The therapy of these pathological forms is naturally based on the removal of the above-mentioned pathogenic factors which we can summarize as follows:
sterilization of urine and obstacle to reinfections
protection of the bladder mucosa
reconstitution of parietal GAGs.
Below is the therapeutic protocol that we commonly use and that we presented both at the World Congress of the American Urological Association and at the Congress of the European Urological Association with the title "Long Lasting Therapy for Recurrent Urinary Tract Infections in Women". Click to download an abstract
LONG LASTING THERAPY FOR RECURRENT URINARY TRACT INFECTION IN WOMEN
We remember that before starting any therapeutic protocol, we must naturally try to eliminate or at least minimize all the factors predisposing the disease (repeated and risky intercourse, spermicides, alterations of the bowel, prolapses, etc.). We must also abolish those lifestyle and eating habits that are potentially harmful or predisposing to cystitis. You must also reach a water intake of at least 1.5 liters per day.
The therapeutic protocol consists of two different phases, of which the first (usually 10 days) serves to re-establish a situation of basic bacterial sterility, while the second (usually 6 months) serves to maintain this situation over time.
Let's remember that bacterial sterility, in the first phase, will have to be achieved in the three compartments affected by the disease, that is, in the bladder (primarily!) but also in the vagina and rectum.
The recommended treatment will therefore be as follows:
IN THE FIRST 10 days. and after an initial urine culture:
- Full-dose quinolones (bladder sterilization).
- Rifamixin (intestinal sterilization).
New generation humanised lactic ferments (reconstitution of intestinal flora). - Vaginal tablets/ovules based on Doderlein's lactobacillus (sterilization and reconstitution of vaginal flora).
- Acidifying vaginal tablets/ovules (vaginal flora protection).
IN THE NEXT 6 months:
Minimum dose quinolones administered every 3 days. but also one hour before each sexual intercourse.
Vaginal acidifiers in cycles of 10 days/month.
Waterfall D-Mannose (see below)
At the end of each month, even in situations of perfect well-being, a urine culture with antibiogram should always be repeated in order to early highlight the appearance of resistant asymptomatic bacteriuria!
ACCESSORY THERAPIES
In the presence of particularly serious or degenerative situations or in any case more resistant situations, we associate other therapeutic measures to the above therapeutic scheme:
- Hyaluronic Acid+Chondroitin sulphate for intravesical instillations (see below).
- E. Coli vaccine
Amitriptyline (see below). - Diets free of proinflammatory substances or nickel-free
Local treatment of any trigger points (Stanford Protocol).
EXPLANATION OF SOME OF THE ILLUSTRATED HEADS
D-MANNOSE
Mannose is a simple sugar or a monosaccharide. It is reabsorbed eight times slower than glucose. Once absorbed, it has the specific characteristic of not being able to be transformed into glycogen and therefore cannot be used as nourishment, but transported as is in the blood, and is filtered by the kidneys, reaching high concentrations in the urinary tract.
D-Mannose is an absolutely harmless and natural substance, i.e. a glyconutrient normally also present in the cells of our body and without the toxicity of antibiotics. D-mannose binds to the receptors (lectins) present in the cilia of the E.coli bacterium (cause of 90% of urinary infections) creating the complexed form mannose+pathogen which thus instead of nesting in the walls of the mucous membranes, remains in the flow of urine, and is brought out with the physiological urination phase. It should also be remembered that D-Mannose is particularly rich in the aforementioned Tamm Horsfall protein which has the ability to bind with bacterial lectins. Finally, D-Mannose inhibits the formation of bacterial biofilms. Biofilms are a prerogative of some bacteria to agglomerate in colonies and to produce a mucopolysaccharide layer around these which makes them resistant to antibiotics. In this state the bacteria can remain silent, even for months, unless they start to reproduce again and therefore cause the disease, when the organic defenses decrease (e.g. end of antibiotic therapy) or the factors favoring the infection increase (e.g. mental or physical stress , intake of irritants, etc.).
HYALURONIC ACID+CHONDROITIN SULFATE (HYALURIL)
The association of these two substances in a single product to be instilled in the bladder has the ability to significantly reduce the production of pro-inflammatory cytokines so as to allow the correct repair of the protective urothelial layer. Let's remember that this layer is made up of GAGs which are precisely hyaluronic acid and chondroitin sulphate. In fact, this layer, if compromised, has the physiological, albeit partial, ability to reconstitute itself in approximately 72 hours. The exogenous instillation of GAGs increases both the speed and the extent of this repair process, promoting the formation of a "neolayer" and blocking the intraparietal penetration of potentially harmful molecules.
AMITRIPTILINE
This high-dose drug is an older generation tricyclic antidepressant. However, we know that, at low doses, it is a "channel blocker", that is, it selectively blocks the sodium channels (but also the potassium channels and presumably also the calcium channels) present on the peripheral nerve fibers which are responsible for the conduction of the impulse. along a nerve fiber. When a nerve fiber "inflames" the sodium channels multiply disproportionately.
Amitriptyline blocks the "excess" sodium channels and, therefore, has an anti-inflammatory activity on the nerve fiber with the effect of slowing down, to the point of blocking, the transmission of the painful impulse. Once nervous inflammation (inflammation) has been blocked, the tissue tends to return to normal conditions, since the inflammation is no longer maintained by the neuropeptides released by the "inflamed" fiber (substance P, which activates the mast cells, primarily ).