Analysing CYP2D6*4 Allele frequency in Patients with Schizophrenia

2017 ◽  
Vol 41 (S1) ◽  
pp. S101-S102
Author(s):  
V. Djordjevic ◽  
T. Jevtovic Stoimenov
Keyword(s):  
Allele Frequency ◽  
Plasma Concentrations ◽  
Clinical Severity ◽  
Genotype Distribution ◽  
Healthy Individuals ◽  
Wild Type ◽  
Specific Pcr ◽  
Significant Difference ◽  
Schizophrenic Patients ◽  
The Right

IntroductionSchizophrenia is treated with antipsychotics and other psychotropic medications, many of which are substrates for the highly polymorphic CYP2D6 enzyme. The most frequent variant allele is CYP2D6*4- leading cause of poor metabolism (PM) phenotype. PM causes the reduction of therapeutic response, increase the risk of adverse drug reactions and increase the plasma concentration of both drug and its metabolites above the levels of toxicity.The AimAnalysing CYP2D6*4 allele frequency among schizophrenic patients for further individualisation and rationalisation of therapy.Patients and methodsResearch was conducted on 38 schizophrenic patients and 110 healthy individuals. CYP2D6*4 allele was detected with allele specific PCR.ResultsBoth wild type allele carriers are 55% of the schizophrenic patients, 45% are wild type/*4heterozygous, and *4/*4 homozygous are not identified. There is a statistically significant difference in the genotype distribution (P < 0.05) between schizophrenic patients and healthy individuals. Significantly higher *4 allele frequency (37%) comparing to healthy individuals (P < 0.0001) indicates the necessary caution in administration of CYP2D6 substrates. A lower frequency of PMs in schizophrenic patients than in healthy individuals could be explained with CYP2D6 neuroactive substrate metabolism. Forty-five percent of the schizophrenic patients are intermediate metabolisers carrying the higher risk of adverse response to CYP2D6 substrates comparing to wild type homozygous. As none of the analyzed patients was PM, exceeded plasma concentrations of medications above toxic levels are not expected when administrating the right dosage.ConclusionAltered CYP2D6 metabolism may contribute to the vulnerability, clinical severity and treatment outcome of schizophrenia.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The −670G>A polymorphism in the FAS gene promoter region influences the susceptibility to systemic sclerosis

2008 ◽  
Vol 68 (4) ◽  
pp. 584-590 ◽  
Author(s):  
V Liakouli ◽  
M Manetti ◽  
A Pacini ◽  
B Tolusso ◽  
C Fatini ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Topoisomerase I ◽  
Gene Promoter ◽  
Serum Levels ◽  
Scleroderma Renal Crisis ◽  
Genotype Distribution ◽  
Healthy Individuals ◽  
Soluble Fas ◽  
Significant Difference ◽  
Pulmonary Arterial

Objective:To evaluate the role of the single-nucleotide polymorphism (SNP) at position −670 in the FAS gene promoter (FAS−670G>A) in influencing the susceptibility, clinical features and severity of systemic sclerosis (SSc).Methods:350 white Italian SSc patients (259 with limited cutaneous SSc (lcSSc) and 91 with diffuse cutaneous SSc (dcSSc)) and 232 healthy individuals were studied. Patients were assessed for the presence of autoantibodies (anticentromere, anti-topoisomerase I (anti-Scl-70) antibodies), interstitial lung disease (ILD), pulmonary arterial hypertension and scleroderma renal crisis. FAS−670G>A SNP was genotyped by PCR restriction fragment length polymorphism assay. Serum levels of soluble FAS (sFAS) were analysed by ELISA.Results:A significant difference in FAS−670 genotype distribution was observed between SSc patients and healthy individuals (p = 0.001). The frequency of the FAS−670A allele was significantly greater in SSc than in controls (p = 0.001). No significant difference in genotype distribution and allele frequencies was observed between lcSSc and dcSSc, although a greater frequency of the FAS−670A allele was found in dcSSc. The FAS−670AA genotype significantly influenced the predisposition to SSc (OR 1.97, 95% CI 1.35 to 2.88, p = 0.001) and to both lcSSc (OR 1.84, 95% CI 1.23 to 2.75, p = 0.003) and dcSSc (OR 2.37, 95% CI 1.41 to 3.99, p = 0.001). FAS−670A allele frequency was greater, although not significantly, in anti-Scl-70 antibody-positive dcSSc and ILD dcSSc. sFAS was significantly higher in patients and controls carrying the FAS−670AA genotype compared with those carrying the FAS−670GG genotype (p = 0.003 in SSc, p = 0.004 in controls).Conclusion:The FAS−670A allele is significantly associated with susceptibility to SSc, suggesting a role for a genetic control of apoptosis in the pathogenesis of the disease.

