Vitamin K is an essential fat-soluble vitamin. It comprises a group of related compounds known as 2-methyl-1,4-naphthoquinones. Vitamin K₁ (phylloquinone) is the primary dietary form, while vitamin K₂ (menaquinones, MK-4 to MK-13) differs in tissue distribution and metabolic characteristics. Vitamin K plays a central role in the gamma-carboxylation of proteins involved in coagulation, bone health, and vascular regulation [8].

Dietary sources of vitamin K₁ include leafy green vegetables such as spinach, broccoli, brussels sprouts, kale, parsley, and lettuce. Vitamin K₂ is found mainly in fermented foods such as natto, sauerkraut, and certain cheeses, as well as in animal products such as egg yolks and dairy [8, 9].

The absorption of phylloquinone (vitamin K₁) occurs mainly in the jejunum and ileum and depends on adequate bile and pancreatic enzymes. While free phylloquinone can be absorbed efficiently, absorption from food sources is much lower because it is tightly bound to plant chloroplasts. As a result, dietary absorption may be only 4–17%. Absorption improves when vitamin K is consumed with dietary fat because of its fat-soluble nature [10].

After absorption, phylloquinone is incorporated into chylomicrons and very-low-density lipoproteins, transported through the lymphatic system, and released into the bloodstream [10]. It is then taken up by hepatocytes and stored in the liver, with smaller amounts distributed to extrahepatic tissues such as skeletal and cardiac muscle.

Menaquinones (vitamin K₂) are produced primarily by intestinal bacteria or are obtained from fermented foods such as natto, cheese, and yogurt [11]. Because these foods typically contain more fat, vitamin K₂ is absorbed more efficiently than vitamin K₁ is. Menaquinones are absorbed in the distal small intestine and colon and transported in lipoproteins to the liver and other tissues [8].

Vitamin K is essential for several physiological processes, most notably blood coagulation [8]. It is required for the synthesis and activation of prothrombin and other vitamin K–dependent clotting factors. Blood coagulation involves two interacting pathways: the intrinsic pathway and the extrinsic pathway [12, 13].

Vitamin K is also required for synthesis of natural anticoagulant proteins C and S. Vitamin K–dependent factors can therefore be grouped into three categories: procoagulant factors (II, VII, IX, X), anticoagulant proteins (C and S) [14, 15].

Deficiency of vitamin K results in incomplete carboxylation, leading to dysfunctional clotting factors and an increased risk of bleeding and anemia [15]. Women had anemia are easily had menstrual bleeding, as their bodies may have decrease capacity to compensate for blood loss [16].

The causes of vitamin K deficiency differ between adults and children. In adults, deficiency is relatively uncommon but may occur because of poor dietary intake, impaired absorption, or medication effects [17]. Low consumption of vitamin K–rich foods such as leafy green vegetables and fermented products remains one of the primary contributors. The recommended daily intake is 90 µg/day for women and 120 µg/day for men [6].

A major cause of deficiency is impaired intestinal absorption. Disorders that interfere with fat absorption, including inflammatory bowel disease, cystic fibrosis, and celiac disease [17], reduce the uptake of this fat-soluble vitamin. Medications also play a significant role. The prolonged use of broad-spectrum antibiotics disrupts the gut flora responsible for synthesizing vitamin K₂, whereas antacids and certain lipid-lowering agents can reduce absorption [17]. Warfarin and other vitamin K antagonists inhibit the vitamin K epoxide reductase complex, thereby decreasing the activation of vitamin K–dependent clotting factors [13, 14, 15, 16, 17]. Novel oral anticoagulants do not affect vitamin K metabolism [15].

Vitamin K deficiency can lead to a variety of clinical manifestations, most notably bleeding disorders, although osteoporosis and atherosclerosis may also occur [8]. This review focuses on bleeding manifestations, as they are most relevant to menorrhagia. Clinical presentation varies depending on which vitamin K–dependent proteins are affected, and symptoms may include bleeding only, thrombosis only, or a combination of the two [6, 15].

