Uterine disorders and iron deficiency anemia

Abnormal uterine bleeding (AUB) is a clinical entity which can lead to iron deficiency anemia. Classification according to the acronym PALM-COEIN (polyp, adenomyosis, leiomyoma, malignancy, and hyperplasia; coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, and not otherwise classified) provides a structured approach to establish the cause of AUB. The goal of this review is to discuss the different mechanisms and the relationship between uterine disorders and AUB. Heavy menstrual bleeding, a subgroup of AUB, is more closely related to the presence of uterine fibroids. The relationship between heavy menstrual bleeding and uterine fibroids remains poorly characterized, particularly the understanding of endometrial function in women with structural myometrial features such as leiomyomas. A number of theories have been proposed in the literature and are discussed in this review. Uterine adenomyosis is also a frequent cause of AUB, and its pathogenesis is still far from being fully elucidated. The mechanisms contributing to its development are multifactorial. Many theories lean toward invasion of the myometrium by endometrial cells. Both clinical and basic studies favor the theory of direct invasion, although de novo development of adenomyosis from Müllerian rests or stem cells has not been ruled out. Development of adenomyotic lesions involves repeated tissue injury and repair. In addition, this review describes the other causes of AUB such as endometrial polyps, cesarean scar defects, and uterine vascular abnormalities. Endometrial polyps are often asymptomatic, but approximately 68% of women have concomitant AUB. Histologic alterations in the lower uterine segment in patients who had undergone cesarean sections were identified and may explain the cause of AUB. Abnormal uterine bleeding (AUB) is a clinical entity which can lead to iron deficiency anemia. Classification according to the acronym PALM-COEIN (polyp, adenomyosis, leiomyoma, malignancy, and hyperplasia; coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, and not otherwise classified) provides a structured approach to establish the cause of AUB. The goal of this review is to discuss the different mechanisms and the relationship between uterine disorders and AUB. Heavy menstrual bleeding, a subgroup of AUB, is more closely related to the presence of uterine fibroids. The relationship between heavy menstrual bleeding and uterine fibroids remains poorly characterized, particularly the understanding of endometrial function in women with structural myometrial features such as leiomyomas. A number of theories have been proposed in the literature and are discussed in this review. Uterine adenomyosis is also a frequent cause of AUB, and its pathogenesis is still far from being fully elucidated. The mechanisms contributing to its development are multifactorial. Many theories lean toward invasion of the myometrium by endometrial cells. Both clinical and basic studies favor the theory of direct invasion, although de novo development of adenomyosis from Müllerian rests or stem cells has not been ruled out. Development of adenomyotic lesions involves repeated tissue injury and repair. In addition, this review describes the other causes of AUB such as endometrial polyps, cesarean scar defects, and uterine vascular abnormalities. Endometrial polyps are often asymptomatic, but approximately 68% of women have concomitant AUB. Histologic alterations in the lower uterine segment in patients who had undergone cesarean sections were identified and may explain the cause of AUB.