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Primary bile acids (BAs), synthesized from cholesterol in the liver, after their secretion with bile into the intestinal lumen, are transformed by gut microbiota to secondary BAs. As natural detergents, BAs play a key role in the digestion and absorption of lipids and liposoluble vitamins. However, they have also been recognized as important signaling molecules involved in numerous metabolic processes. The close bidirectional interactions between BAs and gut microbiota occur since BAs influence microbiota composition, whereas microbiota determines BA metabolism. In particular, it is well established that BAs modulate Clostridioides difficile life cycle in vivo. C. difficile is a cause of common nosocomial infections that have become a growing concern. The aim of this review is to summarize the current knowledge regarding the impact of BAs on the pathogenesis, prevention, and treatment of C. difficile infection.

Background: This SRMA reviewed and assessed the changes in the severity of disorders of gut‐brain interaction (DGBI) symptoms during the COVID‐19 pandemic, and evaluated factors associated with symptom severity changes. Methods: Electronic databases were searched until February 2024, for articles reporting on changes in symptom severity in DGBI patients during the COVID‐19 pandemic. The proportion of DGBI patients who reported a change in their symptom severity were pooled using a random‐effects model, and subgroup analyses were conducted to assess the effect of socio‐cultural modifiers on symptom severity in DGBI. Key Results: Twelve studies including 3610 DGBI patients found that 31.4% (95% CI, 15.9–52.5) of DGBI patients experienced symptom deterioration, while 24.3% (95% CI, 10.2–47.5) experienced improvement. Countries with high gross domestic product (GDP) had a 43.5% (95% CI, 16.3–75.2) likelihood of symptom deterioration, compared to 9.2% (95% CI, 1.4–42.2) in lower GDP countries. Similarly, countries with low COVID fatality rates had a 60.1% (95% CI, 19.7–90.3) likelihood of symptom deterioration, compared to 18.3% (95% CI, 7.8–36.9) in higher fatality rate countries. Countries with lenient COVID policies had a 58.4% (95% CI, 14.1–92.3) likelihood of symptom deterioration, compared to 19% (95% CI, 8.2–38.1) in countries with stricter policies. Patients in high vaccine hesitancy countries had a 51.4% (95% CI, 19.5–82.2) likelihood of symptom deterioration, compared to 10.6% (95% CI, 2.7–33.4) in low vaccine hesitancy countries. Conclusions & Inferences: This meta‐analysis reveals that a significantly higher proportion of DGBI patients experienced deterioration of symptoms during the COVID‐19 pandemic. Various sociocultural, economic and environmental factors potentially modify the effects of the COVID‐19 pandemic on DGBI. [ABSTRACT FROM AUTHOR]

Background and Aims Methods Key Results Conclusions and Inferences The endocannabinoid (eCB) system includes ligands (anandamide and 2‐arachidonoyl glycerol, 2‐AG), receptors and catabolizing enzymes (fatty acid amide hydrolase, FAAH and monoacylglycerol lipase) expressed in both the brain and gut. We investigated whether the FAAH inhibitor, URB597, influenced visceral pain to colorectal distension (CRD) in an acute stress‐related model of visceral hypersensitivity induced by the selective corticotropin‐releasing factor receptor subtype 1 (CRF1) agonist, cortagine.Male Sprague–Dawley rats were injected subcutaneously (SC) with URB597 (3 mg/kg) or vehicle and 2 h later, intraperitoneally with cortagine (10 μg/kg) or vehicle. The visceromotor responses (VMR) were assessed to a first CRD (baseline) before injections, and to a second CRD 15 min after the last treatment. Brain, jejunum, and proximal colon were collected from treated and naïve rats for levels quantification of three fatty acid amides (FAAs) [anandamide (arachidonyl‐ethanolamide, AEA), oleoyl‐ethanolamide (OEA) and palmitoyl‐ethanolamide (PEA)], and 2‐AG. In separate animals, defecation/diarrhea were monitored after URB597 and cortagine.URB597 inhibited cortagine‐induced increased VMR at 40 mmHg (89.0 ± 14.8% vs. 132.5 ± 15.6% for vehicle SC, p < 0.05) and 60 mmHg (107.5 ± 16.1% vs. 176.9 ± 24.4% for vehicle SC, p < 0.001) while not influencing basal VMR. In URB597 plus cortagine group, FAAs levels increased in the brain and intestinal tissue while 2‐AG did not change. URB597 did not modify cortagine‐induced defecation/diarrhea versus vehicle.URB597 shows efficacy to elevate brain and intestinal FAAs and to counteract the colonic hypersensitivity induced by peripheral activation of CRF1 signaling supporting a potential strategy of FAAH inhibitors to alleviate stress‐related visceral hypersensitivity. [ABSTRACT FROM AUTHOR]

