Relation between male obesity and male infertility in a Tunisian population.

Obesity is associated with significant disturbance in the hormonal milieu that can affect the reproductive system. Male infertility affects approximately 6% of reproductive-aged men. It has been suggested that overweight men or men with obese body mass index (BMI) experience prolonged time to pregnancy, although the influence of male BMI on fertility remains understudied. We hypothesised that BMI is inversely correlated with fertility, manifested by reduced sperm concentration and varicocele. Males of mean age 32.74 ± 6.96 years with semen analyses and self-reported BMI were included (n = 98). Patient parameters analysed included age, BMI, pubertal timing, the development of varicocele, and leutinizing hormone, follicle-stimulating hormone and testosterone (n = 18). The mean age of the study population was 32.74 ± 6.96 years. The incidence of azospermia, oligozoospermia, normospermia and the development of varicocele did not vary across BMI categories. Male obesity is not associated with the incidence of sperm concentration and the development of varicocele.

[Impulsivity and externalization and internalization problems in adolescents]. / Impulsivité et problèmes d'internalisation et d'externalisation chez l'adolescent.

OBJECTIVES: The multidimensional aspect of the concept of impulsivity is proven by the composite structure of the rating scales of impulsivity. Several studies have already found correlations between trait-impulsivity and externalizing disorders. However, the studies interested in the relationship between trait-impulsivity and internalizing problems are rare. We have tried to explore correlations between impulsivity and externalization and internalization problems, in a population of adolescent outpatients. METHODS: We recruited 31 adolescent out-patients in the child and adolescent psychiatry department in the University Hospital of Monastir, Tunisia. The Barratt Impulsivity Scale (BIS) was used to evaluate a multidimensional concept of trait-impulsivity, including the dimensions of "Motor", "Non-planning" and "Attentional" impulsivities. The Strength and Difficulties Scales (SDQ) was used to assess different domains of externalizing and internalizing problems, including "Emotional symptoms", "Conduct problems", "Hyperactivity" and "Peer problems". RESULTS: The sex-ratio was 1.21. The mean age was 15.19±1.27 years. All patients but one were attending school. The diagnosis was "Major Depressive Episode" in 32% and "Behavior Disorder" in 38%. The means of the scores of externalizing and internalizing problems were 9.35±4.41 and 9.65±3.26, respectively. The total score of the BIS was significantly related to both scores of externalizing and internalizing problems. The "Motor" impulsivity was specially correlated with the externalizing dimension of the SDQ. The non-planning impulsivity was correlated with both scores of externalizing and internalizing problems, but it was mainly related to internalizing problems. The attentional impulsivity was also correlated with both dimensions of externalizing and internalizing problems. CONCLUSION: The dimensions of trait-impulsivity were correlated with various dimensions of the SDQ concerning externalizing and internalizing problems. That confirms the hypothesis that the impulsiveness is associated with wide domains of the psychopathology of the teenager which are not limited to behavior disorders. We can process these problems by influencing the "Motor impulsivity" and "Non-planning impulsivity". The cognitive and behavioral therapy and the selective serotonin reuptake inhibitor may be efficient.

Chromosomal instability associated with a novel BLM frameshift mutation (c.1980-1982delAA) in two unrelated Tunisian families with Bloom syndrome.

The Bloom syndrome (BS) is an autosomal recessive disorder associated with dwarfism, immunodeficiency, reduced fertility and cancer risk. BS cells show genomic instability, particularly an hyper exchange between the sister chromatids due to a defective processing of the DNA replication intermediates. It is caused by mutations in the BLM gene which encodes a member of the RecQ family of DExH box DNA helicases. In this study, we reported cytogenetic, BLM linkage and mutational analyses for two affected Tunisian families. The Cytogenetic parameters were performed by chromosomal aberration (CA) and sister chromatid exchange (SCE) assays and results showed a significant increase in mean frequency of CA and SCE in BS cells. BLM linkage performed by microsatellite genotyping revealed homozygous haplotypes for the BS patients, evidence of linkage to BLM gene. Mutational analysis by direct DNA sequencing revealed a novel frameshift mutation (c.1980-1982delAA) in exon 8 of BLM gene, resulting in a truncated protein (p.Lys662fsX5). The truncated protein could explain genomic instability and its related symptoms in the BS patients. The screening of this mutation is useful for BS diagnosis confirmation in Tunisian families.

