RESUMEN
BACKGROUND: Vitamin K deficiency can lead to severe coagulation dysfunction, which may be dangerous and fatal, especially in patients undergoing surgery. METHODS: We report an 84-year-old male patient with gallstones and cholecystitis who had a severe coagulation disorder without bleeding symptoms after endoscopic papillary balloon dilation for removal of bile duct stones. After vitamin K supplementation, the coagulation dysfunction was corrected the next day. RESULTS: In this case, long-term antibiotic treatment, inadequate diet, and abnormal liver function led to coagulation dysfunction. After vitamin K supplementation, the blood coagulation disorder was corrected and serious consequences were prevented. Significantly elevated coagulation function was considered to be caused by vitamin K deficiency. CONCLUSIONS: This case indicates that coagulation dysfunction caused by vitamin K deficiency may occur within a few days. Laboratory personnel should fully understand the risks of vitamin K deficiency in elderly patients undergoing surgery with severely restricted diet, impaired absorption, and long-term use of cephalosporin anti-inflammatory therapy, and promptly remind clinical doctors.
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Trastornos de la Coagulación Sanguínea , Cálculos Biliares , Deficiencia de Vitamina K , Masculino , Humanos , Anciano , Anciano de 80 o más Años , Deficiencia de Vitamina K/complicaciones , Vitamina K/uso terapéutico , Cálculos Biliares/complicaciones , Cálculos Biliares/tratamiento farmacológico , Antibacterianos/uso terapéuticoRESUMEN
OBJECTIVE: Patients on dialysis treatment have poor functional vitamin K status, and this may increase the risk of vascular calcification. Vitamin K supplementation may therefore be relevant in patients on dialysis, but the procoagulant effects have not been studied. We evaluated effects of menaquinone-7 (MK-7) supplementation on biomarkers of coagulation in patients on dialysis. METHODS: Double-blinded, placebo-controlled study in 123 patients on dialysis randomized to 52 weeks of vitamin K (MK-7, 360 µg/daily, n = 61) or placebo (n = 62). Measurements at baseline and after 52 weeks of intervention included thrombin generation (endogenous thrombin potential, peak thrombin concentration, time to peak, and lag time); clot activities of vitamin K-dependent coagulation factors (F) II, VII, IX, and X; prothrombin fragment 1 + 2 (F1+2); and proteins induced by vitamin K absence II (PIVKA-II). Between-group differences (vitamin K vs. placebo) at 52 weeks were determined with an analysis of covariance. Within-group changes in vitamin K and placebo groups were analyzed with a paired t-test. Vascular adverse events and serious adverse events were registered based on hospital records, laboratory data, and participant interviews and compared between groups using Fisher's exact test or Pearson's Chi-Squared test. RESULTS: A between-group difference at 52 weeks was observed for PIVKA-II (P < .001). PIVKA-II decreased significantly from baseline to 52 weeks in the vitamin K group, but not in the placebo group. We observed no between-group differences or within-group changes for biomarkers of coagulation, except for FVII clot activity which was reduced in the placebo group (P = .04), and no between-group differences in adverse events and serious adverse events. CONCLUSION: One year of vitamin K supplementation in patients on dialysis has no detectable effects on biomarkers of coagulation activation, clot activities of vitamin K-dependent coagulation factors, and vascular events or death, indicating no procoagulant effects of this treatment.
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Coagulación Sanguínea , Suplementos Dietéticos , Diálisis Renal , Vitamina K 2 , Deficiencia de Vitamina K , Humanos , Masculino , Femenino , Método Doble Ciego , Deficiencia de Vitamina K/tratamiento farmacológico , Deficiencia de Vitamina K/complicaciones , Persona de Mediana Edad , Coagulación Sanguínea/efectos de los fármacos , Anciano , Vitamina K 2/farmacología , Vitamina K 2/uso terapéutico , Vitamina K 2/análogos & derivados , Biomarcadores/sangre , Protrombina , Vitamina K/farmacología , Vitamina K/uso terapéuticoRESUMEN
Nutritional support is essential for patients with severe motor and intellectual disabilities (SMID) to ensure the smooth provision of medical care. These patients often require long-term tube feeding with enteral formulas, potentially leading to deficiencies in vitamins and trace elements. Additionally, frequent antibiotic use for infections often disrupts gut microbiota, inhibiting vitamin K2 production by intestinal bacteria. We assessed the serum protein induced by vitamin K absence or antagonists-II (PIVKA-II) and undercarboxylated osteocalcin (ucOC) levels to assess the vitamin K status in 20 patients with SMID (median age: 44.1 years, 11 men and 9 women) undergoing long-term tube feeding for durations ranging from 3 to 31 years. Thirteen (65%) and nine (45%) patients had elevated PIVKA-II (<40 mAU/mL) and serum ucOC levels (reference value < 4.50 ng/mL), respectively. Dietary vitamin K1 intake did not differ between patients with and without elevated PIVKA-II levels. Vitamin K2 supplementation for 3 months decreased serum PIVKA-II levels near those within the reference range. Approximately half of the patients with SMID on tube feeding had subclinical vitamin K deficiency. Further studies are needed to ascertain if long-term vitamin K2 supplementation effectively prevents vitamin K deficiency-induced hypercoagulation, osteoporosis, and vascular calcification in patients with SMID.