Background: Disorders of gut–brain interaction (DGBI) are characterized by debilitating symptoms not explained by structural or biochemical abnormalities. While functional conditions present with complex, likely heterogeneous pathophysiology, we aimed to investigate if proxy measures of sociocultural and environmental factors are associated with the prevalence of various DGBI in populations across the world. Method s : We performed an ecological study utilizing peer‐reviewed published datasets reporting for 26 countries prevalence rates of DGBI (Rome Foundation Global Epidemiology Study, RFGES), with six independent variables: Helicobacter pylori prevalence and household size as proxy measures for orofecal infections, gross domestic product per capita (GDP), and median age as a proxy measures for socioeconomic development, density of fast food outlets (FFO) per 100,000 population as proxy measure for processed food exposure, and suicide mortality rate per 100,000 people, and world happiness scores were used as a proxy for psychological stress. The data were retrieved from publicly accessible datasets (United Nations, CIA World Factbook, World Bank, World Happiness Report, commercial/financial reports of a global FFO chain). We used linear regression to assess variables in univariate and multivariate analysis and report standardized β coefficients with 95% confidence intervals (CI). Key Results: The regression model revealed that the overall prevalence of DGBI was inversely associated with both GDP per capita (β = −0.57, 95% CI: −0.92, −0.22, p = 0.002) and happiness scores (β = −0.433 95% CI: 0.821, −0.065, p = 0.023), while being positively associated with H. pylori prevalence (β = 0.40, 95% CI: 0.008, 0.81, p = 0.046). The prevalence of functional constipation (FC) was also inversely associated with GDP per capita (β = −0.50, 95% CI: −0.86, −0.13, p = 0.01) and happiness scores (β = −0.497, 95% CI: −0.863, −0.132, p = 0.01), while being positively associated with H. pylori prevalence (β = 0.53, 95% CI: 0.16, 0.91, p = 0.007). The Multivariate model analysis revealed that combining the factors of H. pylori prevalence, suicide rate, household size and happiness scores showed statistically significant association with FC (p = 0.039). Household size (β = −0.43, 95% CI: −0.82, 0.038, p = 0.033) and suicide rates (β = 0.55, 95% CI: 0.19, 0.90, p = 0.004) were statistically significantly associated with functional diarrhea. Irritable bowel syndrome (IBS) was associated with GDP per capita (β = −0.40, 95% CI: −0.79, −0.014, p = 0.043) and happiness scores (β = −0.390, 95% CI: −0.778, −0.003, p = 0.049). Conclusions & Inferences: Utilizing publicly available data, the prevalence of DGBI across diverse countries is linked to various socio‐cultural and environmental factors. Collectively, the data suggests that the prevalence of DGBI is increased in less prosperous regions of the world. [ABSTRACT FROM AUTHOR]

