administering omalizumab versus placebo to asthmatics in a randomized, double-blind placebo-controlled investigation. The primary outcome for both trials compared lower respiratory tract symptoms (LRTSs) between study groups over the first 4 days of infection. RESULTS: Frequent comparisons of symptoms, lung function, and blood eosinophil counts revealed differences that were more pronounced among allergic asthmatics than among controls by days 2 and 3 after virus inoculation. Additionally, an augmentation of upper respiratory tract symptom scores and LRTS scores occurred among the atopic asthmatics versus the controls during the resolution of symptoms (P < .01 for upper respiratory symptom tract scores and P < .001 for LRTS scores). The beneficial effects of administering omalizumab on reducing LRTSs and improving lung function were strongest over the first 4 days. CONCLUSIONS: LRTSs and blood eosinophil counts were augmented and lung function was reduced among allergic asthmatics early after rhinovirus inoculation but increased late in the infection during symptom resolution. The effect of administering omalizumab on the response to rhinovirus was most pronounced during the early/innate phase of the infection.

Toll-like receptor 3 blockade in rhinovirus-induced experimental asthma exacerbations: A randomized controlled study.

BACKGROUND: Human rhinoviruses (HRVs) commonly precipitate asthma exacerbations. Toll-like receptor 3, an innate pattern recognition receptor, is triggered by HRV, driving inflammation that can worsen asthma. OBJECTIVE: We sought to evaluate an inhibitory mAb to Toll-like receptor 3, CNTO3157, on experimental HRV-16 inoculation in healthy subjects and asthmatic patients. METHODS: In this double-blind, multicenter, randomized, parallel-group study in North America and Europe, healthy subjects and patients with mild-to-moderate stable asthma received single or multiple doses of CNTO3157 or placebo, respectively, and were then inoculated with HRV-16 within 72 hours. All subjects were monitored for respiratory symptoms, lung function, and nasal viral load. The primary end point was maximal decrease in FEV1 during 10 days after inoculation. RESULTS: In asthmatic patients (n = 63) CNTO3157 provided no protection against FEV1 decrease (least squares mean: CNTO3157 [n = 30] = -7.08% [SE, 8.15%]; placebo [n = 25] = -5.98% [SE, 8.56%]) or symptoms after inoculation. In healthy subjects (n = 12) CNTO3157 versus placebo significantly attenuated upper (P = .03) and lower (P = .02) airway symptom scores, with area-under-the-curve increases of 9.1 (15.1) versus 34.9 (17.6) and 13.0 (18.4) versus 50.4 (25.9) for the CNTO3157 (n = 8) and placebo (n = 4) groups, respectively, after inoculation. All of the severe and 4 of the nonserious asthma exacerbations occurred while receiving CNTO3157. CONCLUSION: In summary, CNTO3157 was ineffective in attenuating the effect of HRV-16 challenge on lung function, asthma control, and symptoms in asthmatic patients but suppressed cold symptoms in healthy subjects. Other approaches, including blockade of multiple pathways or antiviral agents, need to be sought for this high unmet medical need.

Single-Cell Tracking Reveals a Role for Pre-Existing CCR5+ Memory Th1 Cells in the Control of Rhinovirus-A39 After Experimental Challenge in Humans.

Background: Little is known about T cells that respond to human rhinovirus in vivo, due to timing of infection, viral diversity, and complex T-cell specificities. We tracked circulating CD4+ T cells with identical epitope specificities that responded to intranasal challenge with rhinovirus (RV)-A39, and we assessed T-cell signatures in the nose. Methods: Cells were monitored using a mixture of 2 capsid-specific major histocompatibility complex II tetramers over a 7-week period, before and after RV-A39 challenge, in 16 human leukocyte antigen-DR4+ subjects who participated in a trial of Bifidobacterium lactis (Bl-04) supplementation. Results: Pre-existing tetramer+ T cells were linked to delayed viral shedding, enriched for activated CCR5+ Th1 effectors, and included a minor interleukin-21+ T follicular helper cell subset. After RV challenge, expansion and activation of virus-specific CCR5+ Th1 effectors was restricted to subjects who had a rise in neutralizing antibodies, and tetramer-negative CCR5+ effector memory types were comodulated. In the nose, CXCR3-CCR5+ T cells present during acute infection were activated effector memory type, whereas CXCR3+ cells were central memory type, and cognate chemokine ligands were elevated over baseline. Probiotic had no T-cell effects. Conclusions: We conclude that virus-specific CCR5+ effector memory CD4+ T cells primed by previous exposure to related viruses contribute to the control of rhinovirus.