Bleeding is the predominant symptom of factor X deficiency. Although rare, with a prevalence of approximately 1 in 1,500,000, both homozygous and heterozygous mutations are typically symptomatic. Patients may experience severe hemorrhage, including intracranial bleeding, deep hematomas, and joint bleeding. Thrombosis may occur in individuals with deficiencies of protein C or protein S, both of which are natural anticoagulants. Their deficiency increases the risk of thrombotic events. Combined bleeding and thrombosis can occur in patients with deficiencies of prothrombin (factor II), factor VII, and factor IX. When prothrombin levels are markedly reduced, bleeding is usually prominent and may be spontaneous because of minor trauma [18]. Hemorrhage can occur at various sites, including the skin, mucous membranes (such as epistaxis), gastrointestinal tract (hematemesis, melena), respiratory tract (hemoptysis), and urinary tract (hematuria); in women, the reproductive system presents as menorrhagia [15]. Given these patterns, this review places particular emphasis on how vitamin K deficiency may contribute to excessive menstrual bleeding and why it should be considered in women who present with unexplained menorrhagia.

Menorrhagia refers to abnormally heavy or prolonged menstrual bleeding that can interfere with daily functioning, reduce quality of life, and lead to iron deficiency anemia [19]. In severe cases, it may become life-threatening. It is a common condition, affecting a substantial proportion of menstruating women, and the World Health Organization estimates that nearly 18 million women worldwide experience menorrhagia [4]. Menstruation is a physiological process involving cyclic shedding of the endometrium under hormonal regulation by the hypothalamic–pituitary–ovarian axis [20]. A typical cycle occurs every 25–35 days, lasts 3–7 days, and results in an average blood loss of approximately 30 mL.

Menorrhagia is classically defined as menstrual blood loss exceeding 80 mL per cycle [4]. Because objective measurement is often impractical, several clinical criteria are used. These include menses lasting longer than 7 days, bleeding that requires changing sanitary products every two hours, the use of more than 12 pads or tampons per cycle, the need for double protection, the passage of large clots, or a woman’s perception of abnormally heavy bleeding compared with her usual pattern [1]. More recent definitions emphasize functional impact, describing menorrhagia as menstrual bleeding that adversely affects physical, emotional, or social well-being. Approximately one-third of women with menorrhagia develop iron deficiency anemia, which contributes to fatigue and reduces quality of life. Pictorial blood loss assessment charts may be used in clinical practice to estimate menstrual blood loss and assist in diagnosis [1].

Structural causes of menorrhagia are among the most common and include uterine fibroids, endometrial or cervical polyps, adenomyosis, endometriosis, intrauterine devices, and endometrial hyperplasia or malignancy [16, 20]. These abnormalities can disrupt the endometrial environment and impair hormonal or hemostatic regulation, leading to excessive menstrual bleeding [21]. Structural causes are generally detected through routine gynecological assessment and standard imaging modalities. When no structural abnormality is found, nonstructural causes should be considered. These include hormonal imbalances, hematologic disorders, and medication-related factors. Hormonal abnormalities may arise from dysfunction of the hypothalamic–pituitary–ovarian axis, such as pituitary tumors, or from ovarian dysfunction, such as polycystic ovary syndrome, which alters estrogen and progesterone secretion. Thyroid disorders, including both hypothyroidism and hyperthyroidism, can also contribute to heavy bleeding [4]. Medications such as anticoagulants, antiplatelet agents, and chemotherapeutic drugs are additional nonstructural causes. Hematologic conditions frequently associated with menorrhagia include von Willebrand disease, platelet function defects, and deficiencies in coagulation factors.