Background: Fibroblast growth factor 21 (FGF21) is a stress-inducible hormone that regulates nutrient and metabolic homeostasis. Inflammatory state is one of the stimulators of FGF21 secretion. The aim of the study was to assess correlations between serum FGF21 level and inflammatory markers as well as nutritional status indicators in patients with inflammatory bowel disease (IBD). Methods: Fasting serum FGF21 level was measured using ELISA test in 105 IBD patients and 17 healthy controls. There were 31 subjects with active ulcerative colitis (UC), 16 with inactive UC, 36 with active Crohn's disease (CD), and 22 with inactive CD. Clinical and endoscopic activity of IBD was evaluated based on validated scales and indices. Fecal calprotectin, serum CRP, and selected parameters of nutritional status were tested in all patients. Results: Serum FGF21 level was characterized by fluctuations depending on the IBD activity. FGF21 level was significantly higher in both active UC and CD compared to inactive phases of the diseases and to the controls. A correlation between FGF21 and fecal calprotectin levels was also found in UC and CD. Additionally, in CD, FGF21 level positively correlated with CRP level. In both UC and CD, a negative correlation was noted between FGF21 level and nutritional status parameters including cholesterol, protein, albumin levels, and BMI. Conclusion: The intensity of intestinal inflammation is related to FGF21 level, which correlates negatively with nutritional status indicators in IBD. The disturbances in FGF21 secretion may contribute to the multifactorial pathogenesis of malnutrition and weight loss in IBD patients. [ABSTRACT FROM AUTHOR]

Background: The aim of the study was to assess sex‐ and gender‐related differences in the epidemiology and impact of disorders of gut–brain interaction (DGBI) in Poland. Methods: Data used for the current analysis were derived from the Polish population sample of 2057 subjects (1030 F, 1027 M) collected via the Internet survey that included the Rome IV diagnostic questionnaire and 80 supplementary questions. Key Results: The overall prevalence of DGBI in Poland was 46.0% (51.7% in women and 40.3% in men, p < 0.001). Comparing women versus men, esophageal disorders were observed in 6.3% vs. 6.0%, respectively (p > 0.05), gastroduodenal disorders in 14.0% vs. 7.8% (p < 0.001), bowel disorders in 44.3% vs. 33.9% (p < 0.001), and anorectal disorders in 9.9% vs. 7.7% (p > 0.05). The six most common DGBI included functional constipation 14.2%, functional dyspepsia 8.3%, proctalgia fugax 6.6%, functional bloating 4.8%, functional diarrhea 4.5%, and irritable bowel syndrome (IBS) 4.4%. All these disorders, except for functional diarrhea, were more common in women. The DGBI overlap was significantly higher in women than in men (16.7% vs. 11.2%, p < 0.001). A higher number of overlapping DGBI correlated positively with IBS severity, higher level of somatization, anxiety and depression, poorer quality of life (QoL), and increased healthcare utilization. Conclusions and Inferences: This is the first comprehensive report on significant sex/gender‐related differences in the prevalence and burden of DGBI in Poland. The revealed differences between women and men with DGBI in the clinical profile, psychosocial variables, and healthcare utilization may have important diagnostic and therapeutic implications. [ABSTRACT FROM AUTHOR]

Recently, the concept of the brain-gut-microbiota (BGM) axis disturbances in the pathogenesis of Alzheimer's disease (AD) has been receiving growing attention. At the same time, accumulating data revealing complex interplay between bile acids (BAs), gut microbiota, and host metabolism have shed new light on a potential impact of BAs on the BGM axis. The crosstalk between BAs and gut microbiota is based on reciprocal interactions since microbiota determines BA metabolism, while BAs affect gut microbiota composition. Secondary BAs as microbe-derived neuroactive molecules may affect each of three main routes through which interactions within the BGM axis occur including neural, immune, and neuroendocrine pathways. BAs participate in the regulation of multiple gut-derived molecule release since their receptors are expressed on various cells. The presence of BAs and their receptors in the brain implies a direct effect of BAs on the regulation of neurological functions. Experimental and clinical data confirm that disturbances in BA signaling are present in the course of AD. Disturbed ratio of primary to secondary BAs as well as alterations in BA concertation in serum and brain samples have been reported. An age-related shift in the gut microbiota composition associated with its decreased diversity and stability observed in AD patients may significantly affect BA metabolism and signaling. Given recent evidence on BA neuroprotective and anti-inflammatory effects, new therapeutic targets have been explored including gut microbiota modulation by probiotics and dietary interventions, ursodeoxycholic acid supplementation, and use of BA receptor agonists. [ABSTRACT FROM AUTHOR]