Basal salivary cortisol secretion and susceptibility to upper respiratory infection.

The immunosuppressive effects of glucocorticoids (GCs) are well-established. However, whether the net effect of GC-elicited alterations in immune function is sufficient to influence a clinically relevant outcome in healthy adults has yet to be shown. The aim of the present study was to investigate whether inter-individual differences in basal salivary cortisol production are associated with increased risk and severity of infection and subsequent illness following experimental exposure to a virus that causes the common cold. The present analyses combine archival data from three viral-challenge studies. Participants were 608 healthy adults, aged 18 to 55 years (49.2% female; 65.8% white), who each completed a three-day saliva collection protocol; was subsequently exposed to a virus that causes the common cold; and monitored for 5 days for objective signs of infection (presence of challenge virus in nasal secretions) and clinical illness (mucus weight, mucociliary clearance time). Basal cortisol production (operationalized as the calculated area-under-the-curve averaged across the 3 days) showed a graded association with infection risk, with those producing higher levels of cortisol being at greater risk. Cortisol also showed a continuous association with duration of viral shedding, an indicator of viral replication and continuing infection, such that higher cortisol concentrations predicted more days of shedding. Cortisol was not, however, related to severity of objective illness. These findings are the first to demonstrate in healthy adults an association between basal cortisol production and an objectively measured and clinically relevant infectious disease outcome.

Treatment of Acute Cough Due to the Common Cold: Multi-component, Multi-symptom Therapy is Preferable to Single-Component, Single-Symptom Therapy--A Pro/Con Debate.

Acute viral upper respiratory tract infection, or, the common cold, affects essentially every human being, and cough is reported as its most frequent associated symptom. Billions of dollars are spent worldwide annually by individuals seeking relief from this multi-symptom syndrome. Thousands of non-prescription, over-the-counter products are available worldwide, aimed at relieving the various bothersome symptoms induced by the common cold. Differences of opinion exist as to whether optimal therapy for cough associated with the common cold consists of multi-component, multi-symptom cough/cold preparations, or, whether single-component medications, aimed at relief of specific symptoms, represent the optimal therapeutic approach. The 5th American Cough Conference, held in Washington, D.C. in June, 2015, provided an ideal forum for discussion and debate of this issue between two internationally recognized experts in the field of the common cold and its treatment.

Acute Flaccid Paralysis Associated with Novel Enterovirus C105.

An outbreak of acute flaccid paralysis among children in the United States during summer 2014 was tentatively associated with enterovirus D68 infection. This syndrome in a child in fall 2014 was associated with enterovirus C105 infection. The presence of this virus strain in North America may pose a diagnostic challenge.

Does hugging provide stress-buffering social support? A study of susceptibility to upper respiratory infection and illness.

Perceived social support has been hypothesized to protect against the pathogenic effects of stress. How such protection might be conferred, however, is not well understood. Using a sample of 404 healthy adults, we examined the roles of perceived social support and received hugs in buffering against interpersonal stress-induced susceptibility to infectious disease. Perceived support was assessed by questionnaire, and daily interpersonal conflict and receipt of hugs were assessed by telephone interviews on 14 consecutive evenings. Subsequently, participants were exposed to a virus that causes a common cold and were monitored in quarantine to assess infection and illness signs. Perceived support protected against the rise in infection risk associated with increasing frequency of conflict. A similar stress-buffering effect emerged for hugging, which explained 32% of the attenuating effect of support. Among infected participants, greater perceived support and more-frequent hugs each predicted less-severe illness signs. These data suggest that hugging may effectively convey social support.

