Urinary tract infections (UTIs) are among the most common human infections, second only to respiratory tract infections. Women are about 50 times more likely to develop UTIs than men: in fact, about 60% of women experience at least one UTI in their life time and 20% report recurrent episodes following a first acute episode. The most frequently observed condition is cystitis, that appears as an inflammation of the bladder often associated with urethritis.
Escherichia Coli is responsible for more than 85%of urinary tract infections
Manifold risks are associated with this syndrome, as follows:
Therapy is mainly based on the administration of antibiotics.
This type of treatment is often inconclusive, especiallyin case of recurrent urinarytract infections, because ofantibiotic resistance phenomenon.
Frequent risk of recurrences which may be treated or prevented with food supplements and probiotics.In most cases, recurrent cystitis is due to a re-infection caused by the same strain.
The increased antibiotic resistance to the most frequently used antibiotics for the treatment of urinary tract infections encouraged the search for new therapeutic approaches for the treatment of these pathologies.
UTI recurrence has always been related to bacterial ability to adhere to the urothelial surface by means of specific proteins (UPI), thus exerting their pathogenic activity. Conventional therapies aimed at fighting bacterial adhesion did not show sufficient efficacy to consider bacterial adhesion the sole cause of the phenomenon.
Recent studies pointed out the role of bacterial internalization as main cause of bacterial persistence and antibiotic resistance observed for certain antimicrobial agents.
is a newly developed patented product, able to take effective action against all stages of bacterial infection, by reducing the risk of recurrences and limiting antibiotic resistance phenomena.
To treat and prevent the onset of urinary tract infections and avoid antibiotic resistance phenomena, femistina innovative patent provides the use of a triple-fit mechanism acting on the three key steps of bacterial infection process.
patent ep 2895180
Thanks to two ingredients that
• hinder E. Coli ability to adhereto epithelial cells
• act in two distinct momentsensuring a 24-hour coverage
The antibacterial activity of the two ingredients counteracts bacteria abilityto settle within urothelial cells.
By favouring externalization, the patented combination of these three ingredients exposes bacteria to antibiotic action.
Thanks to the patented triple-fit mechanism of action, the use of FEMISTINA and FEMISTINA PLUS, increases antibiotic action and decreases recurrence rate.
Polycystic ovary syndrome (PCOS) is a complex syndrome characterizedby the presence of enlarged and micropolycystic ovaries.This condition involves a number of endocrine and metabolic changesthat may lead to major health problems over the long term.It is one of the most common disorder in women of childbearing potential(6-10%) and represents one of the most frequent causes of infertility.PCOS often manifests around the time of puberty and presents withsymptoms such as menstrual disorders, hirsutism and obesity.
Manifold risks are associated with this syndrome, as follows:
such as:
ovarian dysfunctions, infertility, endometrial hyperplasia, endometrial cancer.
such as:
metabolic syndrome, gestational diabetes, type 2 diabetes, dyslipidaemia, hypertension cardiovascular risks.
such as:
poor psychological well-being, depression, anxiety, low self-esteem.
PCOS often manifests with obesity, frequently associated with a condition of hyperinsulinism related to insulin resistance, with important endocrine as well as metabolic disorders.
irregular menstrual periods (80% of cases)
amenorrhoea (50-60% of cases)
functional bleeding (25% of cases)
infertility (70-85% of cases)
hyperandrogenism (60% of cases)
hirsutism, acne, alopecia
obesity (50% of cases)
glucose intolerance,
diabetes mellitus,
fibrinolytic defects, with hyperfibrinogenemia, dyslipidaemias
hypertension with consequent increase in cardiovascular risks.
PCOS is the result of a number of different pathogenetic mechanisms that tend to feed off each other, thus determining the onset and the worsening of symptoms.
Usually, the condition of hyperinsulinaemia is related to a condition of hyperandrogenism, that triggers an excessive acyclic estrone production which, in its turn, determines a gonadotropin hyper production, mainly LH. The imbalance in LH/FSH ratio reduces follicular maturation, resulting in anovulation and hyperstimulation of theca cells, with androgen hyperproduction. Concomitantly, a reduced conversion of androgens into estrogens occurs, inducing follicular maturation regression or chronic follicular atresia
Since we are dealing with a disorder having a genetic basis, it is not possible to modify one’s own predisposition.In the presence of risk factors (prepubertal and/or early pubertal hypertrichosis and overweight), the only preventive measures currently in use take into consideration a reduction in the caloric intake and an increase in physical activity.The pharmacological therapy, scheduling the administration of one or more hormonal substances – implying remarkable undesirable effects – is reserved to the most serious cases.