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Discapacidad Intelectual , Deficiencia de Vitamina K , Masculino , Humanos , Femenino , Adulto , Vitamina K 2 , Nutrición Enteral , Protrombina/metabolismo , Biomarcadores , Vitamina K , Osteocalcina , Suplementos Dietéticos , Vitamina K 1RESUMEN
BACKGROUND: It is rare for newly diagnosed (de novo) or newly treated acute myeloid leukemia (AML) complicated with thrombotic complications, especially combined arterial and venous thrombosis. METHODS: We reported a 13-year-old boy diagnosed with AML and leukocytosis, who developed right femoral vein and right dorsal artery thrombosis during chemotherapy. After treatment with low molecular weight heparin, diosmin, and alprostadil, symptoms were relieved. Unfortunately, the child suffered from coagulopathy afterward, which was unexpectedly caused by vitamin K deficiency. RESULTS: After supplementation with vitamin K and prothrombin complex concentrate, coagulation function recovered. CONCLUSION: For childhood AML patients with high thrombotic risks, close monitoring during anticoagulant treatment was necessary. Concomitantly, we should be alert to past medication history and combined medication use, especially those that may lead to vitamin K deficiency, secondary bleeding, and coagulation disorders. Rational use of antibiotics, anticoagulants, and antitumor drugs must be guaranteed.
Asunto(s)
Trastornos de la Coagulación Sanguínea , Leucemia Mieloide Aguda , Trombosis , Deficiencia de Vitamina K , Masculino , Humanos , Niño , Adolescente , Vena Femoral/patología , Anticoagulantes , Trombosis/etiología , Trastornos de la Coagulación Sanguínea/inducido químicamente , Leucemia Mieloide Aguda/complicaciones , Leucemia Mieloide Aguda/tratamiento farmacológico , Leucemia Mieloide Aguda/patología , Deficiencia de Vitamina K/complicaciones , ArteriasRESUMEN
OBJECTIVES: To identified vitamin K2 deficiency rate and risk factors among newborns in China and assess the importance of high-risk maternal intakes of vitamin K2. METHODS: This retrospective study was performed at the Neonatology Department, the Affiliated Hospital of Guangdong Medical University, China. Routinely collected mother-neonate hospitalization data from July 2020 to January 2021 were analyzed. In total, data from 200 neonates who had completed vitamin K2 tests were utilized to assess the prevalence of vitamin K2 deficiency and identify the potential risk factors. According to the vitamin K2 level, the neonates were divided into 2 groups: cases (vitamin K2 deficiency) and controls (no vitamin K2 deficiency). The potential risk factors for vitamin K2 deficiency were evaluated by univariate and multivariate logistic regression. RESULTS: The vitamin K2 level in 24 of the 200 neonates was undetectable (<0.05 ng/mL). The prevalence of low serum vitamin K2 (<0.1 ng/ml) was 33%. Study subjects with antenatal corticosteroids use had an approximately 5-fold greater risk of developing vitamin K2 deficiency. In the univariate analyses, small-for-gestational-age (SGA), caesarean section, maternal gestational diabetes and premature rupture of the membranes were risk factors for vitamin K2 deficiency. In the multivariate logistic regression analysis, high antenatal corticosteroids use, cesarean section, and SGA were independently associated with vitamin K2 deficiency. CONCLUSION: The present study demonstrated that antenatal corticosteroids use is independently associated with vitamin K2 deficiency. This finding highlights the importance of routine vitamin K2 supplementation in late-stage pregnant women and neonates in China.