Introduction: Chronic inflammatory demyelinating polyneuropathy (CIDP) is a complex autoimmune disease caused by dysregulated response to not fully recognized antigens. Some association between CIDP and inflammatory bowel disease (IBD) has been reported, but the exact pathophysiological links of these disorders are not well understood. Aim of the Study: To evaluate fecal calprotectin as a biomarker of gut inflammation in CIDP patients without IBD. Methods: Fifteen patients with CIDP and 15 healthy controls were included in the study. The CIDP diagnosis was based on the EFNS/PNS criteria. The occurrence of bowel symptoms was assessed based on a questionnaire. The quantitative evaluation of fecal calprotectin level was performed by the ELISA test. Results: The fecal calprotectin level (μg/g) expressed as median along with the lower and upper quartiles [25Q–75Q] was significantly higher in CIDP patients compared to the controls: 26.6 [17.5–109.0] vs 15.6 [7.1–24.1], p = 0.0066. Abnormal fecal calprotectin level (>50 μg/g) was found in 33% of all CIDP patients and in none of the control subjects. The patients with abnormal fecal calprotectin level did not differ from the rest of the study group regarding the neurological status. The most common bowel symptoms reported by CIDP patients included constipation (33%), feeling of incomplete evacuation (33%), bloating (27%), and alternating bowel movement pattern (27%). Conclusion: In one-third of CIDP patients the signs of gut immune system activation have been observed. This finding may be associated with CIDP pathogenesis and induction of autoimmune response as well as concomitant dysautonomia with gastrointestinal symptoms. [ABSTRACT FROM AUTHOR]

Background: Gastroparesis is a condition characterized by epigastric symptoms and delayed gastric emptying (GE) rate in the absence of any mechanical obstruction. The condition is challenging in clinical practice by the lack of guidance concerning diagnosis and management of gastroparesis. Methods: A Delphi consensus was undertaken by 40 experts from 19 European countries who conducted a literature summary and voting process on 89 statements. Quality of evidence was evaluated using grading of recommendations assessment, development, and evaluation criteria. Consensus (defined as ≥80% agreement) was reached for 25 statements. Results: The European consensus defined gastroparesis as the presence of symptoms associated with delayed GE in the absence of mechanical obstruction. Nausea and vomiting were identified as cardinal symptoms, with often coexisting postprandial distress syndrome symptoms of dyspepsia. The true epidemiology of gastroparesis is not known in detail, but diabetes, gastric surgery, certain neurological and connective tissue diseases, and the use of certain drugs recognized as risk factors. While the panel agreed that severely impaired gastric motor function is present in these patients, there was no consensus on underlying pathophysiology. The panel agreed that an upper endoscopy and a GE test are required for diagnosis. Only dietary therapy, dopamine‐2 antagonists and 5‐HT4 receptor agonists were considered appropriate therapies, in addition to nutritional support in case of severe weight loss. No consensus was reached on the use of proton pump inhibitors, other classes of antiemetics or prokinetics, neuromodulators, complimentary, psychological, or more invasive therapies. Finally, there was consensus that gastroparesis adversely impacts on quality of life and healthcare costs and that the long‐term prognosis of gastroparesis depends on the cause. Conclusions and Inferences: A multinational group of European experts summarized the current state of consensus on definition, symptom characteristics, pathophysiology, diagnosis, and management of gastroparesis. Key Summary: Current knowledge The epidemiology of gastroparesis is not well known.Diagnosis and treatment of gastroparesis is challenging due to uncertainties in definition and optimal therapeutic approach. What is new here A Delphi panel consisting of 40 experts from 19 European countries established the level of consensus on 89 statements regarding gastroparesis.The statements reaching consensus serve to guide clinicians in recognizing, diagnosing and treating gastroparesis in clinical practice.The statements without consensus identify areas in need of future research. [ABSTRACT FROM AUTHOR]

