Department of Medical Laboratory Diagnostics, Division of Clinical Chemistry and LaboratoryHaematology, Wroclaw Medical University, ul. Borowska 211A, 50-556 Wroclaw, Poland
Dr. Mariola Śliwińska-Mossoń
Department of Medical Laboratory Diagnostics, Division of Clinical Chemistry and LaboratoryHaematology, Wroclaw Medical University, ul. Borowska 211A, 50-556 Wroclaw, Poland
Diabetes is one of the most common metabolic disorders and emerges secondary to an interaction between genetic, environmental and lifestyle factors. This work provides an overview of the impact of smoking on the development of vascular complications in this condition and also provides an overview of the potential role of smoking in predisposition to diabetes. There are many studies documenting the impact of smoking on health (not focused on patients with diabetes), suggesting that the health exposure in these individuals is at least comparable to that observed in the general population. Distinct studies of smoking in patients with diabetes have unambiguously confirmed an increased prevalence and a higher risk of early death associated with the development of macrovascular complications. Smoking is also associated with premature development of microvascular complications and may contribute to the pathogenesis of type 2 diabetes. It has been shown that smoking is a predictor of the progression of glucose intolerance at both the transition from normoglycaemia to impaired glucose tolerance status and the increased risk of developing diabetes. The mechanisms explaining the relationship between smoking and the development of diabetes are not fully understood, although a number of hypotheses have been put forward. Current evidence indicates that smoking cessation is not only important to prevent macrovascular complications in diabetes, but also has a role in limiting microvascular disease and may also facilitate glycaemic management in this condition.
Lung cancer is the most often diagnosed cancer in the world and the most frequent cause of cancer death. The prognosis for lung cancer is relatively poor and 75% of patients are diagnosed at its advanced stage. The currently used diagnostic tools are not sensitive enough and do not enable diagnosis at the early stage of the disease. Therefore, searching for new methods of early and accurate diagnosis of lung cancer is crucial for its effective treatment. Lung cancer is the result of multistage carcinogenesis with gradually increasing genetic and epigenetic changes. Screening for the characteristic genetic markers could enable the diagnosis of lung cancer at its early stage. The aim of this review was the summarization of both the preclinical and clinical approaches in the genetic diagnostics of lung cancer. The advancement of molecular strategies and analytic platforms makes it possible to analyze the genome changes leading to cancer development—i.e., the potential biomarkers of lung cancer. In the reviewed studies, the diagnostic values of microsatellite changes, DNA hypermethylation, and p53 and KRAS gene mutations, as well as microRNAs expression, have been analyzed as potential genetic markers. It seems that microRNAs and their expression profiles have the greatest diagnostic potential value in lung cancer diagnosis, but their quantification requires standardization.
Acute pancreatitis (AP) is an acute inflammation of the pancreas associated with high morbidity and mortality. Endocrine pancreatic insufficiency secondary to AP has drawn increasing attention in recent years. The aim of this paper is to analyze the available clinical and experimental literature to determine the cause and effect relationship of diabetes type 3c (T3cDM; pancreatogenic diabetes) after acute pancreatitis. The clinico-pathological features and management challenges of pancreatogenic diabetes overlap with other secondary causes of diabetes. A complex pathogenesis involving pancreatic exocrine insufficiency, dysfunction of insulin secretion, and insulin resistance is likely the cause of T3cDM after AP. To obtain an improved understanding of the pathophysiology of diabetes after AP, more research is now needed to understand the risk of complications related to the pancreas and diabetes in these patients.
Type 2 diabetes mellitus (T2D) affects millions of people around the world, and its complications have serious health consequences. In addition to external factors, the causes of morbidity and increased risk were also sought in the variability of the human genome. A phenomenon that can answer these questions is the occurrence of single-nucleotide polymorphisms (SNP). They constitute a field for research into genetic determinants responsible for the increase in the risk of the discussed metabolic disease. This article presents the outline of two enzymes: metalloproteinases 2 and 9 (MMP-2, MMP-9), their biological activity and the effect caused by differences in individual alleles in the population, as well as the reports on the importance of these DNA sequence variations in the occurrence of diabetes mellitus type 2 and associated conditions. The results of the conducted research indicate a relationship between two MMP-2 polymorphisms (rs243865, rs243866) and two MMP-9 polymorphisms (rs3918242, rs17576) and the presence of T2D. This could offer a promising possibility to use them as predictive and diagnostic markers. However, due to the low number of reports, more research is needed to clearly confirm the link between these SNPs and diabetes.
29 December 2017 in Advances in Clinical and Experimental Medicine
The aim of this study was to review the diagnostic significance of pancreatic polypeptide (PP) in pancreatic diseases. PP may play a significant role in monitoring the development of the disease and the patient's healing process, particularly after the removal of a portion of the pancreas. Determining PP in acute pancreatitis is quite controversial. At the 1st stage of severe pancreatic damage, there is excessive PP release followed by its fall. In patients with chronic pancreatitis, a significant decrease in PP secretion was found in the presence of a food stimulant. In this case, PP could be a good marker for determining the stage of pancreatitis. Pancreatic polypeptide also functions as a hepatic glucose regulator. PP increases hepatic insulin sensitivity, resulting in reduced hepatic glucose production. Therefore, impaired hepatic insulin sensitivity in chronic pancreatitis is abrogated after the PP administration. Endocrine pancreatic tumors initially grow without specific symptoms. In contrast, they are almost always correlated with elevated serum pancreatic polypeptide. Therefore, the level of PP may be a good diagnostic parameter confirming the presence of pancreatic cancer. Depending on the type of disease, the polypeptide concentration can be increased or decreased, evidencing the disease progress or regression.