This study describes the experience of radical mastectomies with simultaneous breast reconstruction using TRAM flap in patients with inflammatory breast cancer. The study aimed to evaluate the effectiveness of primary breast reconstruction using the TRAM-flap procedure in patients with an inflammatory form of breast cancer. Our work is associated with some deviation from generally accepted standards: delayed breast reconstruction after radical mastectomy for inflammatory breast cancer. We describe the experience of radical mastectomies with the simultaneous reconstruction of the breast using a TRAM flap in patients with inflammatory breast cancer. This study included 12 patients diagnosed with breast cancer stages IIIB and IIIC. Almost all patients (eleven out of twelve patients) underwent radical mastectomy with one-stage reconstruction using a TRAM flap after chemotherapy. Two years later, one patient (8.3%) showed disease progression in the form of distant metastases in the bones of the spine. One patient (8.3%) had a regional relapse in the displaced flap near the postoperative scar. The rest of the patients (83.4%) showed no signs of continuing the disease. Patients with one-stage breast reconstruction improved socially, and their subjective well-being was better than those who underwent radical mastectomy without reconstruction. Experience in performing one-stage reconstructions in the surgical treatment of patients with inflammatory breast cancer is a reason for restrained optimism regarding the possibility and feasibility of these operations.

Objective. Brain-derived neurotrophic factor (BDNF) is identified as an important growth factor involved in learning and memory. Patients with Hashimoto’s thyroiditis can suffer from cognitive dysfunction, whereas BDNF is directly regulated by thyroid hormones. It seems reasonable to propose that changes in BDNF expression underlie some of the persistent neurological impairments associated with hypothyroidism. Methods. The study involved a total of 153 patients with various forms of thyroid pathology. BDNF levels in the sera of the patients and healthy individuals were quantified using enzyme-linked immunosorbent assay with highly sensitive Human BDNF ELISA Kit. Genotyping of the BDNF (rs6265) gene polymorphism using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions. Results. Distribution rs6265 variants in the patients depending on the different types of thyroid pathology showed no significant difference in the relative frequency of BDNF polymorphic variants. Presence of hypothyroidism, regardless of its cause (autoimmune or postoperative), there was a decrease in the serum BDNF levels in all genotypes carriers compared with the control group. The analysis of the correlation between BDNF levels and the levels of thyroid-stimulating hormone (TSH), thyroxine (T4), anti-thyroglobulin (anti-Tg), and anti-thyroid peroxidase (anti-TPO) antibodies showed a significant inverse relationship between BDNF and TSH levels (p<0.001), a direct correlation between BDNF and T4 levels in the blood (p<0.001), and a weak direct relationship between anti-Tg and BDNF levels (p=0.0157). Conclusion. The C allele presence is protective and associates with the lowest chances for reduced serum BDNF levels in thyroid pathology patients in the West-Ukrainian population. However, the T-allele increases the risk of low BDNF levels almost 10 times in observed subjects.

The study aim was to analyse the frequency of polymorphic variants of angiotensinogen gene polymorphism (AGT 704T>C, rs699) in essential arterial hypertension (EAH) patients. METHODS: Seventy-two individuals with EAH and hypertension-mediated organ damage (stage 2), moderate, high or very high cardiovascular risks were involved in the case-control study. Among them, 70.84 % (51) were females and 29.16 % (21) were males; mean age was 59.87±7.98 y. The control group consisted of fi fty practically healthy individuals at relevant age (49.13±6.28 y) and with relevant sex distribution (62 % were females, 38 % were males). AGT (704T>C) gene polymorphism was examined by RT-PCR. RESULTS: The distribution of genotypes in the study group was as follows: TT -14 %, TC -60 %, CC -26 %, which corresponded to the distribution in the control group -16 %, 54 % and 30 %, respectively, and did not deviate from the Hardy-Weinberg equilibrium. Smoking, type 2 diabetes mellitus (DM2) and obesity increased the relative risk of EAH in the examined population 2.5 times [OR=2.81; p=0.049], 3.75 times [OR=4.68; p=0.005] and almost twofold [OR=2.90; p=0.004], respectively. The probability of EAH increases fourfold with the angiotensin II elevation in the serum. Genotypes and alleles of the AGT (704T>C) gene were not signifi cant risk factors for EAH and DM2 in the studied population. However, the TC-genotype (lesser T-allele) increases the risk of obesity in EAH patients more than 1.5 times [OR=2.93; p=0.03]. In addition, the T-allele increases the risk for blood pressure (BP) to elevate up to grade 2-3 [OR=3.64; p < 0.001]. CONCLUSIONS: One-way ANOVA analysis confi rmed the AGT (704T>C) gene polymorphism to be associated with systolic and diastolic BP elevation (F=7.80; p < 0.001 and F=4.90; p=0.01, respectively), especially in TT-genotype carriers (p < 0.05), and with body mass index increase, albeit only in women (F=13.94; p < 0.001) (Tab. 4, Fig. 3, Ref. 26).