Screening of SLC26A4 gene in autoimmune thyroid diseases.

The Pendred syndrome (PS) gene, SLC26A4, was involved in the genetic susceptibility of autoimmune thyroid disease (AITD) in Tunisian population. Recently, functional assays have shown a differential expression of SLC26A4 gene between Graves' disease (GD) and Hashimoto's thyroiditis (HT). Here, by the mean of DHPLC and HRM, we explored the 21 exons and their flanking intronic sequences of 128 patients affected with GD (n = 64) or HT (n = 64). The pathogenic effect of identified variations on splice was investigated using the web server HSF. Eighteen allelic variations were identified and ranged on missense, sens and splice variations. Nine identified variations (c.-66C>G, c.898A>C, c.1002-9A>C, c.1061T>C, c.1544 + 9G>T, c.1545-5T>G, c.1790T>C, c.1826T>G, c.2139T>G) were previously reported in hearing impairment studies. Forty-seven per cent (30/64) of GD patients and 37,5% (24/64) of HT patients present at least one variant in the explored sequences. Moreover, the analysis of the variant distribution between HT (9 (5'UTR), 12 exonic and 13 intronic) and GD (18 (5'UTR), 13 exonic and 5 intronic) patients showed a significant difference (χ² = 6.54, 2df, P = 0.03). Interestingly, missense changes (I300L, p.M283I, F354S and p.L597S) affected conserved residues of pendrin. On the other hand, the HSF analyses ascertain that some variants identified in HT disease are predicted to have a pathogenic effect on splice. In conclusion, our analysis of SLC26A4 sequence variations suggested a distinct genetics basis between HT and GD patients, which should be confirmed on a large cohort.

The autosomal recessive isolated deafness, DFNB2, and the Usher 1B syndrome are allelic defects of the myosin-VIIA gene.

Hereditary non-syndromic profound deafness affects about 1 in 2000 children prior to language acquisition. In 80% of the cases, the mode of transmission is autosomal recessive. The number of genes involved in these recessive forms of isolated deafness (DFNB genes) has been estimated to between 30 and 100. So far, ten DFNB genes have been mapped to human chromosomes, one of which has been isolated. By linkage analysis of a single family whose members were affected with profound deafness, some of them presenting with vestibular dysfunction, DFNB2 has been mapped to chromosome 11q13 (ref. 3). The gene responsible for a form of Usher syndrome type I, USH1B, has been assigned to the same chromosomal region. Usher syndrome associates profound congenital deafness and vestibular dysfunction with retinitis pigmentosa. In the homologous murine region are located the shaker-1 mutations responsible for deafness and vestibular dysfunction. It has been demonstrated that the murine shaker-1 and human USH1B phenotypes result from mutations in the gene encoding myosin-VIIA. Based on mapping data as well as on the similarities between the phenotypes of DFNB2-affected patients and shaker-1 mouse mutants, we have proposed that a defective myosin-VIIA may also be responsible for DFNB2 (ref. 1). Sequence analysis of each of the coding exons of the myosin-VIIA gene (MYO7A) was thus undertaken in the DFNB2-affected family. In the last nucleotide of exon 15, a G to A transition was detected, a type of mutation that is known to decrease the efficiency of splicing. Accordingly, this result shows that different mutations in MYO7A result in either an isolated or a syndromic form of deafness.

Association study of CARD8 (p.C10X) and NLRP3 (p.Q705K) variants with rheumatoid arthritis in French and Tunisian populations.

The objective of the study was to investigate the association of caspase activating and recruitment domain 8 (CARD8) and nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3) polymorphisms with rheumatoid arthritis (RA) in Tunisian and French populations. CARD8 (c.30T>A, rs2043211) and NLRP3 (c.2113C>A, rs35829419) single nucleotide polymorphisms (SNPs) were genotyped in 100 French RA trio families and 141 Tunisian patients with RA and 191 unrelated healthy controls, using TaqMan(®) allelic discrimination assay. The genetic analyses for the association and linkage in French families were performed using the comparison of allelic frequencies (AFBAC), the genotype relative risk (GRR) and the transmission disequilibrium test (TDT). Data for case and control samples were analysed by chi-square-test, GRR and odds ratio (OR). No significant differences between alleles and genotypes frequencies were detected in French trio and Tunisian patients with RA and controls, either with CARD8 or with NLRP3 SNPs both in French and in Tunisian populations. Moreover, stratifying patients according to the presence of rheumatoid factor (RF), anti-cyclic peptides antibodies (ACPA), erosion, nodules, other autoimmune disease or HLA-DRB1*04-positive subgroups did not show any significant association with CARD8 or NLRP3 (P ≥ 0.05). This study suggests that variations in the innate immunity genes CARD8 (p.C10X) and NLRP3 (p.Q705K) have no effect on RA susceptibility either in the Tunisian or in the French population.

