Dysfunctional Uterine Bleeding or Anovulation
The normal menstrual cycle usually consists of a mean interval of 28 days (± 6 days) with a mean duration of 4 days (±2 to 3 days). Normal blood loss is approximately 30 mL per cycle, with an upper limit of 60 to 80 mL. Thirty percent of women who present with a complaint of AUB have clinically significant menorrhagia.[1] The mean age of menarche in the United States is 12.8 years, with the range from 9.1 to 17.7 years.[2]
Physiology
The normal menstrual cycle is divided into proliferative, ovulatory, and secretory phases. In the proliferative phase, gonadotropin-releasing hormone (GnRH) is secreted in a pulsatile fashion by the hypothalamus and stimulates the pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). FSH stimulates a group of ovarian follicular cells to grow, from which one dominant follicle is selected. The dominant follicle produces increasing amounts of estradiol. Estradiol stimulates the endometrium to proliferate and develop many progesterone receptors. When estradiol reaches a certain sustained level, a surge of LH is released from the pituitary, causing the dominant follicle to ovulate (ovulatory phase) and become the corpus luteum, which then produces estrogen and progesterone. Progesterone halts endometrial growth and stabilizes the endometrium (secretory phase). Involution of the corpus luteum in the absence of a conception causes a rapid decline in estrogen and progesterone. The endometrium collapses and sheds as menstruation occurs, approximately 14 days after ovulation. Menstrual flow stops as a result of the combined effect of prolonged vasoconstriction, tissue collapse, vascular stasis, and estrogen-induced "healing." Thrombin generation as a result of extravasation of blood is essential for hemostasis.
Therefore, normal ovulatory cycles involve regular cyclic production of estradiol, initiating ovarian follicular growth and endometrial proliferation. Following ovulation, the production of progesterone stabilizes the endometrium. Without ovulation and subsequent progesterone production, a state of "unopposed" continuous estrogen secretion occurs. This stimulates excessive dilation of the spiral arterial supply in the endometrium and abnormal endometrial growth without adequate structural support. The consequence is spontaneous breakage and sloughing of the endometrium with unpredictable bleeding. Eventually, continued elevated estrogen levels have a negative feedback effect on the hypothalamic-pituitary-ovarian axis, causing a decrease in FSH, LH, and estrogen.[3,4] This results in a vasoconstriction and collapse of the thickened hyperplastic endometrial lining with heavy and often prolonged bleeding. In anovulatory cycles, the estrogen levels can either be high or low. With chronic high levels, there is intermittent heavy bleeding, and chronically low levels may result in prolonged light bleeding.[5]
The maturation of the hypothalamic-pituitary-ovarian axis occurs slowly in the first 18 to 24 months after menarche in the adolescent female. Anovulatory cycles may last up to 5 years.
Information concerning the age that adolescents become ovulatory is conflicting. McDonough and Gantt[6] observed anovulation in 55 to 82% of adolescents between menarche and 2 years postmenarche, 30 to 55% from 2 to 4 years postmenarche, and 20% from 4 to 5 years postmenarche. The World Health Organization (WHO) conducted a 2-year longitudinal study on menstrual and ovulatory patterns in females aged 11 to 15 and found that 19% of girls had regular cycles within the first three cycles and 67% had regular cycles by the end of 2 years.[7] In addition, adolescents with earlier menarche tend to develop ovulatory cycles sooner than those with later onset of menarche.[8] Gynecologic age, defined as the number of years from menarche, is therefore a much stronger predictor of ovulatory cycles than chronological age. Apter and colleagues[9] found that the majority of cycles were still anovulatory by a gynecologic age of 2 years, but after 5 years more than 80% achieved ovulation as measured by midluteal phase progesterone levels.
Besides physiologic causes, anovulation can also have organic pathologic causes. These include hyperandrogenic states (e.g., polycystic ovary syndrome [PCOS]), hypothalamic dysfunction (e.g., anorexia nervosa and excessive exercise), endocrinopathies, and premature ovarian failure. Occasionally, the bleeding is caused by an anatomic cause (e.g., polyps or fibroids), although this is very rare in adolescents. Therefore, the differential diagnosis of DUB in adolescents prioritizes differently than does the differential diagnosis in adult women.[10]
J Midwifery Womens Health. 2003;48(3) © 2003 Elsevier Science, Inc.
Cite this: Abnormal Uterine Bleeding in Adolescents - Medscape - Jun 01, 2003.
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