Objective:Hypertension and dyslipidemia represent two of the most relevant modifiable cardiovascular risk factors and they often coexist. The aim of the research was to study lipid disorders and essential arterial hypertension (EAH) risk depending on AGTR1 (rs5186) and VDR (rs2228570) genes polymorphism.Design and method:100 subjects with EAH and target-organ damaging (2nd stage), moderate, high or very high cardiovascular risk were involved in the case-control study. Among them, 70,83% females and 29,17% males, mean age 57,86 ± 7,81y.o. Control group consisted of 60 practically healthy individuals of relevant age. The lipid panel parameters, such as: TC (Total cholesterol), TG (Triglycerides), LDL-C (Low-density lipoprotein cholesterol), HDL-C (High-density lipoprotein cholesterol) were investigated in blood plasma, using diagnostic kits “Accent 200” (Poland). The atherogenic index (IA) was calculated by the formula: (TC – HDL-C)/ HDL-C. Gene polymorphism of AGTR1 (rs5186) and VDR (rs2228570), was detected by polymerase chain reaction (PCR).Results:Decreased HDL-C is associated with 2nd and 3d degrees of EAH (p = 0,048). The risk of EAH increases in C-allele carriers of AGTR1 (rs5186) gene with hypercholesterolemia (TC> 5,0mmol/l) 1,5 times (OR–2,50;p = 0,048), with an increase in LDL-C and IA – 1,58 and 2,12 times (OR–10,80;p = 0,019), respectively. Homozygous carriers of the minor A-allele had extremely higher concentrations of TC, atherogenic LDL-C and IA, than GG-carriers – by 9,29%, 11,11% and 12,80% (pAA<0,05), respectively. Risk of EAH increases with hypertriglycerolemia 1,89 times (OR–2,93;p = 0,03) and with the increase in LDL-C – 1,26 times (OR–3,60;p = 0,038) in AA-genotype carriers of VDR (rs2228570) gene. Risk of EAH synergistically escalates almost twice in A-allele carriers of VDR (rs2228570) gene with a decrease of HDL-C (OR–2,88;p = 0,046) and the increase of IA (OR–2,70;p = 0,039), significantly only in AG-carriers though. ANOVA analysis confirmed the association of VDR (rs2228570) gene with the increase in IA (F = 3,80;p = 0,05).Conclusions: The EAH risk escalates with hypercholesterolemia, elevated both LDL-C and IA in C-allele carriers of AGTR1 (rs5186) gene, as well as with decreased HDL-C and increased IA in A-allele carriers VDR (rs2228570) in the observed.

Aim of the study: Among the key genes involved in the development of non-alcoholic fatty liver disease (NAFLD) are genes encoding the synthesis of glutathione S-transferase (GST). Material and methods: Deletion polymorphism of GSTT1 and GSTM1 genes was investigated in 104 NAFLD patients and 45 healthy individuals. Biochemical blood analysis, tumor necrosis factor-α (TNF-α), interleukin-10, leptin and adiponectin plasma levels were studied. Results: The distribution of deletion vs. non-deletion genotypes of the GSTT1 gene in NAFLD patients was 18 (17.3%) vs. 86 (82.7%) patients and in healthy people it was 6 (13.3%) vs. 39 (86.7%) individuals. The genotype distribution of the GSTM1 gene was as follows: 52 (50.0%) NAFLD patients had null genotype vs. 52 patients (50.0%) with non-deletion genotype; in the control group-23 (51.1%) vs. 22 (48.9%) individuals. Deletion of the GSTT1 gene in NAFLD patients was associated with twice as high (p = 0.01) TNF-α level in the blood as compared to patients with normal genotype. Higher concentration of leptin in blood by 37.1% (p = 0.04) was observed in patients with null genotype of the GSTM1 gene, as compared to those with normal genotype. Conclusions: Deletion polymorphism of GSTT1 and GSTM1 genes distribution among NAFLD patients did not differ as compared to healthy individuals. Null-genotype GSTT1 gene carriers were characterized by higher TNF-α concentration and null-genotype GSTM1 gene carriers were characterized by elevated leptin level as compared to normal genotype carriers.