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Enfermedades del Recién Nacido , Esteroides , Vitamina K 2 , Deficiencia de Vitamina K , Femenino , Humanos , Recién Nacido , Embarazo , Corticoesteroides , Cesárea , Pueblos del Este de Asia , Recién Nacido Pequeño para la Edad Gestacional , Estudios Retrospectivos , Factores de Riesgo , Esteroides/efectos adversos , Deficiencia de Vitamina K/epidemiología , Exposición MaternaRESUMEN
Patients with cystic fibrosis (CF) are at high risk of fat-soluble vitamin deficiencies, even with supplementation. The contribution of a suboptimal vitamin K status to respiratory and endocrine pathophysiology in CF has been inadequately characterized. This is a cross-sectional study in adult CF patients (≥18 years old) from the Montreal Cystic Fibrosis Cohort. Vitamin K1 (VK1) was measured with high-performance liquid chromatography, using fasted serum samples collected during an oral glucose tolerance test (OGTT: 2 h with plasma glucose and insulin every 30 min) (n = 168). Patients were categorized according to VK1 status (suboptimal defined as <0.30 nmol/L). Suboptimal VK1 levels were observed in 66% of patients. Patients with a suboptimal VK1 status have a higher risk of colonization with Pseudomonas aeruginosa (p = 0.001), have lower body mass index (BMI) (p = 0.003), and were more likely to have exocrine pancreatic insufficiency (p = 0.002). Using an established threshold for VK1, we did show significantly reduced OGTT-derived measures of insulin secretion in patients with a VK1 status below 0.30 nmol/L (first- and second-phase area under the curve (AUC)INS/GLU (p = 0.002 and p = 0.006), AUCINS (p = 0.012) and AUCINS/GLU (p = 0.004)). Subclinical vitamin K deficiency is more common than other fat-soluble vitamin deficiencies in patients with CF. We demonstrate an association between a suboptimal VK1 status and measures of insulin secretion. We highlight the potential associations of mild vitamin K deficiency with pseudomonal colonization and lower BMI, although these need to be validated in prospective studies.
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Avitaminosis , Fibrosis Quística , Deficiencia de Vitamina K , Adulto , Humanos , Avitaminosis/complicaciones , Índice de Masa Corporal , Estudios Transversales , Fibrosis Quística/complicaciones , Secreción de Insulina , Estudios Prospectivos , Vitamina K , Deficiencia de Vitamina K/complicaciones , VitaminasRESUMEN
Vitamin K acts a cofactor for the gamma-carboxylation of several proteins in the coagulation cascade. The clinical spectrum of vitamin K deficiency (VKD) can be asymptomatic to a significant bleeding. VKD is classically seen in newborns. However, this can manifest later in patients with risks such as sub-optimal nutrition, fat malabsorption, medications including antibiotics. A 17-year-old male with spinal muscular atrophy (SMA) Type 1, tracheostomy with ventilator dependent, gastrostomy tube feeding was seen by the gastroenterologist following treatment for small intestinal bacterial overgrowth (SIBO). Investigations showed coagulopathy following which he was transferred to the Pediatric ICU. Labs revealed prothrombin time (PT) 114 s [Normal 9.4-12.5 s], INR (International normalized ratio) 12.6 [Normal < 1.1] and partial thromboplastin time (PTT) 90 s [Normal 25.1-36.5 s]. Mixing studies and coagulation assays were consistent with VKD (low Factor VII and Factor IX with normal Factor V). His home blenderized feeding regimen met the caloric requirement but not the adequate intake (AI) values for vitamin K and other minerals. He received intravenous vitamin K (phytonadione) for five consecutive days with resolution of the coagulopathy (PT 13.2 s, PTT 37.1 s, INR 1.2). The patient was discharged on enteral vitamin K and additional supplements following dietary review by a nutritionist. Clinicians should be cognizant of VKD in patients on blenderized tube feeds which may not meet the adequate intake (AI) goals. In patients who are not receiving nutritionally complete formulas or receiving inadequate volumes, it is important to monitor macro and micronutrients.
Asunto(s)
Nutrición Enteral , Deficiencia de Vitamina K , Masculino , Niño , Humanos , Recién Nacido , Adolescente , Deficiencia de Vitamina K/tratamiento farmacológico , Vitamina K/metabolismo , Vitamina K/uso terapéutico , Vitamina K 1/uso terapéutico , Suplementos DietéticosRESUMEN
We present the case of an adult man with cardiofaciocutaneous syndrome, who initially presented to the emergency department with severe abdominal pain and distension, but was diagnosed with cardiac tamponade on CT after distended neck veins and tachycardia were identified on examination. He had emergency pericardial drainage to relieve the haemopericardium and was treated with colchicine. He was further found to be deficient in factors II, VII and X despite not being on warfarin, and was therefore supplemented with vitamin K. This confirms a diagnosis of vitamin K deficiency, likely multifactorial from malabsorption due to chronic intestinal pseudo-obstruction, small bowel obstruction and possibly exacerbated by subsequent ciprofloxacin use for small intestine bacterial overgrowth. This is the first report of spontaneous haemopericardium secondary to vitamin K deficiency in an adult patient not on anticoagulation, and is an important learning point due to the life-threatening progression of the haemopericardium and cardiac tamponade.
