Surgical resection of lung cancer inhibits mRNA expression of GOT2 gene encoding kynurenine aminotransferase in leukocytes.

INTRODUCTION AND OBJECTIVE: Lung cancer is the most common malignant tumour. More than 80% of all diagnosed cases are non-small cell carcinoma which can be effectively treated by radical resection. Despite significant progress in the field of diagnostic and therapeutic methods, the results of lung cancer treatment are still unsatisfactory. Lung cancer is detected relatively late, which leads to an unfavourable prognosis. Kynurenine aminotransferases are an important element of the kynurenine pathway of tryptophan metabolism, which has recently aroused great interest from the aspect of possible use as a target point of personalized therapies in malignant tumours.The aim of the study was to analyze the expression of the selected gene of kynurenine aminotransferases GOT 2 at the mRNA level in peripheral blood leukocytes of patients with lung cancer. MATERIAL AND METHODS: The mRNA expression of the GOT 2 gene was tested on blood samples from 50 patients treated surgically for non-small cell lung cancer.The control group consisted of 15 healthy individuals.The determination of mRNA expression of the GOT 2 gene was performed using the real-time PCR method.The GAPDH gene was used as the endogenous reference level. RESULTS: The mRNA expression of the GOT2 gene on the 6th day after surgery was statistically significantly lower than before surgery (p = 0,05). In the study group, the average LogRQ mRNA expression of the GOT2 gene before the procedure was 0.192082±0.292174 in woman. This was statistically significantly higher than in men whose average LogRQ mRNA expression of the GOT2 gene before the procedure was 0.004210±0.235065 (p=0.0183). CONCLUSIONS: Surgical resection of lung cancer results in inhibition of GOT2 mRNA expression in leukocytes. Further studies are expected to show whether it may be used as a target point for personalized therapies in lung cancer.

Factors influencing serum chemerin and kallistatin concentrations in patients with alcohol-induced liver cirrhosis.

INTRODUCTION: In Poland, an increasing number of patients are hospitalized due to liver diseases. One of the common liver diseases is cirrhosis, which can be caused by alcohol, viral hepatitis, autoimmune processes and metabolic diseases. MATERIAL AND METHODS: The study included 99 patients with alcoholic cirrhosis from the Lublin region of Eastern Poland. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The concentrations of serum kallistatin and chemerin were determined using ELISA kits. OBJECTIVE: The aim of the study is to evaluate serum levels of kallistatin and chemerin in patients with different stages of alcoholic liver cirrhosis. RESULTS: The highest chemerin level was found in the control group - 182.6±80.4 ng/ml. In other stages of liver cirrhosis, the following levels were observed: 175.7±62.7 ng/ml in Child-Pugh stage A (Ch-P A), 150.2±59.7 ng/ml in Ch-P B and 110.3±73.6 ng/ml in Ch-P C. Significant differences in chemerin levels between controls and Ch-P C patients (p=0.01), as well as between the Ch-P A patients and Ch-P C patients (p=0.02), were demonstrated. The highest kallistatin level was demonstrated in the control group - 8.2±3.5 µg/ml. In other stages of liver cirrhosis, the following concentrations were found: 7.2±27 µg/ml in Ch-P A, 4.4±2.2 µg/ml in Ch-P B and 3.5±1.9 µg/ml in Ch-P C. Statistically significant differences were observed between controls and Ch-P B patients (p<0.001), controls and Ch-P C patients (p<0.001), Ch-P A and Ch-P B patients (p=0.01), as well as Ch-P A and Ch-P C patients (<0.001). CONCLUSIONS: The levels of chemerin and kallistatin decrease with progression of liver damage during alcoholic liver cirrhosis. The impairment of its synthetic function leads to reductions in levels of the adipokines studied.

Afamin and adropin in patients with alcohol-induced liver cirrhosis.

The aim of the study was to determine serum concentrations of afamin and adropin in patients with alcoholic liver cirrhosis and to define their correlation with the stage of disease. The study included 99 patients with alcoholic cirrhosis from the region of Lublin, (Eastern Poland). Liver cirrhosis was diagnosed based on clinical features, history of heavy alcohol consumption, laboratory tests and abdominal ultrasonography. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The serum afamin and adropin concentrations were determined using ELISA kits. The concentration of afamin was found to be significantly lower in patients with compensated alcoholic liver cirrhosis, i.e. P-Ch B (85.1±40.6 µg/ml) and P-Ch C (56.4±32.3 µg/ml) individuals, compared to the control group (135.9±43.6 µg/ml); p-value was <0.01 and <0.001, respectively. As far as adropin is concerned, a reverse relationship was demonstrated: the highest concentration was found in patients with P-Ch C (11.7±5.7 ng/ml) cirrhosis. Furthermore, the above concentration was significantly higher compared to patients with P-Ch A cirrhosis (7.2±2.8 ng/ml; p<0.05) and controls (7.5±2.6 ng/ml; p<0.05). The concentration of afamin decreases with the severity of alcoholic liver cirrhosis, which most likely results from impaired hepatic synthesis. Otherwise, the higher the stage of disease according to the Child-Pugh score, the higher the concentration of adropin.

Clinical approach to visceral pain in irritable bowel syndrome - pathophysiology, symptoms, and treatment.

Visceral pain has been defined as a pain resulting from activation of pain receptors localized in mucous membrane, serous membrane, and smooth muscles of hollow organs. The great majority of these organs are innervated by parasympathetic and sympathetic outflows. Afferent nerve fibres are involved in conduction of both acute and persistent pain and hyperalgesia. Visceral pain differs significantly from other types of pain in the way it originates and in clinical presentation. It can be misleading as a symptom, producing several problems in the diagnostic process. Sometimes, severe visceral pain is observed in the course of non-lifethreatening functional gastrointestinal disorders, while slight abdominal discomfort may be a first symptom of malignant tumours. For many years, the treatment of visceral pain has been considered as not satisfactory enough and covered a wide variety of pharmacological substances. For example, the complex therapy of pain and other manifestations associated with irritable bowel syndrome include psychotherapy/behavioural therapy, bulk-forming agents, probiotics, laxatives, antidiarrheals, antibacterial agents, antispasmodics, and antidepressants. The current knowledge about the pathogenesis of visceral pain gives a rationale for the development of new, more efficacious drugs with a positive benefit/risk ratio. Unfortunately, experience gained so far with the use of some agents affecting serotoninergic transmission in the gastrointestinal tract have shown a serious danger associated with their administration for patients with irritable bowel syndrome.