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      <title>Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</title>
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      <description>Table of Contents for Alcohol, Clinical and Experimental Research. List of articles from both the latest and EarlyView issues.</description>
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      <pubDate>Wed, 10 Jun 2026 08:05:54 +0000</pubDate>
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      <dc:title>Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</dc:title>
      <dc:publisher>Wiley</dc:publisher>
      <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
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         <link>https://onlinelibrary.wiley.com/doi/10.1111/acer.70330?af=R</link>
         <pubDate>Fri, 05 Jun 2026 22:58:20 -0700</pubDate>
         <dc:date>2026-06-05T10:58:20-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/29937175?af=R">Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</source>
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         <title>A Systematic Review of International Guidelines for Addressing Alcohol Use Disorder in Pregnancy</title>
         <description>Alcohol, Clinical and Experimental Research, Volume 50, Issue 6, June 2026. </description>
         <dc:description>
Across 18 international guidelines (2014–2024), there was strong agreement on alcohol screening and abstinence counseling in pregnancy, but limited guidance on treating alcohol use disorder. Most took a cautious stance on medications, leaving clinicians and patients to balance known harms of untreated AUD against uncertain medication safety.

ABSTRACT
Despite well‐documented harms of prenatal alcohol exposure, evidence‐based treatment guidelines for alcohol use disorder (AUD) during pregnancy remain limited. We systematically reviewed international clinical practice guidelines to examine how they address the full cascade of AUD care during pregnancy, including diagnosis, engagement, treatment initiation, and retention. We searched over 40 clinical practice guideline databases (including PubMed and Guidelines International Network) and gray literature sources globally, identifying 1045 records. Using the Population, Interventions, Comparators, Attributes, Recommendation Characteristics (PICAR) framework, we evaluated guidelines from medical organizations in English‐speaking nations addressing alcohol use and AUD management in pregnancy. Our final analysis included 18 guidelines from the United States, Canada, the United Kingdom, Australia/New Zealand, and the World Health Organization published from 2014 to the present. Two reviewers independently assessed each guideline using the Appraisal of Guidelines Research and Evaluation‐Recommendations Excellence (AGREE‐REX) framework to evaluate quality and risk of bias. We used narrative synthesis to summarize findings across key concepts and care cascade stages. Nearly all guidelines (94%) described risks of alcohol exposure and recommended counseling on cessation (89%), yet few extended beyond these early cascade stages. Only 44% mentioned medications for AUD (MAUD), and merely 17% discussed specific psychosocial treatments. Among guidelines addressing MAUD, only one cautiously supported use, while three explicitly recommended against it. Most guidelines (61%) ended treatment recommendations at referral to specialty care, with half limiting guidance to acute alcohol withdrawal management. Taken together, our findings reveal a stark misalignment between screening emphasis and treatment guidance. While guidelines consistently recommend universal screening and brief intervention, they provide minimal actionable frameworks for managing AUD throughout pregnancy. This gap leaves clinicians without evidence‐based pathways for comprehensive AUD treatment during the prenatal period, highlighting an urgent need to strengthen both the evidence base and clinical guidance for AUD management in pregnancy.
</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/059fec54-a81b-46af-978b-733dfcc7ecda/acer70330-toc-0001-m.png"
     alt="A Systematic Review of International Guidelines for Addressing Alcohol Use Disorder in Pregnancy"/&gt;
