
Spices have been used for many decades, and although new and improved culinary spices have been developed, black pepper (Piper nigrum) continues to retain its distinguished title as the “King of spices” due to its particular pungent taste. An alkaloid called piperine is the main component in black pepper that, besides generating the well-known taste, imparts well-documented immunomodulatory, anti-inflammatory, antimicrobial, antioxidant, and even anti-cancer properties; these properties have led to rigorous research on black pepper. Studies conducted on cancer cell lines and in animal models with tumors revealed that piperine might influence tumor development and metastasis via various pathways, some of which are quite common for most types of malignant processes, while others are associated with a specific type of cancer. In this review, we summarized the effect of piperine on various types of cancer and the mechanism by which it acts as a carcinopreventive agent.
Non-celiac gluten sensitivity (NCGS) is a debatable condition that affects less than 6% of children. The absence of specific diagnostic markers and standardized diagnostic procedures make the diagnosis of NCGS challenging, covering patients with different and varied symptoms. Generally, the parents of small and younger children introduce a gluten-free diet (GFD) based on their personal experiences and expectations. Additionally, a “fad component” exists, contributing to the recent rise in the popularity of GFD. Thus, celiac disease (CD) and wheat allergy (WA) must be excluded as these also appear in individuals experiencing symptoms similar to those of NCGS, improving and worsening with gluten withdrawal and consumption, respectively. The role of gluten inducing gastrointestinal symptoms in individuals with self-reported NCGS has been skeptically assessed based on evidence in recent years. However, currently, it is unknown whether a strict GFD is necessary for patients with NCGS. Thus, the placebo-controlled gluten challenge remains the gold standard for a challenging diagnosis like NCGS. The present review evaluates the published studies based largely on the adult population and describes the key elements in diagnosing NCGS and differential diagnosis with CD and WA.
The Mediterranean diet (MD) is considered one of the healthiest dietary patterns due to its rich provision of phytochemicals, antioxidants, vitamins, fiber, polyunsaturated, omega-3, and short-chain fatty acids through a variety of foods. The supply of such nutrients and bioactive components can support gut health and reduce systemic inflammation, with accumulating evidence from several human studies demonstrating the utility of the Mediterranean diet in the prevention of chronic and metabolic diseases. Further studies are needed to explore the role of the Mediterranean diet protecting against such diseases and the related mechanisms, including the interplay between components of the MD and gut microbiota. This brief systematic review specifically explores the recent evidence in humans investigating the link between MD and the human microbiota. Herein, over 50 articles were revised and referenced, after a careful vetting process, to produce this manuscript. Articles were ultimately selected based upon the detail and novelty of their content and contribution to the field.
The reactivation of the Varicella-zoster virus (VZV) is a rare cause of acute gastritis in adults. About 30 cases have been reported in the literature, mostly with immunocompromised patients and mainly after bone marrow transplantation or during the development of malignant hematological diseases. Clinically, it is usually accompanied by cutaneous manifestations. Here, we studied a case of VZV gastritis in a liver transplant (LT) patient. We described the main symptoms, endoscopic findings, histologic changes, and treatment of VZV gastritis. Till now, no case of acute gastritis due to the reactivation of VZV after solid organ transplantation had been reported [2–5]. This was the first reported case of acute gastritis by the reactivation of VZV after LT without cutaneous vesicular eruption. Gastrointestinal symptoms usually develop a week before the onset of fever and cutaneous manifestations. However, in some cases, like this one, vesicular rashes may be absent, making the diagnosis quite challenging. In conclusion, through this case, we suggest including VZV gastritis in the differential diagnosis of gastrointestinal symptoms after transplantation and informing about the response of VZV gastritis to treatment with oral acyclovir.
Infants admitted to Neonatal Intensive Care Units (NICUs) are among the most vulnerable patients in medicine and are at risk for a variety of morbidities, many of which require pharmacologic therapy. Gastroesophageal Reflux Disease (GERD) is a common diagnosis in the NICU patient population and may or may not represent a truly pathologic process. Regardless, pharmacologic therapy is provided to many infants, who are already exposed to an inordinate number of pharmacologic agents, of which most are off label and have an inadequate evidence base to establish either efficacy or safety. Furthermore, as infancy represents a time of dramatic growth and development, many conditions resolve over time, making treatment unnecessary and potentially dangerous. Infants with GERD, especially those born prematurely, exemplify the complexity of attempting pharmacologic therapy with unproven consistent benefit versus “watching and waiting.” The following will present physiology of GERD, gastrointestinal tract anatomy and development as well as options for pharmacologic and non-pharmacologic therapies.