scholarly journals Evaluation of PECAM-1 Gene Polymorphism in Patients with Periodontal Disease and Healthy Individuals

2012 ◽  
Vol 2012 ◽  
pp. 1-5
Author(s):  
Mahdi Kdkhodazadeh ◽  
Mehrdad Hajilooi ◽  
Behzad Houshmand ◽  
Sara Khazaei ◽  
Leila Gholami ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Aggressive Periodontitis ◽  
Genotype Distribution ◽  
Nucleotide Polymorphisms ◽  
Healthy Individuals ◽  
Single Nucleotide ◽  
Genotypic Distribution ◽  
Genotype Frequencies ◽  
Significant Difference ◽  
Polymerase Chain

Objective. Our aim in this paper was to investigate the possible genetic association between three Ser563Asn, Leu125Val and Arg670Gly polymorphisms of the PECAM-1 gene and periodontitis. Methods. Genomic DNA was isolated from whole blood of 105 periodontal patient (52 with chronic periodontitis and 53 with aggressive periodontitis) and 101 healthy individuals. Samples were genotyped and analyzed for the three single-nucleotide polymorphisms (SNPs) of PECAM-1 using polymerase chain reaction with sequence-specific primers (PCR-SSPs). Results. A statistically significant difference was found between the genotypic distribution of the Ser563Asn polymorphism in patients with periodontitis compared to controls (P=0.02). But there were no statistically significant difference between the allele frequencies in the different groups (P=0.05). The other two polymorphisms did not show a statistically significant difference in their allele and genotype frequencies between the groups. There was no statistically significant difference found for any of the polymorphisms allele and genotype distribution in aggressive and chronic periodontitis either. Conclusions. No significant association was found between the polymorphism tested and the subgroups of periodontitis, further research is still necessary to determine whether this polymorphism can be used as a genetic marker of periodontitis.

scholarly journals CRP Gene Polymorphism and Their Risk Association With Type 2 Diabetes Mellitus

2019 ◽  
Vol 7 (1) ◽  
pp. 33-37
Author(s):  
Hakim Bahlok Jebur ◽  
Mirza Masroor ◽  
Hafiz Ahmad ◽  
Naushad Ahmad Khan ◽  
Juheb Akther ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gene Polymorphism ◽  
Inflammatory Marker ◽  
Genotype Distribution ◽  
Reactive Protein ◽  
Specific Pcr ◽  
Increased Risk ◽  
Significant Difference ◽  
Allele Specific

