Human papilloma viruses (HPVs) belong to the Papillomaviridae family and are epitheliotropic infecting squamous epithelia (skin and mucosae). HPV is estimated to be the cause of 99% of cervical cancers (there is no evidence of significant genetic predisposition for cervical cancer), 90% of anal cancer, 65% vaginal cancers, 50% vulvar cancers, and 45‑90% oropharyngeal cancers. The route of HPV transmission is primarily through skin‑to‑skin or skin‑to‑mucosa contact. Sexual transmission is the most documented, but there have been studies suggesting non‑sexual courses. The horizontal transfer of HPV includes fomites, fingers, and mouth, skin contact (other than sexual). Self‑inoculation is described in studies as a potential HPV transmission route, as it was certified in female virgins, and in children with genital warts (low‑risk HPV) without a personal history of sexual abuse. Vertical transmission from mother to child is another HPV transfer course. Several studies have emphasized the possibility of infection through the amniotic fluid, or the placenta, or via contact with maternal genital mucosa during natural birth. Waterborne transmission of HPV has never been demonstrated; however, HPV DNA has been detected in water environments. Routine hygiene measures are proven to be inefficient in preventing HPV transmission, as the studies which have evaluated samples of HPV on contaminated medical equipment (after standard disinfection) have found them to be still positive. Annual costs associated with the morbidity and mortality of HPV‑related diseases are estimated at approximately $4 billion. Once the HPV vaccine program in Australia was launched, many studies reported the initial effects: A decrease in the incidence of high‑grade cervical abnormalities, no new genital warts cases in females under 21 years. Promoting greater understanding in the general public about the evident benefits of vaccination can create positive vaccine attitudes and scatter the myths of spurious side effects.

Endocrine‑disrupting chemicals (EDCs) are exogenous chemical compounds ubiquitously found in everyday life of the modern world. EDCs enter the human body where they act similarly to endogenous hormones, altering the functions of the endocrine system and causing adverse effects on human health. Bisphenol A (BPA), the principal representative of this class, is a carbon‑based synthetic plastic, and a key element in manufacturing cans, reusable water bottles and medical equipment. BPA mimics the actions of estrogen on multiple levels by activating estrogen receptors α and β. BPA regulates various processes, such as cell proliferation, migration and apoptosis, leading to neoplastic changes. Considering genetic mechanisms, BPA exerts its functions via multiple oncogenic signaling pathways, including the STAT3, PI3K/AKT and MAPK pathways. Furthermore, BPA is associated with various modifications of the reproductive system in both males and females. These alterations include benign lesions, such as endometrial hyperplasia, the development of ovarian cysts, an increase in the ductal density of mammary gland cells and other preneoplastic lesions. These benign lesions may continue to develop to breast or ovarian cancer; the effects of BPA depend on various molecular and epigenetic mechanisms that dictate whether the endocrine or reproductive system is impacted, wherein preexisting benign lesions can become cancerous. The present review supports the need for continuous research on BPA, considering its widespread use and most available data suggesting a carcinogenic effect of BPA on the female reproductive system. Although most studies on BPA have been conducted in vitro with human cells or in vivo with animal models, it can be argued that more studies should be conducted in vivo with humans to further promote understanding of the impact of BPA.

HELLP syndrome, also known as the syndrome of hemolysis, elevated liver enzymes, and low platelets, represents a severe pregnancy complication typically associated with hypertension. It is associated with increased risks of adverse complications for both mother and fetus. HELLP occurs in 0.2–0.8% of pregnancies, and, in 70–80% of cases, it coexists with preeclampsia (PE). Both of these conditions show a familial tendency. A woman with a history of HELLP pregnancy is at high risk for developing this entity in subsequent pregnancies. We cannot nominate a single worldwide genetic cause for the increased risk of HELLP. Combinations of multiple gene variants, each with a moderate risk, with concurrent maternal and environmental factors are thought to be the etiological mechanisms. This review highlights the significant role of understanding the underlying pathophysiological mechanism of HELLP syndrome. A better knowledge of the disease’s course supports early detection, an accurate diagnosis, and proper management of this life-threatening condition.