The human intestinal microbiota represents a complex microbial community that plays an essential role in the maintenance of host health. Over the last decade, metagenomic and metabolomic analyses have revealed the influence of intestinal microbial diversity and composition on a range of biological functions in the host. While overall taxonomic composition of the intestinal microbiome is informative, changes in spatial dynamics within the community also have profound biological significance as microbial functions are influenced by neighbouring community members and the microenvironment. Critical gaps remain in our understanding of microbiota structure, co-dependences, resilience and response to antimicrobial agents. In this review, we discuss alternative strategies to deconstruct the microbiome to yield better designed and more clinically effective therapies.
To the Editor,Van Kruiningen has recently suggested that the obstruction of the lymphatic vasculature is the fundamental mechanism in the pathogenesis of Crohn´s disease (CD).[1, 2] Accordingly, CD was described as "segmental elephantiasis of the intestine, and sometimes other body parts."This was supported by impressive images of obstructed lymphatic drainage in patients with CD. [1] Van Kruiningen thus dismissed other putative pathogenic factors, such as dysbiosis of the intestinal microbiota and aberrant mucosal immune responses, as being of secondary importance compared to the lymphatic obstruction.We believe, however, that the pathogenesis of CD is considerably OBM Hepatology and Gastroenterology
Several digestive tract reflexes involving the esophagus and its sphincter muscles have been identified, but to date, no comprehensive review has addressed most of these reflexes. The current review presents the known physiology of different esophageal reflexes in which either the esophagus or its sensory or motor portion of the reflex response is elaborated. The current review comprehensively examines the known and possible mechanisms underlying major esophageal reflexes, highlights the huge gaps in current knowledge and limitations of previous research, helps shed light on the physiology of these reflexes, and suggests how the knowledge gaps can be bridged. In conclusion, this review will be very useful for researchers, clinicians, and academicians around the world.
Anti-TNFα Therapy are used to induce remission and as maintenance therapy in refractory ulcerative colitis (UC) to achieve mucosal healing (MH). However, the time at which mucosal healing should be assessed is unclear. We retrospectively examined the optimal timing for colonoscopy and the criteria to determine the need for the continuation of treatment. We evaluated 44 UC patients that were treated with anti-TNFα Therapy and categorized them into the following groups according to the degree of MH within 12 months: MH and non-MH/NMH, early-MH (EMH, healing within three months), and slow MH/SMH (healing between 4-12 months). We compared the Mayo Endoscopic Subscore (MES) between the MH vs. NMH and SMH vs. NMH groups. The Lichtiger index and blood test results were investigated as predictive factors of MH. MH was defined as an MES of ≤ 1. The MES was significantly lower in the MH group at 3, 6, and 12 months, compared to the NMH group. Significant changes were observed in the platelet counts, the Lichtiger index, the levels of C-reactive protein (lower), and hemoglobin (higher) in the MH group at 3- and 6-months following treatment. However, the only significant difference between the SMH and NMH groups was in the endoscopic findings at 6- or 12-months post-treatment. Colonoscopy should be performed three months after treatment with anti-TNFα Therapy. The treatment should be continued in patients who do not achieve mucosal healing at 3-months, and colonoscopy should be repeated at 6- or 12-months to assess the outcomes.
The human gut is a house to approximately 1,000 different species of bacteria. The bacterial composition of gut microbiota is influenced by several factors, including age, sex, mode of delivery, geographical location, ethnicity, diet, drugs, and administration of prebiotics and/or probiotics. Similarly, human health depends on the composition of gut microbiome, with gut bacteria playing a crucial role in human physiology. For instance, gut microbiota synthesizes vitamins and amino acids, and affects the biotransformation of bile acid. Intestinal microbiota produces short-chain fatty acids (SCFAs) that stimulate intestinal gluconeogenesis, protect the host from diet-induced obesity, and may play a role as an energy substrate. Changes in the composition of gut microbiota, termed dysbiosis, due to, for example, change in the diet or uptake of certain drugs, may result in metabolic diseases, autoimmune and allergic diseases, cancers, and many others. Conversely, dysbiosis can be a consequence of a disease in several cases. This review outlines the current knowledge of the associations between human gut microbiota and human health and diseases.