BACKGROUND: C-reactive protein (CRP) is an inflammatory marker associated with T2DM, obesity, insulin resistance, and cardiovascular disease. AIM: The present study evaluates the association of CRP +1059 G/C polymorphism of the CRP gene in 100 T2D cases and 100 healthy controls. METHODS: Present study was done by allele specific PCR method to study the CRP gene polymorphism in study subjects. RESULTS: Study found that CRP (+1059 G/C) genotype distribution among case and controls was found to be significant (p=0.001), Higher CRP C allele frequency (0.16) was observed compared to controls (0.04). CRP +1059 GC and CC had 2.72 (1.12-6.61), 20.56 (1.16-362.1) risk for T2D. It has been observed, HTN, Obesity, Smoking and alcoholism was found to be associated with increased risk of T2D, and a significant difference was observed in biochemical parameters. CONCLUSION: Study concluded that CRP gene polymorphism was found to be associated with risk of Type 2 Diabetes and risk was linked with heterozygosity and mutant homozygosity. Hypertension, Obesity, Smoking and alcoholism increases the risk of occurrence of Type 2 Diabetes.

scholarly journals An Interdependence between Estrogen Receptor 1 Gene Polymorphisms and Susceptibility to Breast Cancer

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Maryam Saneipour ◽  
Abdolkarim Sheikhi ◽  
Abbas Moridnia
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Allele Frequency ◽  
Genetic Alterations ◽  
Recessive Model ◽  
Control Group ◽  
Genotype Distribution ◽  
Increased Risk ◽  
Significant Difference ◽  
Estrogen Receptor 1

Background: Breast cancer (BC) is the most common malignant tumor in women around the world. Genetic factors do play a vital role in the development and progression of BC. Genetic alterations in the ESR1 (estrogen receptor 1) gene can lead to estrogen dysfunction and increased risk for BC. Nevertheless, due to genetic diversity, the information from different studies is contradictory and controversial. Objectives: This study aimed to investigate the potential relationship between the rs1801132 and rs2234693 single nucleotide polymorphism (SNPs) of the ESR1 gene with susceptibility to BC in the Iranian population. Methods: The genotyping of the rs2234693 and rs1801132 SNPs was assessed in 63 BC patients referred to Imam Hasan Mojtaba Center, which is a charity-based foundation for cancer care in Dezful, Iran, from March 2018 to November 2019. Also, 65 healthy women were selected as a control group. The genotyping of the SNPs was performed using the high-resolution melting (HRM) technique and confirmed by DNA sequencing. Results: The genotype distribution and allele frequency of the rs2234693 SNP were significantly different in BC patients compared to the control group (genotype frequency with P = 0.018 and allele frequency with P = 0.004, OR = 2.085, 95% CI = 1.253 -3.468). In genetic models, rs2234693 increased BC risk in recessive model (P = 0.005, OR = 2.813, 95% CI = 1.363 - 5.802). However, there was no significant difference regarding genotype distribution of the rs1801132 SNP between the BC patients and controls. Conclusions: Our results showed that the CC genotype of the rs2234693 SNP is significantly associated with BC. Accordingly, it can be suggested that the rs2234693 SNP be considered for susceptibility to BC.

Differences Between Upper and Lower Limbs in Venous Endothelial Reactivity in Humans

1994 ◽  
Vol 9 (1_suppl) ◽  
pp. 10-14
Author(s):  
O. Bailliart ◽  
L. Boudaoud ◽  
Ph. Bonnin ◽  
C. Bal Dit Sollier ◽  
J. Roussi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Plasminogen Activator ◽  
Plasma Concentrations ◽  
Cell Activity ◽  
Lower Limbs ◽  
Cell Recovery ◽  
Significant Difference ◽  
Cell Release ◽  
The Right ◽  
Pai 1

Objective: To determine the variability of endothelial reactivity to venostasis in the upper and lower limbs of healthy subjects. Participants: Ten healthy volunteers were investigated twice, at an interval of 1-week. Main outcome measures: Plasma concentrations of substances released from endothelial cells were determined in each limb after 10 min of venostasis in a sequential manner. Tissue plasminogen activator (tPA), plasminogen activator inhibiting factor (PAI-1), thrombin–antithrombin complexes (TAT) and D-dimers (D-Di) were used as indicators of the thrombotic process and its reactions; angiotensin converting enzyme (ACE) and endothelin-1 (ET1) were related to endothelial cell activity involved in vascular tone regulation. Results: No difference was observed in endothelial cell recovery following venostasis after an interval of 1 week. A significant difference in endothelial cell release was found between the upper and lower limbs and between the right and left legs. Conclusions: Excellent reproducibility of measurements was observed. In keeping with the higher frequency of venous thrombosis in the lower limbs, the left leg seemed to be less reactive after venostasis, and the endothelium was more reactive in the upper than in the lower limbs.