Beta-thalassemia (BTH), a recessively inherited haemoglobin (Hb) disorder, causes iron overload (IO), extra-medullary haematopoiesis and bone marrow expansion with major clinical impact. The main objective of this review is to address endocrine components (including aspects of reproductive health as fertility potential and pregnancy outcome) in major beta-thalassemia patients, a complex panel known as thalassemic endocrine disease (TED). We included English, full-text articles based on PubMed research (January 2017–June 2022). TED includes hypogonadism (hypoGn), anomalies of GH/IGF1 axes with growth retardation, hypothyroidism (hypoT), hypoparathyroidism (hypoPT), glucose profile anomalies, adrenal insufficiency, reduced bone mineral density (BMD), and deterioration of microarchitecture with increased fracture risk (FR). The prevalence of each ED varies with population, criteria of definition, etc. At least one out of every three to four children below the age of 12 y have one ED. ED correlates with ferritin and poor compliance to therapy, but not all studies agree. Up to 86% of the adult population is affected by an ED. Age is a positive linear predictor for ED. Low IGF1 is found in 95% of the population with GH deficiency (GHD), but also in 93.6% of persons without GHD. HypoT is mostly pituitary-related; it is not clinically manifested in the majority of cases, hence the importance of TSH/FT4 screening. HypoT is found at any age, with the prevalence varying between 8.3% and 30%. Non-compliance to chelation increases the risk of hypoT, yet not all studies confirmed the correlation with chelation history (reversible hypoT under chelation is reported). The pitfalls of TSH interpretation due to hypophyseal IO should be taken into consideration. HypoPT prevalence varies from 6.66% (below the age of 12) to a maximum of 40% (depending on the study). Serum ferritin might act as a stimulator of FGF23. Associated hypocalcaemia transitions from asymptomatic to severe manifestations. HypoPT is mostly found in association with growth retardation and hypoGn. TED-associated adrenal dysfunction is typically mild; an index of suspicion should be considered due to potential life-threatening complications. Periodic check-up by ACTH stimulation test is advised. Adrenal insufficiency/hypocortisolism status is the rarest ED (but some reported a prevalence of up to one third of patients). Significantly, many studies did not routinely perform a dynamic test. Atypical EM sites might be found in adrenals, mimicking an incidentaloma. Between 7.5–10% of children with major BTH have DM; screening starts by the age of 10, and ferritin correlated with glycaemia. Larger studies found DM in up to 34%of cases. Many studies do not take into consideration IGF, IGT, or do not routinely include OGTT. Glucose anomalies are time dependent. Emerging new markers represent promising alternatives, such as insulin secretion-sensitivity index-2. The pitfalls of glucose profile interpretation include the levels of HbA1c and the particular risk of gestational DM. Thalassemia bone disease (TBD) is related to hypoGn-related osteoporosis, renal function anomalies, DM, GHD, malnutrition, chronic hypoxia-induced calcium malabsorption, and transplant-associated protocols. Low BMD was identified in both paediatric and adult population; the prevalence of osteoporosis/TBD in major BTH patients varies; the highest rate is 40–72% depending on age, studied parameters, DXA evaluation and corrections, and screening thoracic–lumbar spine X-ray. Lower TBS and abnormal dynamics of bone turnover markers are reported. The largest cohorts on transfusion-dependent BTH identified the prevalence of hypoGn to be between 44.5% and 82%. Ferritin positively correlates with pubertal delay, and negatively with pituitary volume. Some authors appreciate hypoGn as the most frequent ED below the age of 15. Long-term untreated hypoGn induces a high cardiovascular risk and increased FR. Hormonal replacement therapy is necessary in addition to specific BTH therapy. Infertility underlines TED-related hormonal elements (primary and secondary hypoGn) and IO-induced gonadal toxicity. Males with BTH are at risk of infertility due to germ cell loss. IO induces an excessive amount of free radicals which impair the quality of sperm, iron being a local catalyser of ROS. Adequate chelation might improve fertility issues. Due to the advances in current therapies, the reproductive health of females with major BTH is improving; a low level of statistical significance reflects the pregnancy status in major BTH (limited data on spontaneous pregnancies and growing evidence of the induction of ovulation/assisted reproductive techniques). Pregnancy outcome also depends on TED approach, including factors such as DM control, adequate replacement of hypoT and hypoPT, and vitamin D supplementation for bone health. Asymptomatic TED elements such as subclinical hypothyroidism or IFG/IGT might become overt during pregnancy. Endocrine glands are particularly sensitive to iron deposits, hence TED includes a complicated puzzle of EDs which massively impacts on the overall picture, including the quality of life in major BTH. The BTH prognostic has registered progress in the last decades due to modern therapy, but the medical and social burden remains elevated. Genetic counselling represents a major step in approaching TH individuals, including as part of the pre-conception assessment. A multidisciplinary surveillance team is mandatory.