Utility of animal and in vivo experimental infection of humans with rhinoviruses in the development of therapeutic agents for viral exacerbations of asthma and chronic obstructive pulmonary disease.

There is an association with acute viral infection of the respiratory tract and exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Although these exacerbations are associated with several types of viruses, human rhinoviruses (HRVs) are associated with the vast majority of disease exacerbations. Due to the lack of an animal species that is naturally permissive for HRVs to use as a facile model system, and the limitations associated with animal models of asthma and COPD, studies of controlled experimental infection of humans with HRVs have been used and conducted safely for decades. This review discusses how these experimental infection studies with HRVs have provided a means of understanding the pathophysiology underlying virus-induced exacerbations of asthma and COPD with the goal of developing agents for their prevention and treatment.

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk.

We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1ß, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.

Supportive treatment for children with the common cold.

PURPOSE OF REVIEW: This review summarizes recent developments in the supportive treatment of common cold symptoms in children. RECENT FINDINGS: Conventional common cold therapies are no longer recommended for use in young children because of safety concerns. There are no studies that convincingly demonstrate the efficacy of any therapy for treatment of common cold symptoms in children less than 6 years of age and it is unlikely studies that establish efficacy can be done. Recent studies report a significant effect of probiotics on the occurrence of common cold illnesses in children, and studies in animals provide a plausible mechanism of action. These data suggest that the use of probiotics may have promise for the prevention of common cold illnesses in children. SUMMARY: The effect of treatment on the severity of common cold symptoms cannot be accurately assessed with current study designs. In the absence of convincing evidence of efficacy, treatment of young children with symptomatic therapies cannot be recommended. Preliminary data suggest a small, beneficial effect of probiotics for the prevention of common cold illness.

The effect of probiotic Bifidobacterium lactis Bl-04 on innate antiviral responses invitro.

Consumption of certain probiotic strains may be beneficial for reducing the risk of acute upper respiratory tract infections (URTIs), however, underlying immunological mechanisms are elusive. Bifidobacterium lactis Bl-04™ has been reported in humans to significantly reduce the risk of URTIs, affect the innate immunity in the nasal mucosa, and reduce nasal lavage virus titer after a rhinovirus (RV) challenge. To study the immunological mechanisms, we investigated the effect of Bl-04 on cytokine production and transcriptomes of human monocyte-derived macrophages (Mfs) and dendritic cells (DCs), and further on RV replication and cytokine production in MRC-5 fibroblasts. The results showed that Bl-04 modulates antiviral immune responses and potentiates cytokine production during viral challenge mimic in immune cells. However, effect of Bl-04 on RV replication and cytokine production in fibroblasts was negligible. Overall, the findings suggest that Bl-04 mildly stimulates antiviral immunity in Mfs and DCs, and potentially influences viral replication in fibroblasts that however warrants further investigations.

Childhood socioeconomic status, telomere length, and susceptibility to upper respiratory infection.

Low socioeconomic status (SES) during childhood and adolescence has been found to predict greater susceptibility to common cold viruses in adults. Here, we test whether low childhood SES is associated with shorter leukocyte telomere length in adulthood, and whether telomere length mediates the association between childhood SES and susceptibility to acute upper respiratory disease in adulthood. At baseline, 196 healthy volunteers reported whether they currently owned their home and, for each year of their childhood, whether their parents owned the family home. Volunteers also had blood drawn for assessment of specific antibody to the challenge virus, and for CD8+ CD28- T-lymphocyte telomere length (in a subset, n=135). They were subsequently quarantined in a hotel, exposed to a virus (rhinovirus [RV] 39) that causes a common cold and followed for infection and illness (clinical cold) over five post-exposure days. Lower childhood SES as measured by fewer years of parental home ownership was associated with shorter adult CD8+ CD28- telomere length and with an increased probability of developing infection and clinical illness when exposed to a common cold virus in adulthood. These associations were independent of adult SES, age, sex, race, body mass, neuroticism, and childhood family characteristics. Associations with infections and colds were also independent of pre-challenge viral-specific antibody and season. Further analyses do not support mediating roles for smoking, alcohol consumption or physical activity but suggest that CD8+ CD28- cell telomere length may act as a partial mediator of the associations between childhood SES and infection and childhood SES and colds.