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Taponamiento Cardíaco , Derrame Pericárdico , Deficiencia de Vitamina K , Masculino , Humanos , Adulto , Derrame Pericárdico/diagnóstico por imagen , Derrame Pericárdico/etiología , Taponamiento Cardíaco/diagnóstico por imagen , Taponamiento Cardíaco/etiología , Warfarina/uso terapéuticoRESUMEN
BACKGROUND: There is near-global consensus that all newborns be given parenteral vitamin K1 (VK1 ) at birth as prophylaxis against VK deficiency bleeding (VKDB). Breastmilk has a low VK content and cases of late VKDB are reported in exclusively breastmilk-fed preterm infants despite VK prophylaxis at birth. OBJECTIVES: To assess the prevalence of functional VK insufficiency in preterm infants based on elevated under-γ-carboxylated (Glu) species of Gla proteins, factor II (PIVKA-II), and osteocalcin (GluOC), synthesized by liver and bone, respectively. PATIENTS/METHODS: Prospective, multicenter, observational study in preterm infants born <33 weeks' gestation. Blood samples and dietary history were collected before hospital discharge, and after discharge at 2-3 months' corrected age. Outcome measures were serum VK1 , PIVKA-II, and %GluOC (GluOC as a percentage of the sum of GluOC plus GlaOC) compared between exclusively breastmilk-fed and formula/mixed-fed infants after discharge. RESULTS: After discharge, breastmilk-fed babies had significantly lower serum VK1 (0.15 vs. 1.81 µg/L), higher PIVKA-II (0.10 vs. 0.02 AU/ml) and higher %GluOC (63.6% vs. 8.1%) than those receiving a formula/mixed-feed diet. Pre-discharge (based on elevated PIVKA-II), only one (2%) of 45 breastmilk-fed infants was VK insufficient. After discharge, eight (67%) of 12 exclusively breastmilk-fed babies were VK insufficient versus only one (4%) of 25 formula/mixed-fed babies. CONCLUSIONS: Preterm infants who remain exclusively or predominantly human breastmilk-fed after neonatal unit discharge are at high risk of developing subclinical VK deficiency in early infancy. Routine postdischarge VK1 supplementation of breastfed infants to provide intakes comparable to those from formula milks should prevent this deficiency.
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Leche Humana , Deficiencia de Vitamina K , Lactante , Recién Nacido , Humanos , Recien Nacido Prematuro , Cuidados Posteriores , Estudios Prospectivos , Alta del Paciente , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/epidemiología , Deficiencia de Vitamina K/prevención & control , Vitamina K 1 , Hemorragia , Vitamina KRESUMEN
BACKGROUND: The development of coagulation disorders can be dangerous and fatal in the older people, especially those with multiple medical conditions. Vitamin K-dependent coagulation disorders are easily overlooked when anticoagulant drugs are not used and the patient shows no signs of bleeding. CASE PRESENTATION: We report a case of a 71-year-old male suffering from pulmonary infection with severe coagulation disorder without bleeding symptoms. He also had a history of Parkinson's disease, Alzheimer's disease and cardiac insufficiency. Coagulation tests were normal at the time of admission, prothrombin time (PT) is 13.9 (normal, 9.5-13.1) seconds and the activated partial thromboplastin time (APTT) is 30.2 (normal, 25.1-36.5) seconds. But it turned severely abnormal after 20 days (PT: 136.1 s, APTT: 54.8 s). However, no anticoagulants such as warfarin was used and no bleeding symptoms were observed. Subsequent mixing studies with normal plasma showed a decrease in prothrombin times. Vitamin K deficiency was thought to be the cause of coagulation disorders considering long-term antibiotic therapy, especially cephalosporins, inadequate diet and abnormal liver function. After supplementation with 20 mg of vitamin K, coagulation dysfunction was rescued the next day and serious consequences were effectively prevented. CONCLUSIONS: Overall, timely vitamin K supplementation with antimicrobials that affect vitamin K metabolism requires clinician attention, especially in older patients who are multimorbid, frail or nutritionally compromised, and are admitted to hospital because of an infection that needs antimicrobial therapy are at risk of clotting disorders due to abnormal vitamin K metabolism secondary to altered gut flora, which can exacerbate existing nutritional deficiencies.