&lt;p&gt;Across 18 international guidelines (2014–2024), there was strong agreement on alcohol screening and abstinence counseling in pregnancy, but limited guidance on treating alcohol use disorder. Most took a cautious stance on medications, leaving clinicians and patients to balance known harms of untreated AUD against uncertain medication safety.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Despite well-documented harms of prenatal alcohol exposure, evidence-based treatment guidelines for alcohol use disorder (AUD) during pregnancy remain limited. We systematically reviewed international clinical practice guidelines to examine how they address the full cascade of AUD care during pregnancy, including diagnosis, engagement, treatment initiation, and retention. We searched over 40 clinical practice guideline databases (including PubMed and Guidelines International Network) and gray literature sources globally, identifying 1045 records. Using the Population, Interventions, Comparators, Attributes, Recommendation Characteristics (PICAR) framework, we evaluated guidelines from medical organizations in English-speaking nations addressing alcohol use and AUD management in pregnancy. Our final analysis included 18 guidelines from the United States, Canada, the United Kingdom, Australia/New Zealand, and the World Health Organization published from 2014 to the present. Two reviewers independently assessed each guideline using the Appraisal of Guidelines Research and Evaluation-Recommendations Excellence (AGREE-REX) framework to evaluate quality and risk of bias. We used narrative synthesis to summarize findings across key concepts and care cascade stages. Nearly all guidelines (94%) described risks of alcohol exposure and recommended counseling on cessation (89%), yet few extended beyond these early cascade stages. Only 44% mentioned medications for AUD (MAUD), and merely 17% discussed specific psychosocial treatments. Among guidelines addressing MAUD, only one cautiously supported use, while three explicitly recommended against it. Most guidelines (61%) ended treatment recommendations at referral to specialty care, with half limiting guidance to acute alcohol withdrawal management. Taken together, our findings reveal a stark misalignment between screening emphasis and treatment guidance. While guidelines consistently recommend universal screening and brief intervention, they provide minimal actionable frameworks for managing AUD throughout pregnancy. This gap leaves clinicians without evidence-based pathways for comprehensive AUD treatment during the prenatal period, highlighting an urgent need to strengthen both the evidence base and clinical guidance for AUD management in pregnancy.&lt;/p&gt;</content:encoded>
         <dc:creator>
Caroline B. Cary, 
Emily O.B. Hynes, 
Mishka Terplan, 
Kelly A. McNamara, 
Vitor S. Tardelli, 
Thiago M. Fidalgo, 
Jennifer K. Bello, 
Michelle Doering, 
Richard A. Grucza, 
Hendrée E. Jones, 
Ryan Duggal, 
Jeannie C. Kelly, 
Silvia S. Martins, 
Caitlin E. Martin, 
Kevin Young Xu
</dc:creator>
         <category>CRITICAL REVIEW</category>
         <dc:title>A Systematic Review of International Guidelines for Addressing Alcohol Use Disorder in Pregnancy</dc:title>
         <dc:identifier>10.1111/acer.70330</dc:identifier>
         <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
         <prism:doi>10.1111/acer.70330</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/acer.70330?af=R</prism:url>
         <prism:section>CRITICAL REVIEW</prism:section>
         <prism:volume>50</prism:volume>
         <prism:number>6</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/acer.70331?af=R</link>
         <pubDate>Fri, 05 Jun 2026 04:54:39 -0700</pubDate>
         <dc:date>2026-06-05T04:54:39-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/29937175?af=R">Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</source>
         <prism:coverDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDisplayDate>
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         <title>The Effects of Early Postnatal Alcohol Exposure on Bone Molecular Composition in a Mouse Model</title>
         <description>Alcohol, Clinical and Experimental Research, Volume 50, Issue 6, June 2026. </description>
         <dc:description>
Early postnatal alcohol exposure was associated with long‐term changes in adult bone molecular composition and increased CTX‐I, indicating persistent effects on skeletal biology. Overlap with gavage‐related changes highlights the need to distinguish alcohol‐specific effects from procedural influences.

ABSTRACT

Background
Perinatal exposure to alcohol is a critical risk factor for long‐term skeletal health in humans and has been demonstrated in rodent models. Early postnatal alcohol gavage exposure in mice is used to study third trimester toxicity in humans. However, further research is required to fully characterize the effects of alcohol on bone molecular composition and distinguish them from the alterations associated with gavage‐related stress in mouse models.


