Composition of gut microbiota and its correlations with neurological, intestinal, cardiovascular and metabolic diseases.

The intestinal microbiota is a microenvironment that has been the subject of studies for several decades. Over time, it has been reconsidered as a possible cofactor of multiple acute and chronic human diseases. In fact, alterations of the intestinal bacterial flora have been found in various neurological diseases. There are three modes of interaction between the intestinal microbiota and the gut-brain-axis: chemical signals, neural pathways and immune system. Even at the gastrointestinal level, the gut microbiota plays certainly an important role in the etiopathogenesis of chronic intestinal inflammatory diseases but also in irritable bowel syndrome. An important correlation has also been demonstrated with non-alcoholic fatty liver disease, as well as in other metabolic, cardiovascular and oncological diseases. Bacteria, viruses, fungi and various microorganisms that normally reside in our intestines can also be called into question as protective factors against these diseases. All this evidence leads researchers to consider the gut microbiota as a key element in the determination of aforementioned diseases. Therefore, it would be foreseeable in the future to associate the use of probiotics with the therapies used in the treatment of all these diseases. In this review we have condensed the main current knowledge regarding the link between the most frequent diseases and the gut microbiota.

Inflammatory Bowel Disease Therapies and Acute Liver Injury.

Drug-induced liver disease (DILI) represents one of the main problems in the therapeutic field. There are several non-modifiable risk factors, such as age and sex, and all drugs can cause hepatotoxicity of varying degrees, including those for the treatment of inflammatory bowel diseases (IBD). The aim of this review is to illustrate the adverse effects on the liver of the various drugs used in the treatment of IBD, highlighting which drugs are safest to use based on current knowledge. The mechanism by which drugs cause hepatotoxicity is not fully understood. A possible cause is represented by the formation of toxic metabolites, which in some patients may be increased due to alterations in the enzymatic apparatus involved in drug metabolism. Various studies have shown that the drugs that can most frequently cause hepatotoxicity are immunosuppressants, while mesalazine and biological drugs are, for the most part, less associated with such complications. Therefore, it is possible to assume that in the future, biological therapies could become the first line for the treatment of IBD.

Non-alcoholic fatty liver disease: correlation with hyperuricemia in a European Mediterranean population.

OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) are two pathologies that intersect each other. It was found that there is an association between MetS/NAFLD and hyperuricemia. The aim of our study was to demonstrate this association in a European Mediterranean population. METHODS: We compared 236 patients with NAFLD to 218 patients without NAFLD. We assessed laboratory metabolic parameters (serum uric acid - SUA, fasting glucose, triglycerides, total cholesterol, etc.) and the presence or absence of MetS in a retrospective, cross-sectional, case-control manner. RESULTS: Analysis of the two main variables in study showed a moderate direct correlation (p< 0.01; Pearson coefficient 0.443) between SUA and NAFLD. Evaluation for SUA quartiles showed a decreased risk of NAFLD for the first and second quartiles (OR Q1 = 0.20; OR Q2 = 0.59), but increased for the third and fourth quartiles (OR Q3 = 2.22; OR Q4 = 6.97). In females, the risk of NAFLD was less compared to males for the first three quartiles of SUA, but it was more than double for the fourth quartile (OR Q1 0.21 vs 0.16; OR Q2 0.82 vs 0.45; OR Q3 2.50 vs 2.26; OR Q4 4.50 vs 9.83). In the NAFLD group, hyperuricemia was significantly correlated with sex, obesity, hypertension, and with the number of components of the MetS. In the Control group, SUA directly correlated with age, diabetes, and ALT, but not with obesity. CONCLUSION: We have found a significant correlation between NAFLD and hyperuricemia. The higher SUA levels accompanied the risk of NAFLD.

Triglycerides to high-density lipoprotein cholesterol ratio for diagnosing nonalcoholic fatty liver disease.