Background and Aims. Bile acids (BA) play an important role in the modulation of numerous gut functions. Fibroblast growth factor 19 (FGF19) is the ileal hormone regulating BA homeostasis. The aim of the study was to evaluate serum FGF19 level and its correlation with clinical and endoscopic disease activity indices along with inflammatory biomarkers including serum CRP and fecal calprotectin levels in patients with ulcerative colitis (UC). Methods. Fasting serum FGF19 level was measured using ELISA test in 16 patients with active UC (7 F, 9 M), 15 patients with nonactive UC (8 F, 7 M), and 19 healthy controls (11 F, 8 M). The disease activity was assessed based on the clinical and endoscopic evaluations as well as serum CRP and fecal calprotectin level measurement. Results. The median serum FGF19 level was higher in patients with nonactive UC (175.3 pg/ml (108.7-342.3)) than in patients with active UC (114.3 pg/ml (68.9-155.3), p = 0.093). The median FGF19 level in healthy controls amounted to 151.6 pg/ml (90.6-224.2), and there were no statistically significant differences between the patients with active and nonactive UC compared to the healthy controls. An inverse correlation was observed between FGF19 level and abdominal pain intensity (R = – 0.48 , p = 0.007) as well as fecal calprotectin (R = – 0.38 , p = 0.036) and CRP levels (R = – 0.36 , p = 0.045). The serum FGF19 level was not correlated neither with clinical nor endoscopic disease activity indices. Conclusions. The inverse correlations between FGF19 level and abdominal pain as well as inflammatory markers in UC may imply its potential analgesic and anti-inflammatory effects. [ABSTRACT FROM AUTHOR]

Introduction: A growing body of evidence indicates that neuroendocrine interactions may occur at all levels of the brain-gut-microbiota axis, which is directly involved in the pathogenesis of Parkinson's disease (PD). Areas covered: The review presents some current and emerging concepts regarding the organization and functioning of the neuroendocrine system as well as the role of neuroendocrine disturbances in the pathophysiology and symptomatology of PD. The concept of the brain-gut-microbiota triad interactions in the neuroendocrine system and PD is proposed. In PD, dysregulation of the main neuroendocrine axes coordinated by the hypothalamus is accompanied by disruptions at the peripheral level, which involve enteroendocrine cells producing numerous neuropeptides. Moreover, the important role of the gut microbiota as a main coordinator of immune and neuroendocrine interactions is discussed. The potential diagnostic and therapeutic implications in the context of the recent developments in the fields of neuroendocrinology and neurodegeneration are also presented. Expert opinion: Unraveling complex neuroendocrine interactions in the course of PD may provide crucial diagnostic implications and novel therapeutic approaches including the application of gut neuropeptides and gut microbiota modification. [ABSTRACT FROM AUTHOR]

Introduction: Alpha-synucleinopathy constituting a characteristic feature of Parkinson's disease (PD) occurs at all levels of the brain-gut axis including the enteric nervous system (ENS). Lesions in the ENS may be connected with gut inflammation, increased intestinal permeability and dysmotility contributing to the pathogenesis of PD and its gastrointestinal manifestations. Aims: To evaluate fecal calprotectin and zonulin as biomarkers of gut inflammation and intestinal barrier dysfunction in PD patients. Methods: Quantitative evaluation of fecal biomarkers was performed by ELISA tests in 35 PD patients and 20 healthy controls. Additionally, patients filled out a short questionnaire concerning gastrointestinal symptoms. Results: Median fecal calprotectin level (μg/g) was significantly higher in PD patients compared to the controls: 54.5 (29.0–137.9) vs. 9.7 (5.2–23.3), p < 0.0001. Applying age-related reference ranges, the increased fecal calprotectin level was found in 43% of PD patients and in none of the control subjects (p < 0.001). No correlation between fecal calprotectin level and PD duration was observed. No statistically significant difference between the groups regarding zonulin level was found. The most frequent bowel symptoms reported by PD patients included constipation (69% of subjects), feeling of incomplete evacuation (51%), bloating (51%), abdominal pain (20%), and alternating bowel movement pattern (17%). Conclusion: The evaluation of fecal calprotectin level may be a useful tool to detect the signs of gut immune system activation present in a remarkable number of PD patients, also in the early stage of the disease. Calprotectin may constitute a critical link between amyloid formation and neuroinflammatory cascades serving as a prospective diagnostic and therapeutic target. [ABSTRACT FROM AUTHOR]