Methods
Female mouse pups were assigned to untreated control (C), gavage control (GC), and alcohol‐treated (A) groups. Between postnatal days 3 and 20, the A group received ethanol (3.0 g/kg/day) by intragastric gavage, while the GC group underwent the same gavage procedure without any solution (neither milk nor ethanol). At postnatal day 90, femoral bone molecular composition and bone metabolism were evaluated by attenuated total reflection Fourier‐transform infrared (ATR‐FTIR) spectroscopy and biochemical studies.


Results
Several ATR‐FTIR‐derived matrix and mineral‐related alterations, including reduced total protein‐related indices, lower collagen cross‐link ratio, reduced mineral‐to‐matrix ratio, and increased crystallinity, were observed in both GC and A groups relative to untreated controls, indicating a substantial long‐term influence of the gavage procedure itself. Compared with the GC, the A group showed additional selective differences, most notably reduced relative carbonate content and increased CTX‐I levels. In the C group, serum 25(OH)D, PTH, and calcitonin levels differed from both GC and A groups, whereas osteocalcin was increased in the GC group relative to the C group, and no significant difference was observed between the GC and A groups.


Conclusion
Prolonged neonatal gavage was associated with substantial long‐term changes in bone molecular composition and several circulating bone‐related hormonal markers. Against this background, postnatal alcohol exposure was associated with additional selective differences, particularly in CTX‐I and relative carbonate content. These findings highlight the importance of discriminating between the effect of the procedure and the effect of alcohol in developmental models based on repeated neonatal gavage.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/7af56543-0f0a-4768-890c-bf16fd112468/acer70331-toc-0001-m.png"
     alt="The Effects of Early Postnatal Alcohol Exposure on Bone Molecular Composition in a Mouse Model"/&gt;
&lt;p&gt;Early postnatal alcohol exposure was associated with long-term changes in adult bone molecular composition and increased CTX-I, indicating persistent effects on skeletal biology. Overlap with gavage-related changes highlights the need to distinguish alcohol-specific effects from procedural influences.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Perinatal exposure to alcohol is a critical risk factor for long-term skeletal health in humans and has been demonstrated in rodent models. Early postnatal alcohol gavage exposure in mice is used to study third trimester toxicity in humans. However, further research is required to fully characterize the effects of alcohol on bone molecular composition and distinguish them from the alterations associated with gavage-related stress in mouse models.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Female mouse pups were assigned to untreated control (C), gavage control (GC), and alcohol-treated (A) groups. Between postnatal days 3 and 20, the A group received ethanol (3.0 g/kg/day) by intragastric gavage, while the GC group underwent the same gavage procedure without any solution (neither milk nor ethanol). At postnatal day 90, femoral bone molecular composition and bone metabolism were evaluated by attenuated total reflection Fourier-transform infrared (ATR-FTIR) spectroscopy and biochemical studies.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Several ATR-FTIR-derived matrix and mineral-related alterations, including reduced total protein-related indices, lower collagen cross-link ratio, reduced mineral-to-matrix ratio, and increased crystallinity, were observed in both GC and A groups relative to untreated controls, indicating a substantial long-term influence of the gavage procedure itself. Compared with the GC, the A group showed additional selective differences, most notably reduced relative carbonate content and increased CTX-I levels. In the C group, serum 25(OH)D, PTH, and calcitonin levels differed from both GC and A groups, whereas osteocalcin was increased in the GC group relative to the C group, and no significant difference was observed between the GC and A groups.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Prolonged neonatal gavage was associated with substantial long-term changes in bone molecular composition and several circulating bone-related hormonal markers. Against this background, postnatal alcohol exposure was associated with additional selective differences, particularly in CTX-I and relative carbonate content. These findings highlight the importance of discriminating between the effect of the procedure and the effect of alcohol in developmental models based on repeated neonatal gavage.&lt;/p&gt;</content:encoded>
         <dc:creator>
Ilknur Dursun, 
Birsen Elibol, 
Sebnem Garip Ustaoglu
</dc:creator>
         <category>RESEARCH ARTICLE</category>
         <dc:title>The Effects of Early Postnatal Alcohol Exposure on Bone Molecular Composition in a Mouse Model</dc:title>
         <dc:identifier>10.1111/acer.70331</dc:identifier>
         <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
         <prism:doi>10.1111/acer.70331</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/acer.70331?af=R</prism:url>
         <prism:section>RESEARCH ARTICLE</prism:section>
         <prism:volume>50</prism:volume>
         <prism:number>6</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/acer.70332?af=R</link>
         <pubDate>Fri, 05 Jun 2026 04:49:44 -0700</pubDate>
         <dc:date>2026-06-05T04:49:44-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/29937175?af=R">Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</source>
         <prism:coverDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/acer.70332</guid>
         <title>Baclofen Modulates Neural Intrinsic Functional Connectivity in Treatment‐Seeking Individuals With Alcohol Use Disorder</title>
         <description>Alcohol, Clinical and Experimental Research, Volume 50, Issue 6, June 2026. </description>
         <dc:description>
In a randomized, double‐blind study of individuals with alcohol use disorder, high‐dose baclofen (75 mg/day) compared with placebo was associated with differences in resting‐state functional connectivity, with higher connectivity in reward and stress‐related regions and lower connectivity in attentional and salience networks.