scholarly journals GLU298ASP and 4G/5G Polymorphisms and the Risk of Ischemic Stroke in Young Individuals

2015 ◽  
Vol 42 (5) ◽  
pp. 310-316 ◽  
Author(s):  
Juan Carlos Esparza-García ◽  
David Santiago-Germán ◽  
María Guadalupe Valades-Mejía ◽  
Jesus Hernández-Juárez ◽  
Eberth Aguilar-Sosa ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Allele Frequency ◽  
Plasminogen Activator Inhibitor ◽  
Mexican Population ◽  
Genotype Distribution ◽  
Plasminogen Activator Inhibitor 1 ◽  
Increased Risk ◽  
Significant Difference ◽  
And Gender ◽  
Endothelial Nitric Oxide

AbstractBackground: Polymorphisms in the endothelial nitric oxide synthase (eNOS) and in the plasminogen activator inhibitor -1 (PAI-1) genes have been implicated in stroke pathogenesis but results are still controversial. The aim of this study was to examine the possible contribution of Glu298Asp in the eNOS and 4G/5G in the PAI-1polymorphisms with ischemic stroke in a young Mexican population. Materials and Methods: In a case-control study, conducted between January 2006 and June 2010, 204 patients ≤45 years of age with ischemic stroke and 204 controls matched by age and gender, were recruited. The Glu298Asp and 4G/5G polymorphisms were determined in all participants by polymerase chain reaction-restriction fragment length polymorphism. Results: There was a significant difference in the Glu298Asp genotype distribution (P=0.001) and allele frequency between the two groups (P=0.001). The 4G/5G genotype distribution (P=0.40) and the allele frequency was similar between groups; (P=0.13). There were independent factors for ischemic stroke: Asp carriage (GluAsp+AspAsp) (P=0.02); smoking (P=0.01); hypertension (P=0.03), and familial history of atherothrombotic disease (P=0.04). Conclusions: The Asp allele from the Gu298Asp gene represents an independent risk factor for ischemic stroke in a young Mexican population. In contrast, the 4G/5G was not associated with an increased risk for this disease in the same group of patients, as previously has been demonstrated in other populations.

ACE Insertion/Deletion, But Not −240A>T Polymorphism, Modulates the Severity in Heart Failure

2008 ◽  
Vol 56 (8) ◽  
pp. 1004-1010 ◽  
Author(s):  
Cinzia Fatini ◽  
Elena Sticchi ◽  
Rossella Marcucci ◽  
Abdihakim Abdullahi Said ◽  
Stefano Del Pace ◽  
...  
Keyword(s):  
Heart Failure ◽  
Allele Frequency ◽  
Nyha Class ◽  
Severe Heart Failure ◽  
Genotype Distribution ◽  
Multinomial Regression ◽  
Predisposing Factor ◽  
Significant Difference ◽  
Patients With Heart Failure