Menorrhagia results from a complex interaction of physiological, hormonal, and biochemical mechanisms [22]. Hormonal imbalance is a major contributor to and often reflects dysregulation of the hypothalamic–pituitary–ovarian axis [23]. Normally, the pulsatile secretion of gonadotropin-releasing hormone stimulates the release of follicle-stimulating hormone and luteinizing hormone, which regulate the ovarian production of estrogen and progesterone [24, 25, 26]. Estrogen promotes endometrial proliferation during the follicular phase, whereas progesterone supports endometrial maturation during the secretory phase [23, 24]. If fertilization does not occur, decreasing hormone levels trigger enzymatic breakdown and shedding of the functional endometrial layer. This process involves spiral arteries, and proper menstruation requires adequate vasoconstriction and hemostasis [23, 24]. Disruption at any step in this sequence can lead to heavy bleeding. Anovulatory cycles, characterized by a lack of progesterone, result in unopposed estrogen stimulation and excessive endometrial growth [27]. A thickened endometrium may outstrip its blood supply, causing breakdown and increased bleeding. Systemic conditions such as renal failure or disorders of the hypothalamic–pituitary axis may also alter hormonal balance and contribute to menorrhagia [28]. Biochemical abnormalities further exacerbate bleeding. Elevated prostaglandin E₂ and F₂$\alpha$ levels increase vasodilation and uterine contractility, promoting increased flow. Platelet dysfunction and clotting factor deficiencies, including von Willebrand disease and other coagulopathies, impair normal hemostasis [29, 30]. Dysregulation of angiogenic factors such as vascular endothelial growth factors weakens vascular stability within the endometrium, and chronic inflammation with elevated cytokines and matrix metalloproteinases disrupts tissue repair and extracellular matrix integrity [31]. Structural uterine abnormalities can contribute through similar mechanisms [21]. Fibroids, polyps, and malignant lesions may interfere with hormonal signaling, alter the endometrial surface, or disrupt vascular function, resulting in significant menstrual blood loss. Uterine fibroids, also known as leiomyomas, are benign tumors of the uterus that disproportionately affect women of reproductive age, often leading to significant clinical symptoms such as abnormal bleeding, pelvic pain, and infertility [32].

The diagnosis of menorrhagia begins with a comprehensive patient history followed by targeted investigations [4]. History-taking should include menstrual cycle characteristics (frequency, duration, amount of bleeding, number of sanitary products used, frequency of changes, and passage of clots), associated pelvic pain, symptoms of anemia, use of hormonal contraception or intrauterine devices, and the presence of systemic illness [4]. It also includes pelvic ultrasound and a Papanikolaou (Pap) smear, with additional imaging, such as computed tomography or magnetic resonance imaging, when necessary. Endometrial biopsy may be performed if hyperplasia or malignancy is suspected. If no structural abnormality is identified, laboratory investigations are indicated. These include complete blood count, iron studies, thyroid function tests, hormonal profiles, platelet function tests, and coagulation studies. Coagulation testing should include prothrombin time, activated partial thromboplastin time, platelet function analysis, and assays for von Willebrand factor and individual clotting factors. In cases of unexplained menorrhagia, after structural, endocrine, and common systemic causes have been excluded, evaluation for hemostatic disorders is warranted. Abnormal screening results should prompt further assessment for coagulation factor deficiencies, as these conditions can significantly contribute to heavy menstrual bleeding [3, 4].