Association between telomere length and experimentally induced upper respiratory viral infection in healthy adults.

IMPORTANCE: Although leukocyte telomere length is associated with mortality and many chronic diseases thought to be manifestations of age-related functional decline, it is not known whether it relates to acute disease in younger healthy populations. OBJECTIVE: To determine whether shorter telomeres in leukocytes, especially CD8CD28- T cells, are associated with decreased resistance to upper respiratory infection and clinical illness in young to midlife adults. DESIGN, SETTING, AND PARTICIPANTS: Between 2008 and 2011, telomere length was assessed in peripheral blood mononuclear cells (PBMCs) and T-cell subsets (CD4, CD8CD28+, CD8CD28-) from 152 healthy 18- to 55-year-old residents of Pittsburgh, Pennsylvania. Participants were subsequently quarantined (single rooms), administered nasal drops containing a common cold virus (rhinovirus 39), and monitored for 5 days for development of infection and clinical illness. MAIN OUTCOME MEASURES: Infection (virus shedding or 4-fold increase in virus-specific antibody titer) and clinical illness (verified infection plus objective signs of illness). RESULTS: Rates of infections and clinical illness were 69% (n = 105) and 22% (n = 33), respectively. Shorter telomeres were associated with greater odds of infection, independent of prechallenge virus-specific antibody, demographics, contraceptive use, season, and body mass index (PBMC: odds ratio [OR] per 1-SD decrease in telomere length, 1.71 [95% CI, 1.08-2.72]; n = 128 [shortest tertile 77% infected; middle, 66%; longest, 57%]; CD4: OR, 1.76 [95% CI, 1.15-2.70]; n = 146 [shortest tertile 80% infected; middle, 71%; longest, 54%]; CD8CD28+: OR, 1.93 [95% CI, 1.21-3.09], n = 132 [shortest tertile 84% infected; middle, 64%; longest, 58%]; CD8CD28-: OR, 2.02 [95% CI, 1.29-3.16]; n = 144 [shortest tertile 77% infected; middle, 75%; longest, 50%]). CD8CD28- was the only cell population in which shorter telomeres were associated with greater risk of clinical illness (OR, 1.69 [95% CI, 1.01-2.84]; n = 144 [shortest tertile, 26%; middle, 22%; longest, 13%]). The association between CD8CD28- telomere length and infection increased with age (CD8CD28- telomere length × age interaction, b = 0.09 [95% CI, 0.02-0.16], P = .01, n = 144). CONCLUSION AND RELEVANCE: In this preliminary study among a cohort of healthy 18- to 55-year-olds, shorter CD8CD28- T-cell telomere length was associated with increased risk for experimentally induced acute upper respiratory infection and clinical illness.

A randomized trial of the efficacy of hand disinfection for prevention of rhinovirus infection.

BACKGROUND: Hand disinfection is frequently recommended for prevention of rhinovirus (RV) infection and RV-associated common colds. The effectiveness of this intervention has not been established in a natural setting. The purpose of this study was to determine the effect of hand disinfection on RV infection and RV-associated common cold illness in a natural setting. METHODS: A controlled clinical trial was done in young adult volunteers during 9 weeks of the fall 2009 RV season. Volunteers were randomized to either an antiviral hand treatment containing 2% citric acid and 2% malic acid in 62% ethanol (n = 116) or to a no-treatment control group (n = 96). The hand treatment was applied every 3 hours while the subjects were awake. All volunteers kept a daily diary of symptoms and had a nasal lavage for polymerase chain reaction once each week and 2 additional lavages around the time of each common cold illness. The primary endpoint was the number of RV-associated illnesses. The incidence of RV infection and of common cold illnesses were evaluated as secondary endpoints. RESULTS: The hand treatment did not significantly reduce RV infection or RV-related common cold illnesses. The total number of common cold illnesses was significantly reduced in the intent-to-treat analysis, but this effect was not seen in the per protocol analysis. CONCLUSIONS: In this study, hand disinfection did not reduce RV infection or RV-related common cold illnesses. CLINICAL TRIALS REGISTRATION: NCT00993759.