Signal transducer and activator of transcription and the risk of rheumatoid arthritis and thyroid autoimmune disorders.

OBJECTIVES: The signal transducer and activator of transcription 4 (STAT4) gene localised on chromosome 2q32.2-q32.3 is known to be essential for mediating responses to interleukin 12 in lymphocytes and regulating the differentiation of T helper cells. The aim of this study was to investigate the role of the STAT4 gene in susceptibility to rheumatoid arthritis (RA) and autoimmune thyroid diseases (AITDs) in Tunisian case control studies. METHODS: Genotyping of STAT4 rs7574865 single nucleotide polymorphism (SNP) was performed in 140 patients affected with RA, 159 patients affected with AITDs and 200 healthy controls using TaqMan® allelic discrimination assay. Data were analysed by χ2-test, genotype relative risk (GRR) and odds ratio (OR). RESULTS: Our results revealed that frequencies of the T allele and the T/T genotype were significantly higher among RA patients compared to controls (p=0.008; p=0.003, respectively). However, no significant associations with the risk of autoimmune thyroid diseases were detected. Moreover, the stratification of RA patients subgroups revealed a significant association of both T allele and T/T genotype in patients presented erosion (p=0.003; p=0.004, respectively) as well as anti-cyclic peptides-negative RA (ACPA-) (p=0.002; p=0.0003, respectively). Furthermore, genotypic association was found according to the absence of rheumatoid factor antibody (RF) (p=0.0014). But, no significant differences in allele and genotype frequencies of STAT4 rs7574865 polymorphism were detected according to the presence of another autoimmune disease, nodules and in HLA-DRB1*04 and HLA-DRB1*0404 positive subgroups. CONCLUSIONS: Our results support involvement of the STAT4 gene in the genetic susceptibility to RA but not to AITDs in the Tunisian population.

Two missense mutations in SLC26A4 gene: a molecular and functional study.

Mutations in the SLC26A4 gene encoding pendrin, an anion transporter, are responsible for non-syndromic hearing loss (HL) (DFNB4) and Pendred syndrome (PS). PS is a genetic disorder that causes early HL and affects the thyroid gland. Here, we report eight Tunisian families affected with profound HL. Clinical investigations revealed goiter in few patients. Genotyping using microsatellite makers showed linkage to SLC26A4, and missense mutations p.L445W and p.M147T were identified by sequencing and polymerase chain reaction-restriction fragment length polymorphism. The p.L445W mutation segregated in seven families and haplotype analysis suggested its founder effect. In order to understand the molecular pathogenic mechanisms of p.L445W and p.M147T mutations, SLC26A4 wild-type and mutant cDNA constructs were transiently expressed in COS7 cells and several human cell lines including Thyroid 8305C cells. Reverse transcription-PCR, western blot and immunofluorescence demonstrated that these two mutations abolished complex glycosylation of pendrin and prevented its targeting to the plasma membrane.

[Risk factors for hospital mortality during pulmonary embolism]. / Facteurs de risque de mortalité hospitalière au cours de l'embolie pulmonaire en milieu de pneumologie.

OBJECTIVES: The objective of our work is to identify the risk factors for hospital mortality during pulmonary embolism in a pneumology department. MATERIAL AND METHOD: All patients admitted to the pneumology department of Habib-Bourguiba hospital between 2014 and 2019, with a final diagnosis of PE are analyzed. RESULTS: One hundred patients were included, 62% of whom were female, with an average age of 63±16 years. Pulmonary fibrosis was noted in eight patients. On admission, the mean Simplified Pulmonary Embolism Severity Index score was 1.46±1.05. The mean duration of hospitalization was 10.6±7 days. The hospital mortality rate was 12%. The independent risk factors for intra-hospital mortality were arterial hypotension (OR: 6.13; 95%CI: 2.88-14.35; p=0.001), cancer (OR: 2.66; 95%CI: 1.22-9.54; p=0.026), a VD/LV ratio at echocardiography>0.9 (OR: 1.84; 95%CI: 1.06-7.69; p=0.039) and severe hypoxemia (OR: 4.86; 95%CI: 2.19-11,34; p=0.006). CONCLUSION: Pulmonary embolism mortality remains high despite improvements in diagnostic and therapeutic management. It is important for our country to take these results into consideration for a better management of patients admitted for pulmonary embolism, and to improve survival.