Disturbances along the brain-gut-microbiota axis may significantly contribute to the pathogenesis of neurodegenerative disorders. Alzheimer's disease (AD) is the most frequent cause of dementia characterized by a progressive decline in cognitive function associated with the formation of amyloid beta (Aß) plaques and neurofibrillary tangles. Alterations in the gut microbiota composition induce increased permeability of the gut barrier and immune activation leading to systemic inflammation, which in turn may impair the blood-brain barrier and promote neuroinflammation, neural injury, and ultimately neurodegeneration. Recently, Aß has also been recognized as an antimicrobial peptide participating in the innate immune response. However, in the dysregulated state, Aß may reveal harmful properties. Importantly, bacterial amyloids through molecular mimicry may elicit cross-seeding of misfolding and induce microglial priming. The Aß seeding and propagation may occur at different levels of the brain-gut-microbiota axis. The potential mechanisms of amyloid spreading include neuron-to-neuron or distal neuron spreading, direct blood-brain barrier crossing or via other cells as astrocytes, fibroblasts, microglia, and immune system cells. A growing body of experimental and clinical data confirms a key role of gut dysbiosis and gut microbiota-host interactions in neurodegeneration. The convergence of gut-derived inflammatory response together with aging and poor diet in the elderly contribute to the pathogenesis of AD. Modification of the gut microbiota composition by food-based therapy or by probiotic supplementation may create new preventive and therapeutic options in AD. [ABSTRACT FROM AUTHOR]

Aim. To assess the association of six polymorphisms in serotonin-related genes with depressive or anxiety disorders in patients with irritable bowel syndrome (IBS). Methods. The lifetime prevalence of depressive and anxiety disorders was assessed in 95 IBS patients (85% women) using the Munich version of the Composite International Diagnostic Interview (CIDI). IBS was diagnosed according to the Rome III criteria. SCL6A4 HTTLPR polymorphism (rs4795541) was determined using PCR-based method. Single-nucleotide polymorphisms in HTR1A (rs6295), HTR2A (rs6313 and rs6311), HTR2C (rs6318), and TPH1 (rs1800532) were detected by minisequencing method. Results. IBS patients with depressive disorders were characterized by higher frequency of 5-HTTLPR L allele in comparison to IBS patients with anxiety disorders. The lower frequency of 1438 A allele in HTR2A was found in IBS patients with depressive disorders in comparison to IBS patients without mental disorders. The lower G allele frequency in HTR2C rs6318 polymorphism among IBS patients with anxiety disorders was also observed. Conclusions. Our results provide further evidence for the involvement of SLC6A4 rs4795541 and HTR2A rs6311 polymorphisms in the pathophysiology of depressive disorders in IBS patients. The new findings indicate that HTR2C rs6318 polymorphism may be associated with the susceptibility to anxiety disorders in IBS patients. [ABSTRACT FROM AUTHOR]

Diagnosis of celiac disease in adults is currently based on serologic tests in combination with histopathological assessment of small intestinal biopsy specimens. High titers of celiac-specific antibodies in immunocompetent patients with villous atrophy in a good quality biopsy sample allow us to state a confident diagnosis. The relief of symptoms and histological improvement after embarking on a gluten free diet further support the initial diagnosis. However, in some cases, these conditions are not fulfilled, which requires a critical evaluation of laboratory and histopathology results and a consideration of other potential causes for the observed pathologies. To avoid diagnostic uncertainty, both biopsy and laboratory testing should be performed on a diet containing gluten. Immune deficiency, cross reaction of antibodies and possibilities of seronegative or latent celiac disease should be considered while evaluating serology Results. Uneven distribution and variable intensity of histopathological changes in the small intestine along with multiple disorders presenting a similar specimen image may lead to invalid biopsy Results. Additional laboratory testing and careful examination of a patient's history may deliver important data for a differential diagnosis and a more specific biopsy evaluation. Persistence or recurrence of symptoms, despite the ongoing treatment, requires a revision of the initial diagnosis, an evaluation of the gluten free diet and a search for concurrent disorders or complications. [ABSTRACT FROM AUTHOR]