Asunto(s)
Trastornos de la Coagulación Sanguínea , Neumonía , Deficiencia de Vitamina K , Anciano , Anticoagulantes/farmacología , Anticoagulantes/uso terapéutico , Coagulación Sanguínea , Trastornos de la Coagulación Sanguínea/diagnóstico , Trastornos de la Coagulación Sanguínea/tratamiento farmacológico , Trastornos de la Coagulación Sanguínea/etiología , Humanos , Masculino , Neumonía/complicaciones , Vitamina K , Deficiencia de Vitamina K/complicaciones , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/tratamiento farmacológicoRESUMEN
Chronic kidney disease (CKD) is commonly associated with vitamin K deficiency. Some of the serious complications of CKD are represented by cardiovascular disease (CVD) and skeletal fragility with an increased risk of morbidity and mortality. A complex pathogenetic link between hormonal and ionic disturbances, bone tissue and metabolism alterations, and vascular calcification (VC) exists and has been defined as chronic kidney disease-mineral and bone disorder (CKD-MBD). Poor vitamin K status seems to have a key role in the progression of CKD, but also in the onset and advance of both bone and cardiovascular complications. Three forms of vitamin K are currently known: vitamin K1 (phylloquinone), vitamin K2 (menaquinone), and vitamin K3 (menadione). Vitamin K plays different roles, including in activating vitamin K-dependent proteins (VKDPs) and in modulating bone metabolism and contributing to the inhibition of VC. This review focuses on the biochemical and functional characteristics of vitamin K vitamers, suggesting this nutrient as a possible marker of kidney, CV, and bone damage in the CKD population and exploring its potential use for promoting health in this clinical setting. Treatment strategies for CKD-associated osteoporosis and CV disease should include vitamin K supplementation. However, further randomized clinical studies are needed to assess the safety and the adequate dosage to prevent these CKD complications.
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Enfermedades Cardiovasculares , Trastorno Mineral y Óseo Asociado a la Enfermedad Renal Crónica , Insuficiencia Renal Crónica , Calcificación Vascular , Deficiencia de Vitamina K , Huesos/metabolismo , Enfermedades Cardiovasculares/complicaciones , Trastorno Mineral y Óseo Asociado a la Enfermedad Renal Crónica/complicaciones , Trastorno Mineral y Óseo Asociado a la Enfermedad Renal Crónica/etiología , Femenino , Humanos , Masculino , Insuficiencia Renal Crónica/complicaciones , Insuficiencia Renal Crónica/terapia , Calcificación Vascular/metabolismo , Vitamina K/metabolismo , Vitamina K 1/uso terapéutico , Vitamina K 2/uso terapéutico , Deficiencia de Vitamina K/complicacionesRESUMEN
Vascular calcification (VC) is highly prevalent in Chronic Kidney Disease (CKD) patients, progresses gradually with deterioration of kidney function and is a strong, independent predictor of cardiovascular (CV) mortality. Matrix Gla Protein (MGP), the most potent inhibitor of VC, requires vitamin K as a co-factor to become biologically active. Accumulating epidemiological data have associated vitamin K depletion with VC progression and CV outcomes. CKD patients are characterized by poor vitamin K status and at the same time, pronounced CV calcification. In early and advanced CKD, including end-stage kidney disease, exogenous supplementation of vitamin K (especially with menaquinone 7, its most bioavailable form) might decrease the inactive form of MGP (dephosphorylated, uncarboxylated MGP) and probably retard the progression or even reverse VC. Here, we focus and discuss the interventional human studies of vitamin K supplementation in CKD patients and suggest future directions in this area of interest.
Asunto(s)
Insuficiencia Renal Crónica , Calcificación Vascular , Deficiencia de Vitamina K , Suplementos Dietéticos/efectos adversos , Femenino , Humanos , Masculino , Diálisis Renal/efectos adversos , Insuficiencia Renal Crónica/diagnóstico , Insuficiencia Renal Crónica/tratamiento farmacológico , Insuficiencia Renal Crónica/epidemiología , Calcificación Vascular/metabolismo , Vitamina K , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/tratamiento farmacológico , Deficiencia de Vitamina K/epidemiologíaRESUMEN
RATIONALE: Fetal brain hemorrhage is rare. It is caused mainly by maternal trauma or fetal coagulation disorder, but in some cases, vitamin K deficiency may be the cause. PATIENT CONCERNS: We describe the case of a pregnant woman with bowel obstruction who was susceptible to vitamin K deficiency due to oral diet restriction, decreased intestinal absorption, and limited intravenous vitamin K supplementation. DIAGNOSIS: After 18âdays of intermittent total parenteral nutrition, acute onset of severe fetal brain hemorrhage developed. INTERVENTIONS: After acute onset of fetal brain hemorrhage, the patient underwent an emergency cesarean section at 25â+â3âweeks of gestation due to fetal non-reassuring fetal monitoring. OUTCOMES: The Apgar score at birth was 0/0, and despite cardiopulmonary resuscitation, neonatal death was confirmed. After the baby was delivered, we checked the maternal upper abdominal cavity and found a massive adhesion in the small bowel to the abdominal wall near the liver and stomach with an adhesion band. The adhesion band, presumably a complication of previous hepatobiliary surgery, appeared to have caused small bowel obstruction. Adhesiolysis between the small bowel and abdominal wall was performed. LESSONS: This case demonstrates that even relatively short-term total parenteral nutrition can cause severe fetal brain hemorrhage. Vitamin K supplementation is required for mothers who are expected to be vitamin K deficient, especially if they are on total parenteral nutrition for more than 3âweeks.