Postpartum depression (PPD) is a disabling condition that has recently shown an increase in prevalence, becoming an essential public health problem. This study is a qualitative review summarizing the most frequent risk factors associated with PPD, evaluating molecular aspects of PPD and current approaches to detect and prevent PPD. The most prevalent risk factors were detected in the areas of economic and social factors, obstetrical history, lifestyle, and history of mental illness. Research on the genetic basis for PPD has taken place in recent years to identify the genes responsible for establishing targeted therapeutic methods and understanding its pathogenesis. The most frequently studied candidate gene was the serotonin transporter gene (SERT) associated with PPD. Among biological studies, antidepressants and psychological interventions provided the most evidence of successful intervention. The obstetrician can serve an essential role in screening for and treating PPD. Postpartum women with risk factors should be screened using the Edinburgh Postnatal Depression Scale (EPDS), but, at the moment, there are no prevention programs in Europe. In conclusion, data from this review increase concerns among this vulnerable population and can be used to design a screening tool for high-risk pregnant women and create a prevention program.

Urinary tract infections (UTIs) represent a frequent pathology among the female population that has become more and more difficult to treat in the past decade, considering the increase in antibiotic resistance—a serious global public health problem. A cross-sectional retrospective study was conducted for six months to report an update regarding the rates of resistance and susceptibility of uropathogens necessary for optimal treatment. A total of 5487 patients were screened, of which 524 (9.54%) were female patients who met the criteria for inclusion in the study. Escherichia coli was the most common pathogen, representing 290 cases (55.34%), followed by Enterococcus spp. 82 (15.64%). Escherichia coli presented the highest resistance to amoxicillin-clavulanic acid (R = 33.1%), followed by trimethoprim-sulfamethoxazole (R = 32.41%) and levofloxacin (R = 32.06%). The highest sensitivity rates were observed for fosfomycin (S = 96.55%), followed by imipenem (S = 93.1%). Enterococcus spp. showed the highest resistance to levofloxacin (R = 50.0%), followed by penicillin (R = 39.02%). The highest sensitivity was observed for fosfomycin (S = 90.24%), linezolid (S = 89.02%), and nitrofurantoin (S = 86.58%). The second most frequent Gram-negative uropathogen was represented by Klebsiella spp., which had the highest resistance to amoxicillin-clavulanic acid (R = 35.89%), followed by levofloxacin (R = 25.64) and trimethoprim-suflamethoxazole (R = 24.35%). The most frequently associated pathology was an episode of UTI in the previous year, followed by diabetes and chronic kidney disease. Antibiotic resistance is a serious problem for all clinicians who treat UTIs. An up-to-date knowledge of antibiotic resistance rates is a major necessity to stop its evolution. Overall, the highest resistance rates were observed for aminopenicillins, fluoroquinolones, and trimethoprim-sulfamethoxazole. The best susceptibility rates were observed for fosfomycin, nitrofurantoin, and carbapenems. Our report aims to guide clinicians whenever they are forced to prescribe antibiotics empirically.