ABSTRACT

Background
Chronic alcohol use alters brain networks related to reward and stress regulation, contributing to alcohol use disorder (AUD). Baclofen, a GABAB receptor agonist, reduces cue‐elicited neural responses and alcohol consumption, but its effects on intrinsic functional connectivity remain unclear. This study investigates the dose‐specific effects of baclofen on intrinsic resting‐state functional connectivity in treatment‐seeking individuals with AUD.


Methods
In this double‐blind, placebo‐controlled, randomized clinical trial, 29 participants with AUD were randomized to receive placebo (n = 10), low‐dose baclofen (30 mg/day, n = 10), or high‐dose baclofen (75 mg/day, n = 9) for 12 weeks. Resting‐state fMRI data were collected at rest during week 2. A data‐driven parcellation approach assessed connectivity patterns across the brain and associations with percentage of heavy drinking days and percentage of days abstinent post scan were examined in an exploratory analysis.


Results
Compared to placebo, high‐dose baclofen was associated with significant differences in intrinsic connectivity in brain regions linked with reward, stress, attentional, and salience networks. Higher connectivity was observed between the somatomotor network and regions involved in stress regulation (e.g., hypothalamus) and reward processing, while lower connectivity was observed within salience and attentional networks. These changes were not observed in the low‐dose or placebo groups. Although nonsignificant, associations between MES and clinical outcomes demonstrated moderate, directionally consistent effects for abstinence‐related outcomes.


Conclusions
High‐dose baclofen may modulate intrinsic brain connectivity in key networks implicated in AUD, including systems involved in attention and stress regulation. Although statistically significant relationships between functional connectivity and clinical outcomes were not identified, trends suggest that connectivity differences between high‐dose baclofen and placebo may be relevant to treatment response. These neurobiological findings provide additional support for baclofen as a dose‐dependent pharmacotherapy for AUD and highlight the need for larger samples to clarify the relationship between intrinsic connectivity and clinical outcomes.