Acquired vitamin K deficiency impairs the gamma-carboxylation of coagulation factors II, VII, IX, and X, resulting in defective hemostasis and clinically significant bleeding, including menorrhagia. Common causes of acquired vitamin K deficiency include poor dietary intake, malabsorption (such as that seen in inflammatory bowel disease), and medications (such as warfarin or broad-spectrum antibiotics). In contrast, hereditary deficiencies of vitamin K–dependent clotting factors arise from genetic mutations and require factor replacement therapy rather than vitamin K supplementation [33, 34]. Several case reports have documented that menorrhagia is associated with a deficiency in vitamin K–dependent factors. A 36-year-old woman with hereditary factor II deficiency experienced severe bleeding requiring transfusion and eventually hysterectomy. Deficiencies in factors VII, IX, and X have also been associated with heavy menstrual bleeding. In many women, menorrhagia may be the first or only symptom of an underlying bleeding disorder [15, 34]. More than half of women with unexplained menorrhagia have laboratory abnormalities suggestive of impaired hemostasis, and vitamin K deficiency may be an underrecognized contributor [35]. Despite this, vitamin K deficiency is not commonly considered in clinical evaluations. A retrospective study of 112 women by Knol et al. [4] found that nearly two-thirds had unexplained menorrhagia despite normal gynecological evaluation, yet only two were referred for hematologic assessment. This suggests that hemostatic causes, including vitamin K deficiency, may be overlooked in routine practice. Acquired deficiencies of vitamin K–dependent factors have been described in several additional reports. A 43-year-old woman with a combined deficiency of vitamin K–dependent factors responded to treatment once the deficiency was identified. Other reports describe menorrhagia due to dietary insufficiency or multiple coagulation factor deficiencies, many of which improved with vitamin K replacement. Overall, the literature suggests that although uncommon, vitamin K deficiency can significantly contribute to heavy menstrual bleeding and may be underdiagnosed. Assessing vitamin K status and coagulation factor activity in women with unexplained menorrhagia may improve diagnostic accuracy and guide appropriate management (Table 1, Ref. [31, 35, 36, 37, 38, 39, 40]).

Menorrhagia has been documented in association with both acquired and hereditary deficiencies of vitamin K–dependent clotting factors in multiple case reports and clinical observations. Screening for coagulation factor deficiencies is an important component of the evaluation of unexplained menorrhagia, particularly when structural and endocrine causes have been excluded. Identifying vitamin K deficiency is clinically valuable because correcting this deficiency can improve menstrual bleeding patterns and overall hemostatic function. Management includes increasing dietary intake of vitamin K–rich foods or providing pharmacologic supplementation when appropriate. Treatment of menorrhagia depends on the underlying cause and may include medical therapy, correction of hematologic abnormalities, or surgical intervention. Early identification of vitamin K deficiency can prevent unnecessary invasive procedures and facilitate targeted treatment. The evidence summarized in this review is derived from case reports, case series, and observational studies, which represent a lower level of evidence. Consequently, causal relationships cannot be established, and the findings should be interpreted with caution. These observations are best regarded as hypothesis-generating rather than definitive and should not be overgeneralized to all women with menorrhagia. This narrative review is subject to inherent limitations, including potential selection bias, reliance on predominantly observational evidence and case reports, restriction to English-language publications, and the absence of quantitative synthesis. Larger, well-designed prospective studies are required to confirm these associations, clarify the prevalence of vitamin K deficiency among women with unexplained menorrhagia, and define optimal diagnostic and therapeutic strategies [32, 35, 37].

Clinicians managing women with menorrhagia should consider vitamin K deficiency (acquired) as a potentially overlooked and reversible contributor to abnormal uterine bleeding, particularly when routine gynecologic evaluation fails to identify a structural cause. Beyond standard hematologic assessment, a focused review of dietary intake, gastrointestinal health, medication history (including antibiotics and anticoagulants), and conditions associated with malabsorption should be incorporated into the clinical evaluation. In patients with unexplained menorrhagia or poor response to conventional therapies, assessment of coagulation parameters—such as prothrombin time (PT) and the international normalized ratio (INR)—represent first-line laboratory screening tests in patients with suspected vitamin K deficiency. Direct measurement of vitamin K levels is not routinely recommended because of limited availability and variability but may be considered in selected cases when diagnostic uncertainty persists. Measurement of PIVKA-II (des-$\gamma$-carboxy prothrombin) may provide a functional indicator of vitamin K deficiency in complex or refractory cases, providing indirect evidence of impaired vitamin K–dependent clotting factor activity. When deficiency is suspected, early nutritional correction and targeted supplementation, alongside the management of underlying causes, may reduce bleeding severity and improve quality of life. Importantly, clinicians should adopt a multidisciplinary approach involving gynecology, hematology, and nutritional services when appropriate rather than viewing menorrhagia solely as a gynecologic disorder. Increased clinical awareness of vitamin K status may prevent unnecessary escalation to invasive interventions and support more individualized, preventive care strategies [38, 39].