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Obstrucción Intestinal/etiología , Hemorragias Intracraneales/etiología , Nutrición Parenteral Total/efectos adversos , Deficiencia de Vitamina K/complicaciones , Adulto , Cesárea/efectos adversos , Femenino , Enfermedades Fetales , Humanos , Recién Nacido , Nutrición Parenteral Total/métodos , Embarazo , Vitamina K/administración & dosificaciónRESUMEN
Vitamin K (VK) plays many important functions in the body. The most important of them include the contribution in calcium homeostasis and anticoagulation. Vascular calcification (VC) is one of the most important mechanisms of renal pathology. The most potent inhibitor of this process-matrix Gla protein (MGP) is VK-dependent. Chronic kidney disease (CKD) patients, both non-dialysed and hemodialysed, often have VK deficiency. Elevated uncarboxylated matrix Gla protein (ucMGP) levels indirectly reflected VK deficiency and are associated with a higher risk of cardiovascular events in these patients. It has been suggested that VK intake may reduce the VC and related cardiovascular risk. Vitamin K intake has been suggested to reduce VC and the associated cardiovascular risk. The role and possibility of VK supplementation as well as the impact of anticoagulation therapy on VK deficiency in CKD patients is discussed.
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Insuficiencia Renal Crónica , Calcificación Vascular/prevención & control , Deficiencia de Vitamina K/complicaciones , Vitamina K/administración & dosificación , Anticoagulantes/uso terapéutico , Coagulación Sanguínea/fisiología , Huesos/metabolismo , Calcio/metabolismo , Proteínas de Unión al Calcio/sangre , Proteínas de Unión al Calcio/fisiología , Enfermedades Cardiovasculares/prevención & control , Proteínas de la Matriz Extracelular/sangre , Proteínas de la Matriz Extracelular/fisiología , Humanos , Diálisis Renal , Insuficiencia Renal Crónica/sangre , Insuficiencia Renal Crónica/etiología , Calcificación Vascular/complicaciones , Calcificación Vascular/terapia , Vitamina K/fisiología , Vitamina K 1/administración & dosificación , Vitamina K 1/metabolismo , Vitamina K 2/administración & dosificación , Vitamina K 2/metabolismo , Deficiencia de Vitamina K/terapia , Proteína Gla de la MatrizRESUMEN
BACKGROUND: People with HIV (PWH) experience increased systemic inflammation and monocyte activation, leading to increased risk of cardiovascular events (death, stroke, and myocardial infarction) and higher coronary artery calcium scores (CACs). Vitamins D and K2 have significant anti-inflammatory effects; in addition, vitamin K2 is involved in preventing vascular calcifications in the general population. The roles of vitamins D and K in increased coronary calcifications in successfully treated PWH is less understood. METHODS: We prospectively recruited 237 PWH on antiretroviral treatment (ART) and 67 healthy controls. CACs were derived from noncontrast chest computed tomography (CT) and levels of 25-hydroxyvitamin D (vitamin D) and inactive vitamin K-dependent dephosphorylated-uncarboxylated matrix Gla protein (dp-uc MGP, marker of vitamin K deficiency) were measured in plasma during a fasting state. The relationship between inflammation markers, dp-uc MGP, and vitamin D on CACs were estimated using zero-inflated negative binomial regression. Adjusted models included 25(OH)D, MGP, sex, race, age, and markers of inflammation or monocyte activation. RESULTS: Overall, controls had lower median age (45.8 vs. 48.8; Pâ=â0.03), a larger proportion of female individuals (55.2 vs. 23.6%; Pâ<â0.0001), and nonwhite (33.8 vs. 70%; Pâ<â0.0001). Among PWH, less than 1% had detectable viral load and the median CD4+ cell count was 682 (IQR: 473.00-899.00). 62.17% of the participants had zero CACs and 51.32% were vitamin D-deficient (<20âng/ml). There was no difference in detectable CACs (Pâ=â0.19) or dp-uc MGP (Pâ=â0.42) between PWH and controls. In adjusted models, PWH with nonzero CACs have three times greater expected CAC burden compared with controls. Every 1% increase in MGP (worse K status) decreases the probability of having CACs equal to zero by 21.33% (Pâ=â0.01). Evidence suggests that the effects of 25(OH)D and MGP are inflammation-mediated, specifically through sVCAM, TNF-αRI, and TNF-αRII. CONCLUSION: Vitamin K deficiency is a modifiable preventive factor against coronary calcification in PWH. Further research should determine whether vitamin K supplementation would reduce systemic inflammation, vascular calcification, and risk of cardiovascular events in PWH.