Trial Registration
ClinicalTrials.gov, NCT01711125, https://clinicaltrials.gov/ct2/show/NCT01711125 letter of completion

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/8cd32a1a-0b70-49ab-85b0-390767c44cbc/acer70332-toc-0001-m.png"
     alt="Baclofen Modulates Neural Intrinsic Functional Connectivity in Treatment-Seeking Individuals With Alcohol Use Disorder"/&gt;
&lt;p&gt;In a randomized, double-blind study of individuals with alcohol use disorder, high-dose baclofen (75 mg/day) compared with placebo was associated with differences in resting-state functional connectivity, with higher connectivity in reward and stress-related regions and lower connectivity in attentional and salience networks.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Chronic alcohol use alters brain networks related to reward and stress regulation, contributing to alcohol use disorder (AUD). Baclofen, a GABA&lt;sub&gt;B&lt;/sub&gt; receptor agonist, reduces cue-elicited neural responses and alcohol consumption, but its effects on intrinsic functional connectivity remain unclear. This study investigates the dose-specific effects of baclofen on intrinsic resting-state functional connectivity in treatment-seeking individuals with AUD.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;In this double-blind, placebo-controlled, randomized clinical trial, 29 participants with AUD were randomized to receive placebo (&lt;i&gt;n&lt;/i&gt; = 10), low-dose baclofen (30 mg/day, &lt;i&gt;n&lt;/i&gt; = 10), or high-dose baclofen (75 mg/day, &lt;i&gt;n&lt;/i&gt; = 9) for 12 weeks. Resting-state fMRI data were collected at rest during week 2. A data-driven parcellation approach assessed connectivity patterns across the brain and associations with percentage of heavy drinking days and percentage of days abstinent post scan were examined in an exploratory analysis.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Compared to placebo, high-dose baclofen was associated with significant differences in intrinsic connectivity in brain regions linked with reward, stress, attentional, and salience networks. Higher connectivity was observed between the somatomotor network and regions involved in stress regulation (e.g., hypothalamus) and reward processing, while lower connectivity was observed within salience and attentional networks. These changes were not observed in the low-dose or placebo groups. Although nonsignificant, associations between MES and clinical outcomes demonstrated moderate, directionally consistent effects for abstinence-related outcomes.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;High-dose baclofen may modulate intrinsic brain connectivity in key networks implicated in AUD, including systems involved in attention and stress regulation. Although statistically significant relationships between functional connectivity and clinical outcomes were not identified, trends suggest that connectivity differences between high-dose baclofen and placebo may be relevant to treatment response. These neurobiological findings provide additional support for baclofen as a dose-dependent pharmacotherapy for AUD and highlight the need for larger samples to clarify the relationship between intrinsic connectivity and clinical outcomes.&lt;/p&gt;
&lt;h2&gt;Trial Registration&lt;/h2&gt;
&lt;p&gt;&lt;a target="_blank"
   title="Link to external resource"
   href="http://clinicaltrials.gov"&gt;ClinicalTrials.gov&lt;/a&gt;, NCT01711125, &lt;a target="_blank"
   title="Link to external resource"
   href="https://clinicaltrials.gov/ct2/show/"&gt;https://clinicaltrials.gov/ct2/show/NCT01711125&lt;/a&gt; letter of completion&lt;/p&gt;</content:encoded>
         <dc:creator>
Warren B. Logge, 
Tristan P. Hurzeler, 
Paul S. Haber, 
Laurence Mealing, 
Andrew J. Baillie, 
Kirsten C. Morley
</dc:creator>
         <category>RESEARCH ARTICLE</category>
         <dc:title>Baclofen Modulates Neural Intrinsic Functional Connectivity in Treatment‐Seeking Individuals With Alcohol Use Disorder</dc:title>
         <dc:identifier>10.1111/acer.70332</dc:identifier>
         <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
         <prism:doi>10.1111/acer.70332</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/acer.70332?af=R</prism:url>
         <prism:section>RESEARCH ARTICLE</prism:section>
         <prism:volume>50</prism:volume>
         <prism:number>6</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/acer.70349?af=R</link>
         <pubDate>Fri, 05 Jun 2026 03:37:35 -0700</pubDate>
         <dc:date>2026-06-05T03:37:35-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/29937175?af=R">Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</source>
         <prism:coverDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/acer.70349</guid>
         <title>Issue Information</title>
         <description>Alcohol, Clinical and Experimental Research, Volume 50, Issue 6, June 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator/>
         <category>ISSUE INFORMATION</category>
         <dc:title>Issue Information</dc:title>
         <dc:identifier>10.1111/acer.70349</dc:identifier>
         <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
         <prism:doi>10.1111/acer.70349</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/acer.70349?af=R</prism:url>
         <prism:section>ISSUE INFORMATION</prism:section>
         <prism:volume>50</prism:volume>
         <prism:number>6</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/acer.70329?af=R</link>
         <pubDate>Fri, 05 Jun 2026 03:32:43 -0700</pubDate>
         <dc:date>2026-06-05T03:32:43-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/29937175?af=R">Wiley: Alcohol, Clinical and Experimental Research: Table of Contents</source>
         <prism:coverDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Mon, 01 Jun 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/acer.70329</guid>
         <title>Drinking Patterns and CT/MRI Feature‐Based Nomogram Models Can More Accurately Predict Acute Alcoholic Pancreatitis Recurrence</title>
         <description>Alcohol, Clinical and Experimental Research, Volume 50, Issue 6, June 2026. </description>
         <dc:description>
We retrospectively collected the drinking patterns and CT/MRI features of 152 patients with initial acute alcoholic pancreatitis (AAP), identified their independent risk factors by logistic analysis, and developed a nomogram model. Integrating these factors into the nomogram resulted in an AUC of 0.924 (95% CI 0.871–0.977) in the training set and 0.843 (95% CI 0.714–0.972) in the independent test set. The clinical model alone achieved AUCs of 0.799 and 0.800, and the imaging model achieved AUCs of 0.827 and 0.686, respectively. The model serves as an effective tool for clinical prediction of AAP and helps clinicians in developing personalized prevention and treatment strategies.