This therapy schedules the association of estrogens with a progestin possessing antiandrogenic properties, in order to regulate the menstrual cycle and reduce hyperandrogenism signs.
As an alternative, ovulation induction may be performed by administering gonadotropins, typically FSH, an hormone acting on follicles in the last step of their maturation process.
As with all hormonal therapies, estroprogestinic therapy may present some inconveniences.In addition, women wishing to become pregnant require therapy discontinuation or the administration of clomiphene,a medicine that may cause important undesirable effects.
FSH use may also lead to superovulation phenomena, multiple ovulations and ovarian hyperstimulation syndrome, with consequent hypovolaemia, haemoconcentration, ascites, pleural and pericardial effusions.
It provides the administration of oral hypoglycaemic agents able to reduce the connections between hyperinsulinaemia and hormonal-metabolic changes.
Also this type of therapy has somelimitations.Furthermore, being it a long-termtherapy, it exposes the patient to therisk of permanent pancreatic functionimpairment.
Two physiological events have remarkable consequences on a woman’s life cycle: the menarche and menopause. Both events are regulated by the production of β-estradiol (E2), the major oestrogen produced by ovaries. Menopause does not occur abruptly, but rather it develops over a prolonged time period (years) and involves a range of disturbances heavily affecting women’s life. The hormonal balance resulting from the menopausal period is responsible for a cascade of metabolic (energy metabolism) and endocrine changes called Menopausal Metabolic Syndrome.
MMS is not a pathological condition but it includes a range of disturbances which, due to their concomitant onset, increase the risks of cardiovascular diseases, type 2 diabetes, hypertension and breast cancer.
The factors that outline MMS picture include increased visceral(abdominal) adipose tissue, insulin resistance, blood pressure increase above the normal threshold (hypertension) and lipid profile change (hypertriglyceridaemia).
It is estimated that the metabolic syndrome affects 20-25% of middleaged population, but in menopausal women its prevalence reaches 24% e il 55%. As a matter of fact, after the onset of menopause, women have a 5-fold higher risk of developing diabetes and a 3-fold higher risk of cardiovascular death than men.
During women’s life, oestrogens stimulatefat storage in the gluteo-femoral area.Upon cessation of ovarian-secretedβ-estradiol (E2) production, the storagearea shifts to the visceral (abdominal)region.This accumulation, through a cascadeof events, induces the onset of theMetabolic syndrome.
In fact, the increase in the visceral fat induces insulin resistanceleading to three main consequences:
Insulin resistance causes a decrease in adiponectin (which controls body fat level) and an increase in apo lipoprotein B (apo B) levels. Such increase favours hypertriglyceridaemia and hepatic lipase rise, with consequent LDL increase and HDL decrease. In addition, lipases generate free fatty acids (FFA) which accumulate again as adipose tissue.
Excess circulating insulin reduces SHBP with subsequent further oestrogen - androgen imbalance.
Hyperglycaemia, besides being responsible for the risk of diabetes, is associated with an increased oxidative stress triggered by glucose selfoxidation.
There are different approaches targeted at reducing visceral fat storage or insulin resistance which may lower metabolic syndrome-associated risks.
The hormone replacement therapy represents the treatment of choice to counteract the harmful effects of menopause, including those related to metabolic syndrome. Although this therapeutic approach reduces some symptoms of MMS, several clinical studies and systematic literature reviews pointed out that this treatment appears to be responsible for a major incidence of cardiovascular diseases and breast and endometrial cancers.
There are various medications for insulin control but they have remarkable side effects; therefore they are prescribed only to diabetic patients.
RISKS
Weight gain
Cancer risk
Nausea, diarrhoea
Regular medical control of the hepaticand renal functions
The first intervention to be implemented is a substantial change in lifestyle. An increased physical activity, associated with a controlled diet is able to decrease visceral fat storage and insulin resistance, thus restoring a correct metabolic balance. Though being free of any undesirable effects, this approach was shown to be ineffective, due to the poor compliance of menopausal women.