ObjectiveACE gene is reported to be a candidate gene in heart failure. The insertion/deletion (I/D) polymorphism has been observed to be a predictor of mortality in this disease, but no data are available concerning the role of ACE −240A>T polymorphism. In this study, we investigated the role of ACE I/D and −240A>T polymorphisms in influencing both severity and clinical outcomes in patients with heart failure, according to New York Heart Association (NYHA) class.PatientsWe studied 323 patients with heart failure (258 men/65 women; age, 70.8 ± 11.5 years) followed-up for 11.9 ± 6.6 months.ResultsThe ACE D and −240T allele frequency significantly increased according to the NYHA functional class (P = 0.0002 and P < 0.0001, respectively).No significant difference in ACE polymorphism genotype distribution and allele frequency according to N-terminal pro-brain natriuretic peptide tertiles was observed. At multinomial regression analysis, ACE D but not −240T allele has been evidenced to be a significant and independent predictor of severity for both NYHA III and IV classes (P = 0.01 and P = 0.004, respectively). The ACE D allele prevalence was higher, even if not significantly in both death and rehospitalization groups in comparison with survivors and nonrehospitalized (P = 0.6 and P = 0.9, respectively). No difference in −240T allele frequency has been observed for the ACE −240A>T polymorphism, in relation to both death and rehospitalization (P = 0.1 and P = 0.6, respectively).ConclusionsThis study suggests that ACE I/D polymorphism might represent a predisposing factor to severe heart failure, independently of well-known prognostic markers.

Association of MDM2 Gene Polymorphisms SNP285 and 309 with Myelodysplastic Syndromes (MDS) Susceptibility and Outcome.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2823-2823
Author(s):  
Kathy L. McGraw ◽  
Lan Min Zhang ◽  
William Fulp ◽  
Hui-Yi Lin ◽  
Andres Jerez ◽  
...  
Keyword(s):  
Allele Frequency ◽  
Response Rate ◽  
Disease Onset ◽  
Response Duration ◽  
Negative Regulator ◽  
Genotype Distribution ◽  
Healthy Controls ◽  
Genotype Frequencies ◽  
Increased Risk ◽  
Significant Difference