ABSTRACT

Background
To develop and test a nomogram model based on drinking patterns and computed tomography and magnetic resonance imaging (CT/MRI) characteristics for recurrence of acute alcoholic pancreatitis (AAP) following its first onset.


Methods
Patients with initial AAP at the Affiliated Hospital of North Sichuan Medical College were retrospectively enrolled and categorized them into recurrence and non‐recurrence groups. They were randomly assigned in a 7:3 ratio to form training and independent test sets, and their clinical and imaging data were collected and analyzed. Nomogram models were established to predict the recurrence of AAP.


Results
Among 152 cases of initial AAP, 37 cases were recurrent and 115 were non‐recurrent, with a mean (SD) age of 43.84 ± 10.28 years and 91.45% male participants. In the training set, 26 cases were recurrent and 80 were non‐recurrent; in the independent test set, 11 cases were recurrent and 35 were non‐recurrent. Multivariable logistic regression analysis showed that hyperlipidemia, pre‐onset alcohol consumption, alcohol cessation, the Bedside Index for Severity in AP (BISAP) score, extrapancreatic inflammation on CT/MRI (EPIC/EPIM) score, and CT/MRI severity index (CTSI/MRSI) score were independent predictors of recurrence after initial AAP onset. Integrating these factors into a nomogram prediction model resulted in the area under the curve (AUC), sensitivity, and specificity values of 0.924 (95% CI 0.871–0.977), 0.885, and 0.838 for the training set and 0.843 (95% CI 0.714–0.972), 0.727, and 0.857 for the independent test set. The clinical model alone and the imaging model achieved AUCs of 0.799 (95% CI 0.703–0.896) and 0.827 (95% CI 0.742–0.912) in the training set and 0.800 (95% CI 0.646–0.954) and 0.686 (95% CI 0.492–0.880) in the independent test set, respectively.