The combination of broad screening initiatives and development of effective antiviral therapies have led to a revolution in the treatment of hepatitis C virus and has reduced the proportion of patients with the virus who develop a need for liver transplantation in favor of other etiologies, such as alcohol-related liver disease and non-alcoholic steatohepatitis. However, the opioid epidemic and rise in injection drug use in the United States has simultaneously led to otherwise healthy hepatitis C viremic patients dying of overdoses. The sum total of all of these factors has large implications for the transplant community and those patients on the wait list for multiple different organs: lower numbers of people on transplant wait list have active HCV, while HCV is becoming more common in potential liver, kidney and thoracic organ donors. We will review the history of solid organ transplant from donors with hepatitis C as well as to describe the current understanding of the potential use of these grafts in light of the shifting demographics on the waiting list and potential donor population.
The editors of OBM Hepatology and Gastroenterology would like to express their sincere gratitude to the following reviewers for assessing manuscripts in 2020. We greatly appreciate the contribution of expert reviewers, which is crucial to the journal's editorial process. We aim to recognize reviewer contributions through several mechanisms, of which the annual publication of reviewer names is one. Reviewers receive a voucher entitling them to a discount on their next LIDSEN publication and can download a certificate of recognition directly from our submission system. Additionally, reviewers can sign up to the service Publons (https://publons.com) to receive recognition. Of course, in these initiatives we are careful not to compromise reviewer confidentiality. Many reviewers see their work as a voluntary and often unseen part of their role as researchers. We are grateful to the time reviewers donate to our journals and the contribution they make.
Liver transplantation has steadily increased worldwide resulting in a large number of patients on the waiting list. Due to the opioid epidemic in the US, the pool of Hepatitis C seropositive donors increased significantly in recent years. Direct acting antivirals played an instrumental role in making liver transplantation with hepatitis C positive allograft an acceptable option. Although hepatitis C positive liver transplantation to hepatitis C positive recipients is a common practice, there is limited data and agreement on hepatitis C positive liver transplant to hepatitis C negative recipient. Thus, we review the current literature on this topic.
The current study aimed to investigate the effect of a multi-species probiotic (MSP) on cytokine production by human peripheral blood mononuclear cells (PBMCs) and their immune dialogue with HT-29 colon cancer cells. PBMCs were incubated with MSP and their effect on cell proliferation and TNFα, IL-1β, IL-2, IL-6, IFNγ, IL-10, and IL-1ra production was evaluated. The impact of MSP on the cytokine production by PBMC stimulated by HT-29 cells was detected. Not-stimulated PBMC incubated with MSP showed increased production of TNFα, IL-1β, IL-6, and IL-10, but no change in IL-6, IFNγ, and IL-1ra. The stimulatory effect of MSP on lipopolysaccharide (LPS)-promoted PBMC was less pronounced for TNFα, IL-1β, and IFNγ, and the IL-6 production was decreased; phorbol 12-myristate 13- acetate (PMA)-induced IL-2 and IFNγ secretion was inhibited. The addition of MSP to co-cultures of PBMC and HT-29 cancer cells caused a remarkable increase in TNFα and IL-1β secretion, with no change in remaining cytokines. The multi-species probiotics modulated cytokine production by PBMC and affected the cross-talk between PBMC and HT-29 cancer cells. We conclude that probiotics may serve as supplements to the therapeutic strategies applied for the treatment of chronic inflammatory and malignant diseases, especially colorectal cancers.
The literature on the prevalence of spontaneous bacterial peritonitis (SBP) in cirrhotic outpatients who visited the hospital for therapeutic abdominal paracentesis was reviewed in order to assess the usefulness of urinary strips in this setting. The authors reviewed the studies published as peer-reviewed articles on the prevalence of SBP in ambulatory outpatients who visited the hospital for therapeutic paracentesis. Five such studies were available in the literature. It was found that the prevalence of SBP was in the range of 0%–3.5%. In regard to the use of reagent strips, Multistix8 SG is not useful in this setting, while the PeriscreenTM strip is a consistent screening tool for the rapid detection of SBP, particularly in the outpatients’ setting (negative predictive value: 99.4%–100%). In asymptomatic cirrhotic outpatients undergoing a large volume of paracentesis with low risks of infection, the prevalence of spontaneous bacterial peritonitis is low. In this setting, a systematic analysis of ascitic fluid could be avoided. The use of reagent strips may serve as an alternative. Among the reagent strips tested so far, the PeriscreenTM strip has exhibited the highest diagnostic performance with a high negative predictive value.