Abstract Abstract 2823 Background: Mutations in TP53, or less often its regulators, increases risk for malignant transformation. Murine double minute protein 2 (MDM2), an E3 ubiquitin ligase, targets p53 for proteasomal degradation and is the most well studied negative regulator of p53. Recent investigations have highlighted the emerging importance of p53 in MDS. Haploinsufficiency for ribosomal protein S14 in deletion 5q MDS liberates free ribosomal proteins that bind to and promote degradation of MDM2, thereby activating p53 in erythroid precursors. A single nucleotide polymorphism (SNP) in an MDM2 promoter (SNP309) is linked to younger age of onset of several solid tumors and an increased risk for acute myeloid leukemia (AML) [Knappskog and Lonning. 2011. Transcription 2:207, Xiang et al. 2009. Leuk Res. 33:1454]. The thymine (T) to guanine (G) substitution introduces an additional Sp1 transcription factor binding site causing upregulation of MDM2 transcription. A second SNP in this promoter (SNP285) has also been linked to cancer susceptibility, where a guanine (G) to cytosine (C) exchange is associated with decreased ovarian and breast cancer risk (Knappskog and Lonning. 2011. Oncotarget. 2:251). The C-allele of SNP285 has diminished Sp1 promoter binding compared to the G-allele decreasing MDM2 expression. In this study we investigated genotype distribution of MDM2 SNPs in del(5q) and non-del(5q) MDS patients and compared results to healthy controls. Methods and Results: Using Sanger sequencing, we compared allele and genotype frequencies for SNP285 and SNP309 in 155 healthy controls, 97 non-del(5q), and 119 del(5q) MDS patients. For SNP285, we found no significant difference in genotype or allele frequency among non-del(5q) or del(5q) cases compared to controls (p=0.25 and 0.26, respectively). Although there was no difference in age at diagnosis by genotype in del(5q) MDS (p=0.82), there was a significant difference among non-del(5q) MDS cases [p<0.01, mean (range) for GC:80.8y (75–89) and GG:68.9y (27–91)], however, the frequency of the GC genotype was low [n=5, non-del(5q); n=11, del(5q)] with no CC genotype cases. For SNP309, there was no difference in allele frequency (p=0.68), however genotype frequency differed between controls, non-del5q, and del5q MDS (p=0.06). The genotype distribution was significantly different between non-del(5q) and del(5q) MDS (p=0.01). SNP309 genotype frequencies for controls, non-del(5q), and del(5q) MDS were GG:17.3%, 22.7%, 10.1%; TG: 42.9%, 37.1%, 53.8%; TT: 39.7%, 40.2%, 36.1%, respectively. We found no difference in age of disease onset by SNP309 genotype in either non-del(5q) or del(5q) cases (p=0.08 and 0.97, respectively). There was no significant relationship between SNP285 genotype and IPSS (p=1.0), cytogenetic risk (p=0.66), or WHO classification (p=0.16) in non-del(5q) or del(5q) cases (p=1.0, 0.78, and 0.60, respectively). Similar results were observed for SNP309 [p=0.85, 0.39, and 0.68 for non-del(5q); p= 0.06, 0.98, 0.27 for del(5q), respectively]. For SNP285 there was no difference in overall survival (OS) by genotype in either non-del(5q) (p=0.65) or del(5q) MDS (p=0.72). Progression free survival (PFS) also did not differ by genotype in non-del(5q) (p=0.82) or del(5q) (p=0.58) patients. There was a significant difference in LEN response rate in del(5q) MDS (p=0.04, non-responders: 23.8% GC and 76.2% GG, responders: 4.9% GC and 95.1% GG), however, genotype did not influence response duration (p= 0.40). For SNP309, there were no significant difference in OS by genotype (p=0.42), PFS (p=0.78), LEN response rate (p=0.17), or response duration in del(5q) MDS (p=0.65). In non-del(5q), there was no difference in OS (p=0.42), LEN response rate (p=0.91), or response duration (p=0.47). However, we found a significant difference in PFS by genotype (p=0.03) with more prolonged PFS in patients with the heterozygous TG genotype (60 mo PFS: GG 55.3%, TT 54.1%, and TG 81.7%). Finally, we found no difference in chromosome 5 deletion size or deletion location in del(5q) MDS according to SNP309 genotype. Conclusions: MDM2 SNP309 may be linked to MDS susceptibility, as well as LEN responsiveness and PFS in del(5q) and non-del(5q) MDS, respectively. These data warrant validation in a larger patient cohort. Investigation of the interaction between MDM2 SNPs and the well described TP53 R72P SNP is underway. Disclosures: List: Celgene: Consultancy.

Functional polymorphism of the myeloperoxidase gene (G-463A) in depressive patients

2010 ◽  
Vol 22 (5) ◽  
pp. 218-222 ◽  
Author(s):  
Piotr Gałecki ◽  
Antoni Florkowski ◽  
Kinga Bobińska ◽  
Janusz Śmigielski ◽  
Małgorzata Bieńkiewicz ◽  
...  
Keyword(s):  
Allele Frequency ◽  
Depressive Disorders ◽  
Genotype Distribution ◽  
Functional Polymorphism ◽  
Single Nucleotide ◽  
Significant Difference ◽  
Inflammatory Processes ◽  
Healthy Control ◽  
Depressive Patients

Gałecki P, Florkowski A, Bobińska K, Śmigielski J, Bieńkiewicz M, Szemraj J. Functional polymorphism of the myeloperoxidase gene (G-463A) in depressive patients.Objective:Myeloperoxidase (MPO) is an enzyme involved in the production of hypochloric acid as well as other reactive oxygen species. This enzyme plays a significant role in inflammatory processes. In view of the observed associations between depression and such inflammatory processes, as well as of the reports that confirm the presence of oxidative stress in depression, this study was designed to assess the correlation, if any, between the single nucleotide polymorphism G-463A of the MPO gene and the risk of recurrent depressive disorders (DD).Methods:The study was carried out in a group of 149 patients with recurrent DD and 149 healthy control subjects. Genotyping was performed by PCR/restriction fragment length polymorphism.Results:A comparison between healthy controls and depressive patients showed a statistically significant difference in genotype distribution and allele frequency in the studied groups. Genotype distribution and allele frequency did not correlate with clinical variables of the patients.Conclusion:The obtained results of the study allow us to draw a cautious conclusion about the role of the analysed G-463A MPO polymorphism in recurrent DD development, which, however, requires eventual confirmation in further studies.