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Enfermedades Cardiovasculares , Infecciones por VIH , Calcificación Vascular , Deficiencia de Vitamina K , Biomarcadores , Enfermedades Cardiovasculares/epidemiología , Femenino , Infecciones por VIH/complicaciones , Infecciones por VIH/tratamiento farmacológico , Humanos , Inflamación/complicaciones , Calcificación Vascular/epidemiología , Calcificación Vascular/etiología , Vitamina D , Vitamina K , Deficiencia de Vitamina K/complicaciones , VitaminasRESUMEN
Panitumumab, a fully human anti-epidermal growth factor receptor (EGFR) monoclonal antibody, has been shown to be useful in treating either advanced or recurrent KRAS/NRAS/BRAF wild-type colorectal cancer. We herein report the case of a 60-year-old man with short bowel syndrome who developed hematochezia due to panitumumab-induced colitis with vitamin K deficiency during third-line chemotherapy. The cause of vitamin K deficiency was the lack of intravenous vitamin K supplementation following a change from central venous nutrition to peripheral venous nutrition. We advise clinicians to carefully check for colitis and manage the infusions of chemotherapy patients with short bowel syndrome.
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Antineoplásicos , Colitis , Neoplasias Colorrectales , Síndrome del Intestino Corto , Deficiencia de Vitamina K , Anticuerpos Monoclonales/efectos adversos , Antineoplásicos/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Colitis/tratamiento farmacológico , Neoplasias Colorrectales/tratamiento farmacológico , Hemorragia Gastrointestinal/etiología , Humanos , Masculino , Persona de Mediana Edad , Mutación , Recurrencia Local de Neoplasia/tratamiento farmacológico , Panitumumab/efectos adversos , Proteínas Proto-Oncogénicas p21(ras)/metabolismo , Síndrome del Intestino Corto/tratamiento farmacológico , Deficiencia de Vitamina K/inducido químicamente , Deficiencia de Vitamina K/tratamiento farmacológicoRESUMEN
Chronic kidney disease (CKD) is accompanied with extensive cardiovascular calcification, in part correlating with functional vitamin K deficiency. Here, we sought to determine causes for vitamin K deficiency beyond reduced dietary intake. Initially, vitamin K uptake and distribution into circulating lipoproteins after a single administration of vitamin K1 plus K2 (menaquinone 4 and menaquinone 7, respectively) was determined in patients on dialysis therapy and healthy individuals. The patients incorporated very little menaquinone 7 but more menaquinone 4 into high density lipoprotein (HDL) and low-density lipoprotein particles than did healthy individuals. In contrast to healthy persons, HDL particles from the patients could not be spiked with menaquinone 7 in vitro and HDL uptake was diminished in osteoblasts. A reduced carboxylation activity (low vitamin K activity) of uremic HDL particles spiked with menaquinone 7 vs. that of controls was confirmed in a bioassay using human primary vascular smooth muscle cells. Kidney menaquinone 4 tissue levels were reduced in 5/6-nephrectomized versus sham-operated C57BL/6 mice after four weeks of a vitamin K rich diet. From the analyzed enzymes involved in vitamin K metabolism, kidney HMG-CoA reductase protein was reduced in both rats and patients with CKD. In a trial on the efficacy and safety of atorvastatin in 1051 patients with type 2 diabetes receiving dialysis therapy, no pronounced vitamin K deficiency was noted. However, the highest levels of PIVKA-II (biomarker of subclinical vitamin K deficiency) were noted when a statin was combined with a proton pump inhibitor. Thus, profound disturbances in lipoprotein mediated vitamin K transport and metabolism in uremia suggest that menaquinone 7 supplementation to patients on dialysis therapy has reduced efficacy.
