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Lactose intolerance is a pathology frequently encountered today. It occurs when the activity of lactase in the intestine is reduced or absent, with consequent failure to digest lactose. The global prevalence of this clinical condition is estimated of about 57% with instrumental methods, while the real prevalence exceeds 65%. The absence of lactase determines both the excessive osmotic load in the small intestine and the fermentation of lactose by the bacterial flora with consequent production of short-chain fatty acids and gas. This latter process is responsible for the onset of symptoms associated with lactose intolerance (abdominal pain, bloating, flatulence, etc.) which arise after the intake of lactose. Several studies have shown an increased risk of developing various pathologies for lactose-intolerant subjects (some types of cancer, osteoporosis, etc.). Therefore, it is essential to diagnose and properly treat this pathology. Various options exist for diagnosing lactose intolerance: Hydrogen Breath Test, genetic test, Quick Lactose Intolerant Test, Lactose Tolerance Test, Gaxilose Test. Like diagnostic methods, there are several options for treating intolerance. In addition to a food restriction, the use of exogenous enzymes and/or probiotic and the selection of milk containing specific types of beta-caseins less correlated to the appearance of gastrointestinal symptoms are very useful. The aim of this review is to illustrate the main and most modern diagnostic and therapeutic choices for lactose intolerance currently available.

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.