In recent years, we have discussed the correlation of malignant tumor process with the development of osteoporosis, which can be exacerbated by ongoing chemotherapy and radiation therapy. The aim of the work was to assess the status of bone metabolism in 32 untreated patients with lung cancer without metastasis. Materials and Methods: Patients underwent dual-energy X-ray osteodensitometry of proximal part of femoral bone. Osteopontin (OP), osteocalcin (OC) and alkaline phosphatase (AP) parameters were studied in blood, as well as osteo-associated chemical elements. Results: Lung cancer proceeds with severe disorders of bone metabolism, which is accompanied by an increase in blood levels of OP, OС, AP, phosphorus, lithium, lead, strontium and cobalt against a decrease of calcium, magnesium and manganese, which were observed in 75; 78; 31; 100; 66; 47; 44; 3; 100; 100, and 6% of patients, respectively; such disorder was associated with a morphological variant of the tumor (cobalt) and stage of disease (calcium, magnesium, manganese, strontium), development of osteodeficit (OP, OC, AR, strontium, zinc). Osteodeficit in the form of osteopenia and osteoporosis is observed more common in women, in every second patient, and osteodensimetric T-score depends on the age of patients, directly correlates with the values of the OP and OC, and inversely — with a zincemia rate. Conclusions: The disorders of bone metabolism in patients with lung cancer indicate the need for the development of antiosteoporosis treatment for cancer patients.
Aim: To study the nature of different variants of paraneoplastic syndrome (PNPS) in lung cancer, taking into account the features of the tumorous process and the complications of radiochemotherapy. Patients and Methods: We performed an analysis of the data of 1,669 patients with lung cancer aged between 24 and 87 years, among whom there were 89% of men and 11% of women. The ratio of small cell and non-small-cell histological variants of the lung cancer was 1: 4, IB, IIA, IIB, IIIA, IIIB and IV stages of cancer — 1:2:6:58:43:57. Results: PNPS developed in 16% of the lung cancer patients, in these patients we have detected a marked increase in the disease incidence in women, the peripheral form of the tumor, the apical variant of Pancoast — Tobias and adenocarcinoma, but no cases of the median lower localization of the tumor. The number of the upper lobar pathology was decreased, while the severity of the cancer was significantly greater, which more often occurred with exudative pleurisy, germination of the tumor into the chest wall and compression of the upper vena cava. The 21 components of PNPS pathology were established. We distributed them conditionally into the musculoskeletal system lesions, variants of skin vasculitis and autoimmune processes, the nature of which depended on the localization and course of the tumorous process, its histological variation and severity of the course. Moreover, PNPS negatively affected the development of radiochemotherapy complications and worsened survival rate. Conclusions: The course of PNPS in lung cancer is highly diverse, being a risk factor for a severe tumorous process that worsens the survival of patients
Aim: To evaluate changes in indicators of endothelial function and their relationship with morphological forms of disease, stage of pathological process and tumor markers, by analysis the peripheral blood of lung cancer (LC) patients. Materials and Methods: 38 LC patients without metastases (mean age — 57 years) prior chemo- and radiotherapy were included in the study. The duration of the disease manifestation was 18 months. 21% of patients had small cell LC, and the rest — non-small cell LC. The ratio of patients with stages IA, IB, IIA, IIB, IIIA and IIIB LC was 1 : 3 : 3 : 4 : 4 : 4. The enzyme immunoassay, spectrophotometry, and statistical data analysis were used. Results: Endothelial dysfunction of vessels was characterized by increased blood levels of vascular endothelial growth factor (VEGF), endothelin-1 (ET1), homocysteine (HCys), cyclic guanosine monophosphate (cGMP), P-selectin (PSel) and nitrites (NO2) and simultaneously by decreased values of prostacyclin (PgI2). Those were observed in 100; 90; 76; 71; 50; 53 and 79% of LC cases, respectively. Disturbances of vascular endothelial function were associated with patient’s age, disease duration, and morphological form and LC stage. Such changes were observed in women with higher prevalence. The studied indices correlated with tumor markers, namely transforming growth factor beta (TGFβ1), fibronectin and osteopontin. Conclusion: Indices of vascular endothelial dysfunction in LC can be of diagnostic and prognostic value.
Summary. Aim: To study the state of purine metabolism in gastric (GAC) and pulmonary (PAC) adenocarcinomas and to assess its clinical and pathogenetic significance. Patients and Methods: One hundred and six male patients were examined, among whom were 63 subjects aged 34 to 79 suffering from GAC, and 43 subjects aged 24 to 76 suffering from PAC. In GAC, the ratio of the pyloric, corporeal and antral localization of the tumor and variant of overall gastric lesion accounted to 24:5:1:1; and that of the central and peripheral PAC was 2:1. Serum levels of purine metabolism products (uric acid, oxypurinol, adenine, guanine, xanthine, hypoxanthine) were measured and activities of xanthine oxidase, xanthine deaminase, adenosine deaminase and 5-nucleotidase were analyzed. Results: Purine metabolism disorders are observed in all GAC and 91% of PAC patients; among other things, hyperuricemia is observed in ¾ and ½ of cases, respectively; moreover, the nature of changes is more pronounced in gastric cancer and, in both groups of patients, these indices reflect the disease course severity, are associated with the neoplastic process localization, have a predictive value, trigger the development of metastases. Conclusion: Сhanges in purine metabolism are involved in the pathogenetic patterns of GAC and PAC, reflect the course of the tumor process, are associated with tumor localization and have prognostic significance.
An article deals with the influence of the transforming growth factor beta-1 (TGF-β1) on the carcinogenesis of hepatic cells, as well as attention is given to the role of this factor in the hepatocellular carcinoma (HCC) progression. We monitored two groups of patients: in the treatment group, patients were administered cancer vaccine therapy and anti-relapse immune corrector Arecur®-a complex of exogenous peptides with anti-inflammatory, anti-infective and regenerating properties; in the reference group, patients were not administered immune corrector. The study showed that the cancer vaccine has a positive effect on the activity of T-cell immunity and interleukin-2 expression level. The result of the inclusion of antirelapse immune corrector Arecur® in the patients' management regimen was the reduction of TGF-β1 expression. The lower recurrence rate of HCC in the treatment group suggests that Arecur® may prevent possible recurrences and metastasis of HCC by limiting TGF-β1 expression. Future researches of anti-relapse immune correction regimens for patients with hepatic tumours may improve the therapeutic strategy and prevention of the disease progression in the long term. In addition, immune correction using exogenous peptides is likely capable of preventing the malignancy in patients with chronic hepatitis and liver cirrhosis.
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