Autoimmune thyroid diseases: genetic susceptibility of thyroid-specific genes and thyroid autoantigens contributions.

Autoimmune thyroid diseases are common polygenic multifactorial disorders with the environment contributing importantly to the emergence of the disease phenotype. Some of the disease manifestations, such as severe thyroid-associated ophthalmopathy, pretibial myxedema and thyroid antigen/antibody immune complex nephritis are unusual to rare. The spectrum of autoimmune thyroid diseases includes: Graves' disease (GD), Hashimoto's thyroiditis (HT), atrophic autoimmune thyroiditis, postpartum thyroiditis, painless thyroiditis unrelated to pregnancy and thyroid-associated ophthalmopathy. This spectrum present contrasts in terms of thyroid function, disease duration and spread to other anatomic location. The genetic basis of autoimmune thyroid disease (AITD) is complex and likely to be due to genes of both large and small effects. In GD the autoimmune process results in the production of thyroid-stimulating antibodies and lead to hyperthyroidism, whereas in HT the end result is destruction of thyroid cells and hypothyroidism. Recent studies in the field of autoimmune thyroid diseases have largely focused on (i) the genes involved in immune response and/or thyroid physiology with could influence susceptibility to disease, (ii) the delineation of B-cell autoepitopes recognized by the main autoantigens, thyroglobulin, thyroperoxidase and TSH receptor, to improve our understanding of how these molecules are seen by the immune system and (iii) the regulatory network controlling the synthesis of thyroid hormones and its dysfunction in AITD. The aim of the present review is to summarize the current knowledge regarding the relation existing between some susceptibility genes, autoantigens and dysfunction of thyroid function during AITD.

[Predisposition to autoimmune thyroid diseases within a Tunisian multiplex family]. / Prédisposition aux maladies auto-immunes thyroïdiennes au sein d'une famille tunisienne multiplexe.

The autoimmune thyroid diseases (AITDs) are multifactorial diseases which result from interplays between predisposing genes and triggering environmental factors. In order to study the genetic susceptibility factors to AITDs, we have followed up 115 control members belonging to a large Tunisian family with a high prevalence of AITDs (Akr family) during 15 years between 1990 to 2005. The follow-up of these control members have showed that 13 subjects (11.3%) developed AITDs (G2). The Hashimoto thyroiditis was the most frequently seen in 77% of the cases, whereas the Graves's disease was present in 23% of the cases. One hundred and two members remained controls (G1). High female predominance was noted in the two groups. The mean age of the G1 subjects group was slightly higher than that of G2. The prevalence of positive antithyroglobulin antibody (TgAb) and antithyroperoxydase antibody (TPOAb) was more frequent in G2 group (P=0.27 and P=0.23) respectively. The HLA haplotypes was realized in 42% of control members. The most frequent HLA haplotypes that were found were B37, DRB11 and A1. HLA B37 and DRB11 were significantly more frequent for the patients of G2 (P=0.0001 and P=0.034) respectively. Our study confirms the contribution of the genetic factors in the development of AITDs in 'Akr' family and suggested that the members of this family share the same genetic inheritance.

[Excavated pulmonary opacity in diabetes]. / Une opacité pulmonaire excavée chez un diabétique.

Mucormycosis or zygomycosis is a group of infections caused by filamentous fungi of the mucorales order belonging to the zygomycetes family. They generally appear in patients with uncontrolled diabetes or immunodepression, especially neutropenic immunodepression. Incidence has increased with progress in immunosuppressive therapy and chemotherapy and the absence of the use of antifungal prophylactic agents effective against mucors. We report the case of a diabetic patient presenting with an excavated opacity in the right lung which failed to improve after receiving non-specific antibiotic treatment. Direct examination of the bronchial washing specimen led to the diagnosis of pulmonary mucormycosis. Prognosis depends mainly on early diagnosis, enabling appropriate treatment with amphotericin B. Mortality remains high, around 80%; diagnosis is commonly established post-mortem.