Background. Pancreatolithiasis occurs in less than 1% of the general population and is mainly recognized in patients with chronic pancreatitis. Selection of the appropriate treatment method depends on the location, size and number of stones. Objectives. The aim of the study was to analyze data concerning patients with pancreatic duct stones who were hospitalized at Wroclaw Medical University's Department of Gastroenterology and Hepatology from 2010 to 2014. Material and methods. The study presents data on 16 patients with pancreatic duct stones, who constituted 7% of all 228 patients with chronic pancreatitis hospitalized at the Department in the study period. The clinical data were compared with findings reported in the literature. Results. Epigastric pain was the most common symptom reported by patients with pancreatolithiasis. The sensitivity of imaging tests in the diagnosis of pancreatic duct stones was as follows: abdominal ultrasonography - 31%, endoscopic retrograde cholangiopancreatography (ERCP) - 67%, computed tomography - 71%, endoscopic ultrasonography - 73%. In 6 patients ERCP and sphincterotomy were performed along with stenting of the main pancreatic duct. Three other subjects were qualified for surgical treatment. In 7 selected patients conservative treatment and further observation were applied. Conclusions. Endoscopic ultrasonography is characterized by high sensitivity in the diagnosis of pancreatic duct stones. ERCP is the first-line treatment in the case of a small number of stones with sizes below 5 mm located in the head or body of the pancreas. In the case of stones with sizes ≥ 5 mm, extracorporeal shock wave lithotripsy should be performed before endoscopic drainage during ERCP. Stenosis of the main pancreatic duct is the key risk factor for the recurrence of pancreatolithiasis. [ABSTRACT FROM AUTHOR]

Additionally, numerous microbial metabolites and endotoxins from the gut crossing the gut-blood barrier can impact the lungs and vice versa lung inflammation can affect the gut microbiota (Enaud et al. [5]). Unravelling the association between the gut microbiota alterations in COVID-19 patients and the disease course and severity may result in a new therapeutic avenue based on the gut microbiota modification with the use of pre- and probiotics. Dear Editor, I have read with great interest the latest review paper on the potential benefits of probiotic use during the pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (Bottari et al. [1]). [Extracted from the article]

Sex and gender effects in irritable bowel syndrome (IBS) have been reported in epidemiological, physiological, and clinical treatment studies. The potential role of gonadal hormones is discussed based on the female predominance in IBS and the correlation between lBS symptoms and hormonal status. Several different models have been proposed to examine the role of sex hormones in gastrointestinal (GI) function, including changes in GI symptoms during the menstrual cycle and differences in symptom expression in pre- and post-menopausal women as well as changes during pregnancy, hormonal treatment, or after ovariectomy. Gonadal hormones, in particular estrogens, can significantly modulate various clinical manifestations of IBS, including alterations in GI motility and visceral hypersensitivity. Additionally, sex differences in the stress response of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system are considered to be contributing factors in the pathogenesis of functional bowel disorders, The modulatory effects of estrogens on visceral pain may result from interactions with numerous neurotransmitters at different levels of the brain-gut axis, with a pivotal role of estrogens' interactions with the serotonin and corticotropin-releasing factor (CRF) signaling systems. Estrogens can also modulate neuroimmune interactions triggered by stress via the brain-gut axis. Sex differences in the biological actions, pharmacokinetics, and treatment efficacy of serotonergic medications clearly suggest sex differences in pain pathways that have to be taken into consideration in therapeutic interventions. [ABSTRACT FROM AUTHOR]