Metformin has been widely used as a therapeutic drug for hyperglycemia and diabetes. Sleep is a vital and restorative process that is necessary for the proper functioning of organs. Sleep deprivation can induce multi-organ injury, including damage to the pancreas and liver that may result in hyperglycemia and diabetes. We studied the role of metformin in reversing sleep deprivation-induced hyperglycemia and pancreatic and liver dysfunction in mice. Mice were kept in cages and fed water and food ad libitum. Mice were subjected to a cycle of 1-day sleep deprivation (7:00 am-7:00 pm) and 1-day sleep for 30 days (15 cycles). Metformin (100 or 300 mg/kg/day p.o.) was administered from 16th to 30th day. Animals were killed on day 31. The pancreatic function was analyzed by determining the levels of serum glucose, amylase (AMYL), and insulin. Inflammation of the pancreas and liver was investigated by studying the expression of iNOS and NFĸB, and levels of cytokines. Proteins involved in the GLUT2-PPARγ-pAMPK glycolytic pathway in the liver were analyzed to evaluate the anti-hyperglycemic role of metformin. Sleep deprivation increased blood glucose, AMYL, and GPT levels. Furthermore, it resulted in liver and pancreatic inflammation. However, compared with control, sleep deprivation decreased the levels of proteins involved in the GLUT2-PPARγ-pAMPK glycolytic pathway. Sleep deprivation plus metformin decreased blood glucose and GPT levels and pancreatic inflammation. However, the combination increased the levels of proteins involved in the GLUT2-PPARγ-pAMPK glycolytic pathway. In addition, metformin alone increased the levels of AMYL, as well as resulted in islet atrophy, edge irregularities, and disordered pancreatic acinar cells. Metformin attenuates hyperglycemia and reduces pancreatic and liver inflammation in sleep-deprived mice; however, it may cause pancreatic dysfunction.
Chronic constipation and irritable bowel syndrome (IBS) are two of the most common functional gastrointestinal disorders, both of which negatively affect the quality of life of the patients. Since people may have co-existing symptoms of multiple disorders, chronic constipation and IBS with predominant constipation cannot be clearly distinguished. In this cross-sectional study, data were obtained from self-administered questionnaires to assess the prevalence of chronic constipation and IBS, and their overlap, among female undergraduate students in Japan. We also assessed the participants' mental status, physical activity, lifestyle, and dietary intake, each of which can influence chronic constipation and IBS. These parameters were assessed using a Japanese version of the hospital anxiety and depression scale, and an established semi-quantitative questionnaire available for clinical investigation (FFQg).Among the 131 participants, 9.2% had chronic constipation and 18.0% had IBS, while 2 (1.7%) participants had both constipation and IBS. Increased body mass index and higher dietary intake of protein (energy ratio), fat (energy ratio), cholesterol, animal protein (ratio), animal fat (ratio), and meat and eggs, and decreased carbohydrate energy ratio and vegetable fat ratio, were associated with chronic constipation. A state of anxiety tended to be associated with IBS, but in contrast to the results for chronic constipation, the dietary intake of the nutrients and types of food examined were not associated with IBS, except for the "snacks food group". The results suggest that overlap between chronic constipation and IBS was not common, and that these two disorders had different clinical characteristics and backgrounds.
Patients receiving immunosuppressive therapy for inflammatory bowel disease may be susceptible to non-cirrhotic portal hypertension, now referred to as porto-sinusoidal vascular disease. Here we describe a patient treated with long-term azathioprine for Crohn’s disease who developed porto-sinusoidal vascular disease with obliterative portal venopathy without nodular regenerative hyperplasia on histology. Specific signs of portal hypertension were present, including porto-systemic collaterals on imaging. Histopathologic findings of porto-sinusoidal vascular disease support the hypothesis of endothelial cell injury induced by 6-thioguanine secondary to azathioprine use.
Crohn's disease is part of a group of diseases termed inflammatory bowel disease. Guidelines have long advocated the use of steroids for acute flare up and Current goals of treatment include enhancing long-lasting remission, preventing relapse, reducing the need for surgery, preventing complications and slowing disease progression. No cure currently exists for the disease. Traditionally, the clinical approach to treatment has been symptom-based where patients have had to ‘earn’ their next treatment escalation. However, this approach has evolved rapidly in recent times. Now, treat to target strategies, more intensive monitoring with biomarkers, and use of more biological based therapies appear to give much better clinical outcomes. This review compares traditional approaches to more novel ones and provides an insight for future avenues of therapy.