[A rare localization of solitary plasmocytoma]. / Une localisation rare de plasmocytome solitaire.

INTRODUCTION: Solitary bone plasmocytoma is rare, characterized by malignant plasmocyte proliferation, derived from a sole B lymphocyte clone located on a bony segment without medullar invasion. It, above all, affects the thoracolumbar spine. Costal involvement is rarely described. CASE REPORT: The authors report the case of a 60-year-old man who complained of dyspnea, dry cough, and thoracic pain four months before admission. Thoracic imaging revealed a left apical tissue mass with osteolysis of the first rib. A transparietal biopsy of the mass was not helpful. Surgical biopsy concluded as to the diagnosis of costal plasmocytoma. All of the examinations carried out to search for other localizations were negative confirming the solitary nature of the tumor. The treatment consisted of complementary radiotherapy at a dose of 45Gy. The patient was in remission after eight months. CONCLUSION: Solitary costal plasmocytoma should be called to mind when confronted with a lytic tumor of the rib. The treatment is based on surgery and radiotherapy. The prognosis is dominated by the risk of progression to multiple myeloma.

[Postpartum pericardic tamponade revealing systemic lupus erythematosus]. / Tamponnade péricardique en postpartum révélatrice d'un lupus érythémateux systémique.

Pericarditis is the most common manifestation of systemic lupus erythematosus and is clinically found in 62% of the autopsies. Cardiac tamponade is a deadly but rare complication found in less than 1% of all lupus cases. It is highly revealing. The authors report the case of a 29-year old woman presenting postpartum cardiac tamponade. The diagnosis of systemic lupus erythematosus was based on the association of haematological disorders (anaemia and leukopenia), pericarditis, pleurisy and positive anti-nuclear and anti-native DNA antibodies. The patient was treated with pericardiac drainage and cortisone therapy. The evolution was favourable after 22 months. Using this case study, the authors note the rarity of cardiac tamponade as a manifestation inaugurating lupus and discuss the relationship between pregnancy and lupus disease.

[Lung abscess: Diagnosis and management]. / Abcès du poumon : diagnostic et prise en charge.

Lung abscesses are necrotic cavitary lesions of the lung parenchyma. They are usually caused by anaerobic bacteria or mixed flora and typically occur after aspiration. Primary lung abscesses occur in previously healthy patients with no underlying medical disorders and are usually solitary. Secondary lung abscesses occur in patients with underlying or predisposing conditions and may be multiple. The initial diagnosis is usually made by chest radiography showing a lung cavity with an air-fluid level. Typically, the cavity wall is thick and irregular, and a surrounding pulmonary infiltrate is often present. The differential diagnosis of pulmonary cavitation is wide, including different types of possible infections, neoplasia and malformations of the bronchial tree. Management is usually based on prolonged antibiotic treatment. Failure of conservative management, manifested by the persistence of sepsis and/or other abscess complications, may necessitate drainage with invasive techniques (percutaneous, endoscopic or surgical) or open surgical removal of the lung lesion in patients with good performance status and sufficient respiratory reserve.

Association of IRF5 gene polymorphisms with rheumatoid arthritis in a Tunisian population.

OBJECTIVE: A strong genetic association of rheumatoid arthritis (RA) with the interferon regulatory factor 5 (IRF5) gene has been described previously in a Swedish population, although this result was not confirmed in a French population. We undertook an association study between IRF5 and the RA phenotype, as well as a study with serological markers of RA, in a Tunisian population. METHODS: A single-nucleotide polymorphism (SNP; rs2004640) was genotyped using a Taqman 5' allelic discrimination assay on an ABI 7500 real-time polymerase chain reaction (PCR) instrument in 140 RA patients and 185 controls. Rheumatoid factor (RF) and anti-citrullinated protein/peptide antibodies (ACPA) were determined by enzyme-linked immunosorbent assay (ELISA). Association was assessed based on the chi(2) test and odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: The frequency of the TT genotype of the IRF5 SNP rs2004640 differed significantly between patients and controls (p = 0.01). This difference was greater when a subgroup of patients with another 'autoimmune' disorder was considered (p = 0.007). A weak but significant association was also found in a subgroup of patients who were positive for ACPA (p = 0.04) or erosion (p = 0.01). CONCLUSIONS: Our results indicate that the TT genotype of the IRF5 (rs2004640) dimorphism is associated with RA in a Tunisian population.