BACKGROUND: Nonalcoholic Fatty Liver Disease (NAFLD) is a widespread disease in the western world. It can develop into more serious pathological conditions (i.e. liver cirrhosis). Therefore, it is important to diagnose it in order to prevent this evolution. For diagnosis it is possible to use both imaging methods and biomarkers, such as the Triglycerides To High-Density Lipoprotein Cholesterol Ratio (TG/HDL-C). Aim of our study is to determine whether TG/HDL-C ratio is significantly associated with NAFLD and Metabolic Syndrome (MetS). METHODS: We recruited 231 patients, 131 with and 100 without NAFLD. The Body Mass Index had been calculated and different laboratory parameters had been obtained. TG/HDL-C ratio was calculated for each. RESULTS: In our sample HDL-C was not significantly reduced in NAFLD group (P=0.49), but higher TG and TG/HDL-C ratio were significantly associated with NAFLD: in both P<0.001. According to receiver operating characteristic curve, the best cut-off of TG/HDL-C in NAFLD population was 1.64 (area under the curve [AUC] 0.675 [95% CI 0.604-0.746], P<0.001). TG/HDL-C higher ratio was significantly associated with MetS (P<0.001). The best cut-off of TG/HDL-C in patients with MetS was 2.48 (AUC 0.871 [95% CI 0.808-0.935], P<0.001). CONCLUSIONS: We demonstrated that higher TG/HDL-C ratio is associated with NAFLD and MetS. Though nowadays TG/HDL-C ratio is not a criteria for NAFLD diagnosis, we believe that in the future it could be used as a reliable non-invasive marker in routine diagnostics of NAFLD.

Lactose intolerance: An update on its pathogenesis, diagnosis, and treatment.

Lactose intolerance has a high prevalence worldwide, ranging between 57% and 65%. It is caused by a reduction or loss of the activity of the intestinal enzyme lactase-phlorizin hydrolase, responsible for the digestion of lactose. This alteration determines an increased osmotic load in the small intestine and the fermentation of lactose by the bacterial flora, which leads to a high production of short-chain fatty acids and gas. This is followed by the onset of abdominal pain, diarrhea, and flatulence. In addition to these problems, it was found that subjects with lactose intolerance have an increased risk of developing various extra-intestinal diseases, including cancers. The diagnosis is essential to undertake an adequate treatment and, for this purpose, different methods have been tested. These include genetic test, hydrogen breath test (HBT), quick lactase test, and lactose tolerance test. HBT is the most used method because it is non-invasive, inexpensive, and highly sensitive and specific, as well as easy to perform. In clinical practice, the other methods are mainly used as HBT integration tests. There are also many therapeutic options. An appropriate intervention concerns the dietetic style, such as the consumption of lactose-free foods, but with nutritional characteristics comparable to dairy products. Other valid choices are represented by the use of exogenous enzymes, probiotics, prebiotics, the selection of milk containing specific types of beta-caseins. This review is intended to illustrate the diagnostic methods currently available and the possible therapeutic options for lactose intolerance.

Irritable bowel syndrome and lactose intolerance: the importance of differential diagnosis. A monocentric study.

BACKGROUND: Nowadays irritable bowel syndrome (IBS) and lactose intolerance (LI) are two very frequent diseases. IBS is a functional disorder, while LI is caused by the inability to digest lactose. LI is often incorrectly diagnosed as IBS. The aim of our study is to identify LI patients among IBS patients, so as to set up a correct therapy. METHODS: We enrolled 259 patients with IBS and we compared them to a control group of 108 patients. All patients underwent H2 Breath-Test (HBT) and two questionnaires regarding the symptoms associated with IBS and LI were administered to the intolerant subjects and one questionnaire to IBS patients with no LI. RESULTS: At the HBT, 79.9% (N.=207) of patients with IBS were positive, while in the control group were positive 25.0% (N.=27) of subjects (P<0.001). The questionnaires showed, after a month of therapy, a marked improvement in LI symptoms subjects. In addition, there was also a prevalence of more severe symptoms among subjects with IBS and LI than those with IBS and no LI. CONCLUSIONS: We can affirm that most patients with initial diagnosis of IBS are, instead, lactose intolerant. This diagnosis allows us to undertake an adequate therapy so as to improve symptoms and quality of life. Therefore it is important to include LI in the pathologies with which IBS enters into differential diagnosis.

FIB-4 and APRI scores for predicting severe liver fibrosis in chronic hepatitis HCV patients: a monocentric retrospective study.