Conclusions
Nomogram models based on drinking patterns and CT/MRI characteristics can more accurately predict AAP recurrence. The model serves as an effective tool for clinical prediction of AAP and helps clinicians in developing personalized prevention and treatment strategies.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/05a686e0-fa42-47f6-992a-ee43b5cd2a54/acer70329-toc-0001-m.png"
     alt="Drinking Patterns and CT/MRI Feature-Based Nomogram Models Can More Accurately Predict Acute Alcoholic Pancreatitis Recurrence"/&gt;
&lt;p&gt;We retrospectively collected the drinking patterns and CT/MRI features of 152 patients with initial acute alcoholic pancreatitis (AAP), identified their independent risk factors by logistic analysis, and developed a nomogram model. Integrating these factors into the nomogram resulted in an AUC of 0.924 (95% CI 0.871–0.977) in the training set and 0.843 (95% CI 0.714–0.972) in the independent test set. The clinical model alone achieved AUCs of 0.799 and 0.800, and the imaging model achieved AUCs of 0.827 and 0.686, respectively. The model serves as an effective tool for clinical prediction of AAP and helps clinicians in developing personalized prevention and treatment strategies.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;To develop and test a nomogram model based on drinking patterns and computed tomography and magnetic resonance imaging (CT/MRI) characteristics for recurrence of acute alcoholic pancreatitis (AAP) following its first onset.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Patients with initial AAP at the Affiliated Hospital of North Sichuan Medical College were retrospectively enrolled and categorized them into recurrence and non-recurrence groups. They were randomly assigned in a 7:3 ratio to form training and independent test sets, and their clinical and imaging data were collected and analyzed. Nomogram models were established to predict the recurrence of AAP.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Among 152 cases of initial AAP, 37 cases were recurrent and 115 were non-recurrent, with a mean (SD) age of 43.84 ± 10.28 years and 91.45% male participants. In the training set, 26 cases were recurrent and 80 were non-recurrent; in the independent test set, 11 cases were recurrent and 35 were non-recurrent. Multivariable logistic regression analysis showed that hyperlipidemia, pre-onset alcohol consumption, alcohol cessation, the Bedside Index for Severity in AP (BISAP) score, extrapancreatic inflammation on CT/MRI (EPIC/EPIM) score, and CT/MRI severity index (CTSI/MRSI) score were independent predictors of recurrence after initial AAP onset. Integrating these factors into a nomogram prediction model resulted in the area under the curve (AUC), sensitivity, and specificity values of 0.924 (95% CI 0.871–0.977), 0.885, and 0.838 for the training set and 0.843 (95% CI 0.714–0.972), 0.727, and 0.857 for the independent test set. The clinical model alone and the imaging model achieved AUCs of 0.799 (95% CI 0.703–0.896) and 0.827 (95% CI 0.742–0.912) in the training set and 0.800 (95% CI 0.646–0.954) and 0.686 (95% CI 0.492–0.880) in the independent test set, respectively.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Nomogram models based on drinking patterns and CT/MRI characteristics can more accurately predict AAP recurrence. The model serves as an effective tool for clinical prediction of AAP and helps clinicians in developing personalized prevention and treatment strategies.&lt;/p&gt;</content:encoded>
         <dc:creator>
Xin Yue Zhong, 
Rong Peng, 
Yan Deng, 
Ting Zhang, 
Chao Hua Tang, 
Meng Ting Zhou, 
Yi Fan Ji, 
Xing Hui Li, 
Bi Fei Li, 
Xiao Ming Zhang
</dc:creator>
         <category>RESEARCH ARTICLE</category>
         <dc:title>Drinking Patterns and CT/MRI Feature‐Based Nomogram Models Can More Accurately Predict Acute Alcoholic Pancreatitis Recurrence</dc:title>
         <dc:identifier>10.1111/acer.70329</dc:identifier>
         <prism:publicationName>Alcohol, Clinical and Experimental Research</prism:publicationName>
         <prism:doi>10.1111/acer.70329</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/acer.70329?af=R</prism:url>
         <prism:section>RESEARCH ARTICLE</prism:section>
         <prism:volume>50</prism:volume>
         <prism:number>6</prism:number>
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