Objectives To establish the rates of publication and reporting of results for interventional clinical trials across Polish academic medical centres (AMCs) completed between 2009 and 2013. We aim also to compare the publication and reporting success between adult and paediatric trials. Design Cross-sectional study. Setting AMCs in Poland. Participants AMCs with interventional trials registered on ClinicalTrials.gov. Main outcome measure Results reporting on ClinicalTrials.gov and publishing via journal publication. Results We identified 305 interventional clinical trials registered on ClinicalTrials.gov, completed between 2009 and 2013 and affiliated with at least one AMC. Overall, 243 of the 305 trials (79.7%) had been published as articles or posted their summary results on ClinicalTrials.gov. Results were posted within a year of study completion and/or published within 2 years of study completion for 131 trials (43.0%). Dissemination by both posting and publishing results in a timely manner was achieved by four trials (1.3%). Conclusions Our cross-sectional analysis revealed that Polish AMCs fail to meet the expectation for timely disseminating the findings of all interventional clinical trials. Delayed dissemination and non-dissemination of trial results negatively affects decisions in healthcare.

Polycystic ovary syndrome (PCOS) is a common female endocrinopathy associated with reproductive and metabolic abnormalities. PCOS is characterized by complex pathogenesis and pathophysiology. Its multifactorial etiology and heterogeneous presentation make effective treatment difficult. Endocrine abnormalities in PCOS create a vicious cycle of overriding dysfunction involving the hypothalamic-pituitary-ovarian (HPO) axis. Most research has primarily focused on identifying genetic, epigenetic, or immunological factors underlying PCOS. In recent years, new reports have emerged on the possible involvement of antibodies directed against HPO axis components in the development of PCOS. Some of these have been shown to be able to interfere with hormone receptors or receptor binding by targeting the key domains for their function. However, the evidence is heterogeneous and challenging to interpret, given the overall predisposition to high levels of various autoantibodies found in women with PCOS. This review focuses on autoantibodies affecting the HPO axis in PCOS and their potential role in the pathogenesis of PCOS. The authors discuss PCOS as a potential antibody-mediated autoimmune disease in light of recent reports on its possible pathogenesis.

Background For research with human participants to be ethical, risk must be in a favorable balance with potential benefits. Little is known about the risk/benefit ratio for pediatric cancer phase II trials testing targeted therapies. Objective Our aim was to conduct a systematic review of preliminary efficacy and safety profiles of phase II targeted therapy clinical trials in pediatric oncology. Methods Our protocol was prospectively registered in PROSPERO (CRD42020146491). We searched EMBASE and PubMed for phase II pediatric cancer trials testing targeted agents. We included solid and hematological malignancy studies published between 1 January, 2015 and 27 February, 2020. We measured risk using drug-related grade 3 or higher adverse events, and benefit by response rates. When possible, data were meta-analyzed. All statistical tests were two-sided. Results We identified 34 clinical trials (1202 patients) that met our eligibility criteria. The pooled overall response rate was 24.4% (95% confidence interval [CI] 14.5–34.2) and was lower in solid tumors, 6.4% (95% CI 3.2–9.6), compared with hematological malignancies, 55.1% (95% CI 35.9–74.3); p < 0.001. The overall fatal drug-related (grade 5) adverse event rate was 1.6% (95% CI 0.6–2.5), and the average drug-related grade 3/4 adverse event rate per person was 0.66 (95% CI 0.55–0.78). Conclusions We provide an estimate for the risks and benefits of participation in pediatric phase II cancer trials. These data may be used as an empirical basis for informed communication about benefits and burdens in pediatric oncology research.

Objectives: Human papillomavirus (HPV) infection is one of the most common sexually transmitted diseases. Long-term exposure to the HPV is a known cause of squamous intraepithelial lesions that consequently lead to cervical cancer development. The loop electrosurgical excision procedure (LEEP) conization is an established early cervical cancer treatment method. We aim to assess the remission of HPV infection after LEEP in non-vaccinated patients with pre-cancerous cervical lesions and establish the efficacy of cervical cancer prophylaxis. Material and methods: We analyzed 31 LEEP conizations performed due to low and high-grade squamous intraepithelial lesions in 2019–2020. We obtained molecular test samples and detected DNA of 37 different HPV genotypes. After a six-month follow-up, each patient underwent subsequent high-risk HPV testing and genotyping. Results: We observed that 54.8% of qualified patients were infected with HPV 16. We discovered complete viral remission in 64.5% of cases. After surgery, margins were negative in 71% of the patient's samples. During the follow-up, six patients got infected with new strains of HPV. Conclusions: We found that a correctly performed LEEP conization may contribute to the remission of persistent HPV infection; a more extended follow-up period might be recommended due to a high rate of post-surgery HPV infections. Objectives: Human papillomavirus (HPV) infection is one of the most common sexually transmitted diseases. Long-term exposure to the HPV is a known cause of squamous intraepithelial lesions that consequently lead to cervical cancer development. The loop electrosurgical excision procedure (LEEP) conization is an established early cervical cancer treatment method. We aim to assess the remission of HPV infection after LEEP in non-vaccinated patients with pre-cancerous cervical lesions and establish the efficacy of cervical cancer prophylaxis. Material and methods: We analyzed 31 LEEP conizations performed due to low and high-grade squamous intraepithelial lesions in 2019–2020. We obtained molecular test samples and detected DNA of 37 different HPV genotypes. After a six-month follow-up, each patient underwent subsequent high-risk HPV testing and genotyping. Results: We observed that 54.8% of qualified patients were infected with HPV 16. We discovered complete viral remission in 64.5% of cases. After surgery, margins were negative in 71% of the patient's samples. During the follow-up, six patients got infected with new strains of HPV. Conclusions: We found that a correctly performed LEEP conization may contribute to the remission of persistent HPV infection; a more extended follow-up period might be recommended due to a high rate of post-surgery HPV infections.