AIM OF THE STUDY: Hepatitis C virus (HCV) can cause a chronic liver infection which could then develop into fibrosis, cirrhosis, and hepatocellular carcinoma. Today the diagnosis of liver fibrosis also includes the use of biomarkers. The purpose of our study was to determine the ability of the fibrosis index based on four factors (FIB-4) and aspartate aminotransferase-to-platelet ratio (APRI) to predict the severity of liver fibrosis or cirrhosis. MATERIAL AND METHODS: Medical records of 106 patients with HCV-related liver fibrosis were analyzed. All patients underwent clinical examination, blood tests (complete blood count, total bilirubin, etc.) and transient elastography. FIB-4 and APRI were calculated for each patient. RESULTS: Twenty-six patients (24.52%) had F4 fibrosis, 80 patients (75.48%) had non-F4 fibrosis (F0-F3). There was a statistically significant difference (p < 0.05) between non-F4 fibrosis patients and F4 fibrosis patients in many parameters, including APRI (F4 fibrosis patients had higher values: 2.06 ±3.22 compared to 0.68 ±0.76 of the non-F4 group; p = 0.044) and FIB-4 (F4 fibrosis patients had higher values: 4.84 ±4.14 compared to 2.29 ±2.90 of the non-F4 group; p = 0.006). Receiver operating characteristic (ROC) curve analysis for APRI and FIB-4 revealed that the area under the curve (AUC) of FIB-4 was 0.855 (CI: 0.813-0.936), while the APRI score had an AUC of 0.767 (CI: 0.79-0.932). CONCLUSIONS: In this study, patients with severe fibrosis or cirrhosis were found to have a higher FIB-4 value than APRI in the context of chronic hepatitis C.

Platelet to lymphocyte ratio as a predictive biomarker of liver fibrosis (on elastography) in patients with hepatitis C virus (HCV)-related liver disease.

BACKGROUND: Liver fibrosis is a frequent complication of chronic hepatitis C virus (HCV) infection. Its evaluation is very important for the prognosis of these patients. The aim of this study was to evaluate the possibility of exploiting the platelet to lymphocyte ratio and the neutrophil to lymphocyte ratio as non-invasive predictive markers of liver fibrosis. METHODS: We recruited 120 patients with chronic HCV infection. They were subjected to various clinical investigations to assess the severity of fibrosis. Transient elastography and some serological tests were performed, and the platelet to lymphocyte ratio and the neutrophil to lymphocyte ratio were estimated. RESULTS: Sixty-four patients had F4 fibrosis (defined by elastography) and their platelet to lymphocyte ratio (69.92 ± 26.47) was lower than in patients with non-F4 fibrosis (95.19 ± 48.15) (p = 0.001). The neutrophil to lymphocyte ratio was also estimated, but the difference between the 2 groups of patients was not significant statistically (p = 0.07). CONCLUSION: The platelet to lymphocyte ratio can be used as a predictive biomarker of liver fibrosis, unlike the neutrophil to lymphocyte ratio which is not predictive of this HCV-related chronic hepatitis complication. More studies are needed to validate this hypothesis.

Benign pancreatic hyperenzymemia-Gullo's syndrome: focus on this clinical challenge. A monocentric retrospective study.

BACKGROUND: An abnormal and chronic rise of pancreatic enzymes in the blood is most often due to pancreatic diseases, primarily inflammatory or neoplastic, or to numerous extra-pancreatic pathologies. Benign chronic pancreatic hyperenzymemia was described for the first time - as a separate nosological entity - in 1996 by Lucio Gullo et al. They demonstrated the existence of a benign chronic pancreatic hyperenzymemia in asymptomatic subjects and without clinical implications; however, a follow-up of at least 1-2 years is necessary during which no specific symptomatology or morpho-functional impairment of the pancreas should occur, also evaluated through the aid of instrumental diagnostic investigations such as ultrasonography (US), computed tomography (CT) or magnetic resonance cholangio pancreatography (MRCP). METHODS: This study was performed with the analysis of a group of 43 subjects arrived at the observation of the Gastroenterology Team of Policlinico Hospital G. Rodolico in Catania-Italy which presented a chronic pancreatic hyperenzymemia, in order to establish the actual benignity of this condition over time. RESULTS: During the follow-up, pancreatic alterations and hyperenzymemia were found in 10 patients, while hyperenzymemia was not associated with pancreatic modification in 33 patients. CONCLUSIONS: Because of this enzymatic elevation - often conspicuous and lasting - the patient is often particularly anxious. For the same reason, the patient frequently undergoes very expensive laboratory and instrumental diagnostic methods. Good knowledge of the syndrome makes it possible to manage the event more rationally, also to reduce management costs to a minimum.