scholarly journals Comparison Between Strength of Muscles Rotating the Knee in Healthy Individuals and Patients one Year after an ACL Reconstruction

2014 ◽  
Vol 2 (11_suppl3) ◽  
pp. 2325967114S0014
Author(s):  
Marcın Popieluch ◽  
Robert Śmigıelski ◽  
Darıusz Straszewski ◽  
Marcın Plenzler ◽  
Mıchał Stanıszewski
Keyword(s):  
Muscle Strength ◽  
Internal Rotation ◽  
Acl Reconstruction ◽  
Lower Leg ◽  
Control Group ◽  
Special Device ◽  
Healthy Individuals ◽  
Static State ◽  
Significant Difference ◽  
The Right

Objectives: In this study we have made an attempt to establish torque value of the muscles rotating the knee of patients who had ruptured their ACLs during an amateur football practise on an artificial turf. In this study we presented biomechanical research on torques of muscles responsible for internal and external rotation of the lower leg. We presented a method whereby it is possible to measure the muscle strength before and after the ACL rupture but also during the process of rehabilitation and after its finish. The available literature on measurements of torque of the knee is quite extensive though it mainly describes torques of muscles flexing and extending the joint. In Polish literature there is scarcity of studies focused on torques of muscles rotating the knee. In foreign literature there is an increasing emphasis on the role of lower leg rotation, as the element greatly impacting, for instance, the position of the foot. Methods: The study presents results of 22 patients and 50 healthy individuals (not practising any particular sport regularly) being the control group. All patients had their ACLs reconstructed using the double-bundle technique. The material for the graft was obtained from the hamstrings. The aim was to measure the maximal torque of the muscles responsible for external and internal rotation of the knee (lower leg in a static state using a special device). The device allowed measurement of the torque of muscles rotating the lower leg in its axis by stabilizing the ankle with special emphasis on foot mounting (stabilization of footwear). The special device was connected to a PC with CPS/HMF software. The software enabled observation and recording of increase in the value of the torque until it reached its maximum. The measurements were taken in two knee positions: 30 degrees and 90 degrees flexion. Results: The result were analyzed statistically, means and SDs were calculated. Only right-legged subjects were included in the analysis. The Shapiro-Wilk test was used to test normality of the distribution. Some of the data did not have a normal distribution so in order to compare results of different groups a non-parametric Mann–Whitney U test was used. The groups differed significantly in terms of age (p=0.001), did not differ in terms of body height (p=0.529) or mass (p=0.233). Statistically significant differences (p<0.001) were marked by an asterix symbol (*). Each measurement of the left and right leg was also compared between the groups. The Kruskal–Wallis one-way analysis of variance by ranks was used and significant differences were those with p<0.001. When analyzing it has been noted that there was a statistically significant difference (p<0.001) between the torque value of muscles responsible for internal rotation (S40) when examining the right limb (after ACL reconstruction) in both groups. Significant differences were observed in all starting positions, as well as in both degrees of flexion – 30 and 900. Deficit of muscle strength on the right side – the injured one – when compared to the left was sometimes as high as 30%. Conclusion: 1. Near 30% deficit of strength of muscles responsible for internal rotation of the knee indicates that the knee is rotationally unstable after a year from the surgery. 2. Based on the fact that using the hamstrings tendons – responsible for internal rotation of the knee – in order to reconstruct the ACL, poses a risk of rotational instability of the joint for as long as a year after the procedure, the rehabilitation protocol for such patients should be adjusted or completely changed.

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