Asunto(s)
Insuficiencia Renal Crónica , Deficiencia de Vitamina K , Vitamina K/metabolismo , Animales , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diabetes Mellitus Tipo 2/metabolismo , Humanos , Ratones , Ratones Endogámicos C57BL , Ratas , Insuficiencia Renal Crónica/metabolismo , Distribución Tisular , Vitamina K/uso terapéutico , Vitamina K 1/metabolismo , Vitamina K 1/uso terapéutico , Vitamina K 2/metabolismo , Vitamina K 2/uso terapéutico , Deficiencia de Vitamina K/complicaciones , Deficiencia de Vitamina K/metabolismoRESUMEN
Hyperemesis gravidarum (HG), severe nausea and vomiting in pregnancy, can lead to vitamin deficiencies. Little is known about HG-related vitamin K deficiency. We aimed to summarise available evidence on the occurrence of HG-related vitamin K deficiency and corresponding maternal and neonatal complications. A systematic review was conducted, searching Medline and EMBASE from inception to 12 November 2020. We identified 1564 articles, of which we included fifteen in this study: fourteen case reports (n 21 women) and one retrospective cohort study (n 109 women). Nine out of twenty-one women reported in case reports had a prolonged prothrombin time (PT). The cohort study measured PT in 39/109 women with HG, of whom 10/39 women (26 %) had prolonged PT. In total, 30-50 % women received vitamin K supplementation after vitamin K deficiency had been diagnosed. Four case reports (n 4 women) reported corresponding maternal complications, all consisting of coagulopathy-related haemorrhage. Nine case reports (n 16 neonates) reported corresponding neonatal complications including intracranial haemorrhage (n 2 neonates) and embryopathy (n 14 neonates), which consisted of Binder phenotype (n 14 neonates), chondrodysplasia punctata (n 9 neonates) and grey matter heterotopia (n 3 neonates). In conclusion, vitamin K deficiency and related complications occur among women with HG. In our systematic review, we were unable to assess the incidence rate.
Asunto(s)
Hiperemesis Gravídica , Deficiencia de Vitamina K , Embarazo , Humanos , Femenino , Masculino , Hiperemesis Gravídica/complicaciones , Hiperemesis Gravídica/diagnóstico , Estudios de Cohortes , Estudios Retrospectivos , Deficiencia de Vitamina K/etiología , Vitamina KRESUMEN
BACKGROUND: Hyperphosphataemia is strongly associated with cardiovascular disease and mortality. Recently, phosphate binders (PBs), which are used to bind intestinal phosphate, have been shown to bind vitamin K, thereby potentially aggravating vitamin K deficiency. This vitamin K binding by PBs may offset the beneficial effects of phosphate reduction in reducing vascular calcification (VC). Here we assessed whether combining PBs with vitamin K2 supplementation inhibits VC. METHODS: We performed 3/4 nephrectomy in rats, after which warfarin was given for 3 weeks to induce vitamin K deficiency. Next, animals were fed a high phosphate diet in the presence of low or high vitamin K2 and were randomized to either control or one of four different PBs for 8 weeks. The primary outcome was the amount of thoracic and abdominal aorta VC measured by high-resolution micro-computed tomography (µCT). Vitamin K status was measured by plasma MK7 levels and immunohistochemically analysed in vasculature using uncarboxylated matrix Gla protein (ucMGP) specific antibodies. RESULTS: The combination of a high vitamin K2 diet and PB treatment significantly reduced VC as measured by µCT for both the thoracic (P = 0.026) and abdominal aorta (P = 0.023), compared with MK7 or PB treatment alone. UcMGP stain was significantly more present in the low vitamin K2-treated groups in both the thoracic (P < 0.01) and abdominal aorta (P < 0.01) as compared with high vitamin K2-treated groups. Moreover, a high vitamin K diet and PBs led to reduced vascular oxidative stress. CONCLUSION: In an animal model of kidney failure with vitamin K deficiency, neither PB therapy nor vitamin K2 supplementation alone prevented VC. However, the combination of high vitamin K2 with PB treatment significantly attenuated VC.
Asunto(s)
Insuficiencia Renal , Calcificación Vascular , Deficiencia de Vitamina K , Animales , Femenino , Masculino , Ratas , Proteínas de Unión al Calcio , Proteínas de la Matriz Extracelular , Modelos Animales , Fosfatos , Diálisis Renal , Insuficiencia Renal/complicaciones , Calcificación Vascular/etiología , Calcificación Vascular/prevención & control , Vitamina K , Vitamina K 1/uso terapéutico , Vitamina K 2/farmacología , Vitamina K 2/uso terapéutico , Deficiencia de Vitamina K/complicaciones , Deficiencia de Vitamina K/tratamiento farmacológico , Microtomografía por Rayos XRESUMEN
Over the past few years, growing interest has been shown for the impact of dietary requirements and nutritional factors on chronic diseases. As a result, nutritional programs have been reinforced by public health policies. The precise role of micronutrients in chronic liver disease is currently receiving particular attention since abnormalities in vitamin levels are often detected. At present, treatment programs are focused on correcting vitamin deficiencies, which are frequently correlated to higher rates of comorbidities with poor outcomes. The literature reviewed here indicates that liver diseases are often related to vitamin disorders, due to both liver impairment and abnormal intake. More specific knowledge about the role of vitamins in liver disease is currently emerging from various results and recent evidence. The most significant benefits in this area may be observed when improved vitamin intake is combined with a pharmacological treatment that may also affect the progression of the liver disease, especially in the case of liver tumors. However, further studies are needed.