Association of calpain-10 polymorphisms with type 2 diabetes in the Tunisian population.

BACKGROUND: Genome-wide analyses of the genetic predisposition to type 2 diabetes mellitus (T2DM) in different isolates and populations have identified regions of interest called non insulin-dependent diabetes mellitus (NIDDM) 1, 2, 3 and 4. At the NIDDM1 locus (2q37.3), calpain-10 (CAPN10) encodes for a ubiquitously expressed protease implicated in the two fundamental pathophysiological aspects of T2DM. This is a report of the results of a study of the association of four CAPN10 polymorphisms with T2DM in the Tunisian population. PARTICIPANTS AND METHODS: A total of 222 T2DM patients with a diabetes duration of 10 years or more and 206 healthy controls were enrolled to analyze the frequency distribution of four CAPN10 polymorphisms (UCSNP-43, UCSNP-19, UCSNP-110 and UCSNP-63) using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in the Tunisian population. We also investigated the association of T2DM with different haplotypes and haplotype combinations. RESULTS: Only the A allele of UCSNP-43 showed an association with T2DM (odds ratio, OR=1.86). We also identified a novel combination of haplotypes (121/221) defined by three polymorphisms (UCNSP-43, -19 and -63) that is associated with an increased risk of T2DM (OR=2.38). CONCLUSION: In this study involving the Tunisian population, we identified genetic variants within CAPN10 that are linked with T2DM and a novel haplotype combination, 121/221, associated with an increased susceptibility to T2DM.

Risk genotypes and haplotypes of the GLUT1 gene for type 2 diabetic nephropathy in the Tunisian population.

OBJECTIVE: Diabetic nephropathy (DN) is a long-term complication of both type 1 and type 2 diabetes. Genetic studies on DN have been of little help so far, since several genetic association studies have shown conflicting results. Here we report the findings of a case-control study on five SNPs in the glucose transporter 1 (GLUT1) gene. The study investigated the association of five GLUT1 genotypes and haplotypes with DN. RESEARCH DESIGN AND METHODS: All subjects, 126 DN (cases) and 273 type 2 diabetes (controls), were genotyped using the polymerase chain reaction restriction fragment length polymorphism. RESULTS: The TT and the AA genotypes of the Haell and Enh2 SNP1, increased the risk of DN. The study also identified CGT as the highest risk haplotype (4.4-fold) followed by CAT with an increased risk of DN of 2.6-fold. CONCLUSIONS: The GLUT1 gene confers susceptibility to DN in type 2 diabetes patients in the Tunisian population.

Prognostic Value of BCL2 in Women Patients with Invasive Breast Cancer

Background: Breast cancers are heterogeneous, making it essential to recognize several biomarkers for cancer outcome predictions especially in young women where the classical prediction parameters are not suitable. The goal from this study is to evaluate the impact of B cell lymphoma 2 (BCL2), P53 and Ki-67 proteins expression on survival in young women patients with invasive ductal carcinoma. Patients and methods: Samples and clinical data from 238 patients were collected between 2003 and 2017. They were selected according to 2 criteria: age ≤40 years old and most of them are affected by an Invasive Ductal Carcinoma. We evaluated BCL2, P53 and ki-67 expression by immunochemistry test, and then we assessed correlations of these biomarkers expression with patient's clinicopathological characteristics and survival. Results: Triple negative breast cancer group showed a high frequency among our cohort but we emphasize an almost equitable distribution among all molecular groups. Contrary to other studies which reported that luminal A was correlated with better prognosis, our analysis demonstrated that luminal A is correlated with the Scarff, Bloom and Richardson (SBR) grading 2 or SBR grading 3. To better investigate the prognosis, we analyze three biomarkers known by their impact on physiopathology behavior on breast cancer BCL2, ki-67and P53. BCL2 is the more relevant one, it was correlated with molecular subtypes (p=0.0012) and SBR grading (p=0.0016). BCL2 seems to be the good prognostic biomarker related to survival (p=0.004) with a protective role among patients when endocrine therapy is not provided and Lymph Node (LN) involvement is positive (p=0.021, p=0.000 respectively). Conclusions: The classical prognostic parameters based mainly on the molecular classification in breast cancer seem insufficient in the case of young women. BCL2 protein expression analysis provides a better prognostic value. BCL2 should be clinically associated in current practice when young women specimens are diagnosticated.