Uterine fibroids are the most common benign pelvic tumors in women. It occurs in 20 to 40% of women in reproductive age. They can be clinically evident in 20 to 25% of the cases; the greatest peak of presentation takes place in the fourth to fifth decades, presenting up to 80% of the pathology specimens of the surgically resected uteri, independently of the preoperative diagnosis. It is also known as uterine leiomyomatosis, fibromyomas, leiofibromyomas and fibroleiomas.
They are composed of large amounts of extracellular matrix (collagen, fibronectin and proteoglycans). Collagen type I and II are present in abundant amounts, but the collagen fibers are formed irregularly and disorderly, similar to the keloid formation.
There is evidence that they have a genetic basis and that their growth is related to genetic predisposition, hormonal influence and several growth factors.
Can Fibroids Cause You To Gain Weight?
Uterine fibroids cause an increase in the size of the aforementioned organ, originating weight gain. The large size of some tumors has been described with astonishment over time. The largest case of a uterine fibroids was described by Hunt in 1888 as a finding at a necropsy, with the “amazing” weight of 63.5 kg. This clearly shows that fibroids can cause to gain weight.
It is estimated that only 20 to 50% of women with one uterine fibroid or more experience symptoms that may be attributed directly to the fibroids itself. The symptoms vary and include abnormal uterine bleeding, pelvic pain, pelvic pressure, reduced bladder capacity, constipation, and reproductive dysfunction.
The most common symptom is abnormal uterine bleeding. Symptoms usually correlate with their location, number, size or with some concomitant degenerative change.
Abnormal uterine bleeding: Menorrhagia and hypermenorrhea is the most common pattern of bleeding. Submucosal and intracavitary fibroids tend to produce bleeding more frequently. Here are some of the comments proposed mechanisms:
-An increase of the size of the surface endometrial area.
-Increased vascularity and vascular flow of the uterus.
-Interference with normal uterine contractility.
-Endometrial ulceration of the submucosal fibroids.
-Compression of the venous plexus with the myometrium.
Fibroids undergo regression after menopause, which is accompanied by atrophy of the endometrium allowing the uterine bleeding to stop.
Symptoms of Pelvic Mass: The subserosal fibroids are the most related to this symptom. The size of the myomatous uterus is described in menstrual weeks, as well as in a pregnant uterus.
A myomatous uterus 12 to 20 weeks in size can be palpated on abdominal examination. Pelvic pressure appears when the uterus increases of size. As the uterus grows, pressure on adjacent organs, especially the urinary tract and rectosigmoids, is accentuated. The demonstrations associated with the urinary tract include frequency urinary output obstruction and ureteral obstruction with hydronephrosis. Constipation or tenesmus may be secondary to fibroids in the posterior wall, which exerts pressure on the rectosigmoid.
Pain: It is not a frequent symptom, and it is usually associated with the torsion of a pediatric fibroids, cervical dilatation by a submucosal fibroids, protruding from the lower uterine segment, or by a red degeneration associated with pregnancy.
Infertility: Uterine myomatosis is associated with infertility in 5 to 10% of cases. The intramural and subserosal fibroids tend to produce greater reproductive dysfunction. The suggested mechanisms through which decrease fertility include:
-Alteration of the endometrial contour that interferes with the implantation.
-Aggregation and deformity of the uterine cavity that interferes with sperm transport.
-An anatomical distortion that reduces access to the cervix.
-Altered uterine contracture.
-The persistence of intrauterine bleeding or clots interferes with implantation.
-Subsequent fibroids may interfere with the relationship between anatomical tube-ovarian, and the tubal ostium may be distorted or obstructed.
Fibroids are clearly associated with exposure of estrogen and circulating progesterone.
In fact, they are rarely observed during puberty, and they are more prevalent during the reproductive years, with regression after menopause.
The risk factors associated with this pathology are age, parity, ethnicity, hormone replacement therapy, endogenous hormonal factors, weight, diet, exercise, family history, pregnancy, tissue injury and smoking, among others.