Polycystic ovary syndrome (PCOS) is a prevalent endocrinological condition among women of reproductive age, characterized by several well-known symptoms, including hyperandrogenism, anovulation, irregular menstrual cycles, and insulin resistance. In addition, women suffering from PCOS are also at an increased risk of developing several autoimmune diseases, including thyroid disorders, type 1 diabetes, and rheumatoid arthritis. Furthermore, an elevated prevalence of diverse autoantibodies is observed in women diagnosed with PCOS. These include antibodies specific to autoimmune diseases, e.g., anti-thyroid peroxidase (anti-TPO), anti-thyroglobulin (anti-TG), and antinuclear antibodies (ANAs), as well as those that are non-specific, such as anti-malondialdehyde-modified human serum albumin (anti-HSA-MDA) or anti-α-crystallin. It appears that several mechanisms may be responsible for this phenomenon. PCOS has been observed to co-occur with autoimmune diseases, potentially attributable to shared genetic susceptibility or the presence of hormonal disorders resulting from autoimmune diseases. Moreover, PCOS is a chronic low-grade inflammatory disease that may contribute to immune dysfunction and subsequent overproduction of autoantibodies. A further intriguing aspect may be the yet-unknown role of autoantibodies in the pathogenesis of PCOS, considering PCOS as a disease with an autoimmune etiology.

STUDY QUESTION: Does polycystic ovary syndrome influence the morphology of the uterus and the prevalence of congenital uterine anomalies? SUMMARY ANSWER: Available evidence of very low quality shows a possible association between PCOS and some uterine anomalies. WHAT IS KNOWN ALREADY: Congenital uterine malformations range from subtle changes in uterine shapes to major morphologic deformities It is postulated that major anomalies result from the abnormal development of Mullerian ducts. However, the etiology of minor deformities is a subject of speculation. Many factors may impact the development of the uterus and its morphology in utero and after birth. Many researchers have reported on the increased prevalence of uterine anomalies in PCOS patients, yet the synthesis of evidence has not been performed. STUDY DESIGN, SIZE, DURATION: A systematic review and meta-analysis were performed. We systematically searched the PubMed, Scopus, Embase, and Cochrane Library databases using a complex search strategy including terms such as e.g. ‘uterus’, ‘polycystic ovary syndrome’, ‘morphology’, ‘dimensions’, ‘congenital uterine anomalies’, and their synonyms. No language or date restrictions were applied during the literature search. The meta-analysis was based on odds ratio (OR) and 95% CIs using the Mantel–Haenszel random effects model. PARTICIPANTS/MATERIALS, SETTING, METHODS: The primary outcomes included uterine malformations, dimensions, and volume, assessed using non-invasive and invasive methods in observational studies comparing PCOS and non-PCOS patients. We excluded case reports, case series, reviews, studies without control groups, and articles reporting exclusively on polycystic ovary morphology. The modified Newcastle–Ottawa scale was used to assess the quality of the included research. MAIN RESULTS AND THE ROLE OF CHANCE: Our search retrieved 1929 identified publications, 11 of which were included in the systematic review (10 581 women). The majority of the studies were of poor quality. PCOS was associated with higher prevalence of uterine anomalies (OR = 5.96; 95% CI = 1.22–29.17, P = 0.028). The general count of uterine malformations was significantly higher in the PCOS group (25.0%, 95% CI 6.9–43.2, range 0–49%) than in the non-PCOS group (5.3%, 95% CI 0.5–14.8, range 0–23.1%). The studies had a very high heterogeneity. The scope of uterine malformations possibly linked to PCOS included septate, didelphys, I-shaped (morphology that is not recognized by any main classifications), and dysmorphic uteri. The septate uterus was the most often reported malformation. Altered dimensions included fundal indentation depth and angle. Available research used four classification systems: the most frequently reported was that of the American Fertility Society 1988 (3/11). Six studies did not use any classification. The assessment methods included 2- and 3-dimensional ultrasound, magnetic resonance imagining, hysterosalpingography, laparoscopy, and hysteroscopy. LIMITATIONS, REASONS FOR CAUTION: Most of the available studies are of very low quality, use inadequate assessment methods and classifications, and are prone to a high risk of selection bias. Additionally, the differences between PCOS phenotypes and their hormonal aspects are poorly addressed and do not sufficiently explain the etiology of observed changes. The included research displays a varying level of heterogeneity. WIDER IMPLICATIONS OF THE FINDINGS: Further research is needed to (i) confirm whether the association between uterine anomalies and PCOS is clinically relevant, (ii) evaluate whether the prevalence of the uterine anomalies varies between women with different hormonal disturbances (e.g. hyperandrogenism), (iii) assess the benefit of any intervention for uterine anomalies in women with PCOS. STUDY FUNDING/COMPETING INTEREST(S): This study received no funding. The authors have no conflicts to disclose. REGISTRATION NUMBER: CRD42024527964; http://www.crd.york.ac.uk/prospero/