Parenthood and host resistance to the common cold.

OBJECTIVE: To determine whether parenthood predicts host resistance to the common cold among healthy volunteers experimentally exposed to a common cold virus. METHODS: Participants were 795 healthy volunteers (age range = 18-55 years) enrolled in one of three viral-challenge studies conducted from 1993 to 2004. After reporting parenthood status, participants were quarantined, administered nasal drops containing one of four common cold viruses, and monitored for the development of a clinical cold (infection in the presence of objective signs of illness) on the day before and for 5 to 6 days after exposure. All analyses included controls for immunity to the experimental virus (prechallenge specific antibody titers), viral strain, season, age, sex, race/ethnicity, marital status, body mass, study, employment status, and education. RESULTS: Parents were less likely to develop colds than nonparents were (odds ratio [OR] = 0.48, 95% confidence interval [CI] = 0.31-0.73). This was true for both parents with one to two children (OR = 0.52, 95% CI = 0.33-0.83) and three or more children (OR = 0.39, 95% CI = 0.22-0.70). Parenthood was associated with a decreased risk of colds for both those with at least one child living at home (OR = 0.46, 95% CI = 0.24-0.87) and those whose children all lived away from home (OR = 0.27, 95% CI = 0.12-0.60). The relationship between parenthood and colds was not observed in parents aged 18 to 24 years but was pronounced among older parents. CONCLUSIONS: Parenthood was associated with greater host resistance to common cold viruses.

Molecular Analysis of Pancreatic Cyst Fluid for the Management of Intraductal Papillary Mucinous Neoplasms.

Pancreatic cancer is one of the most lethal human cancers. Early detection and diagnosis of precursor lesions for pancreatic malignancy is essential to improve the morbidity and mortality associated with this diagnosis. Of the cystic precursor lesions, branch duct intraductal papillary mucinous neoplasm (IPMN) is the most frequently identified lesion and has a wide range of malignant potential. Currently, Carcinogenic embryonic antigen (CEA) levels in the cyst fluid and cytology are the two most often utilized tools to diagnose these lesions; however, their diagnostic and risk stratification capabilities are somewhat limited. Within the last decade, the use of endoscopic ultrasound-guided fine-needle aspiration has opened the door for molecular analysis of cystic fluid as an option to enhance both the diagnosis and risk stratification of these lesions. The first step is to differentiate branch duct IPMNs from other lesions. KRAS and GNAS alterations have been shown to be accurate markers for this purpose. Following cyst type identification, mutational analysis, telomere fusion, microRNAs, long non-coding RNA, and DNA methylation have been identified as potential targets for stratifying malignant potential using the cystic fluid. In this review, we will examine the various targets of cyst fluid molecular analysis and their utility in the diagnosis and risk stratification of branch duct IPMNs.

Application of Artificial Intelligence in the Management of Pancreatic Cystic Lesions.

The rate of incidentally detected pancreatic cystic lesions (PCLs) has increased over the past decade and was recently reported at 8%. These lesions pose a unique challenge, as each subtype of PCL carries a different risk of malignant transformation, ranging from 0% (pancreatic pseudocyst) to 34-68% (main duct intraductal papillary mucinous neoplasm). It is imperative to correctly risk-stratify the malignant potential of these lesions in order to provide the correct care course for the patient, ranging from monitoring to surgical intervention. Even with the multiplicity of guidelines (i.e., the American Gastroenterology Association guidelines and Fukuoka/International Consensus guidelines) and multitude of diagnostic information, risk stratification of PCLs falls short. Studies have reported that 25-64% of patients undergoing PCL resection have pancreatic cysts with no malignant potential, and up to 78% of mucin-producing cysts resected harbor no malignant potential on pathological evaluation. Clinicians are now incorporating artificial intelligence technology to aid in the management of these difficult lesions. This review article focuses on advancements in artificial intelligence within digital pathomics, radiomics, and genomics as they apply to the diagnosis and risk stratification of PCLs.