RESUMEN
Vitamin K is essential for the process of coagulation. In its absence, severe and sometimes fatal bleeding events can occur, especially in newborns. Vitamin K prophylaxis at birth has been shown to prevent morbidity and mortality associated with vitamin K deficiency bleeding (VKDB) and is recommended by multiple organizations including the American Academy of Pediatrics and the World Health Organization. Pediatricians should feel comfortable explaining the risks and benefits of vitamin K prophylaxis to families and should be equipped to recognize signs of VKDB, especially given increasing rates of parental refusal. This article aims to improve understanding of VKDB, including prevention, early recognition, and treatment. [Pediatr Ann. 2023;52(2):e42-e45.].
Asunto(s)
Sangrado por Deficiencia de Vitamina K , Deficiencia de Vitamina K , Recién Nacido , Humanos , Niño , Deficiencia de Vitamina K/complicaciones , Deficiencia de Vitamina K/diagnóstico , Vitamina K/uso terapéutico , Sangrado por Deficiencia de Vitamina K/diagnóstico , Sangrado por Deficiencia de Vitamina K/prevención & control , Hemorragia/etiología , Hemorragia/prevención & controlRESUMEN
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.
Asunto(s)
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
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
We report a probable case of abetalipoproteinemia in an infant who presented with unusual symptoms of late-onset vitamin K deficiency. Abetalipoproteinemia is a rare autosomal recessive disease caused by mutation of the microsomal triglyceride transfer protein gene, resulting in the absence of microsomal triglyceride transfer protein function in the small bowel. It is characterized by the absence of plasma apolipoprotein B-containing lipoproteins, fat malabsorption, hypocholesterolemia, retinitis pigmentosa, progressive neuropathy, myopathy, and acanthocytosis. A biopsy of the small intestine characteristically shows marked lipid accumulation in the villi of enterocytes. Large supplements of fat-soluble vitamins A, D, E, and K have been shown to limit neurologic and ocular manifestations. Dietary fat intake is limited to medium-chain triglycerides.
Asunto(s)
Abetalipoproteinemia/complicaciones , Deficiencia de Vitamina K/complicaciones , Abetalipoproteinemia/sangre , Abetalipoproteinemia/diagnóstico , Abetalipoproteinemia/patología , Duodeno/patología , Enterocitos/patología , Femenino , Humanos , Lactante , Recién Nacido , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/patologíaRESUMEN
Background: A low vitamin K status is common in patients on haemodialysis, and this is considered one of the reasons for the accelerated atherosclerosis in these patients. The vitamin is essential in activation of the protein Matrix Gla Protein (MGP), and the inactive form, dp-ucMGP, is used to measure vitamin K status. The purpose of this study was to investigate possible underlying causes of low vitamin K status, which could potentially be low intake, washout during dialysis or inhibited absorption capacity. Moreover, the aim was to investigate whether the biomarker dp-ucMGP is affected in these patients. Method: Vitamin K intake was assessed by a Food Frequency Questionnaire (FFQ) and absorption capacity by means of D-xylose testing. dp-ucMGP was measured in plasma before and after dialysis, and phylloquinine (vitamin K1) and dp-ucMGP were measured in the dialysate. Changes in dp-ucMGP were measured after 14 days of protein supplementation. Results: All patients had plasma dp-ucMGP above 750 pmol/L, and a low intake of vitamin K. The absorption capacity was normal. The difference in dp-ucMGP before and after dialysis was -1022 pmol/L (p < 0.001). Vitamin K1 was not present in the dialysate but dp-ucMGP was at a high concentration. The change in dp-ucMGP before and after protein supplementation was -165 pmol/L (p = 0.06). Conclusion: All patients had vitamin K deficiency. The reason for the low vitamin K status is not due to removal of vitamin K during dialysis or decreased absorption but is plausibly due to a low intake of vitamin K in food. dp-ucMGP is washed out during dialysis, but not affected by protein intake to a clinically relevant degree.
Asunto(s)
Ingestión de Alimentos/fisiología , Conducta Alimentaria/fisiología , Fenómenos Fisiológicos de la Nutrición/fisiología , Diálisis Renal , Deficiencia de Vitamina K/etiología , Vitamina K/administración & dosificación , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Proteínas de Unión al Calcio/sangre , Proteínas de la Matriz Extracelular/sangre , Femenino , Humanos , Masculino , Persona de Mediana Edad , Encuestas y Cuestionarios , Vitamina K/metabolismo , Deficiencia de Vitamina K/diagnóstico , Proteína Gla de la MatrizRESUMEN
BACKGROUND: An increase in serum undercarboxylated osteocalcin concentrations suggests vitamin K deficiency. Clinical intervention studies suggested that the vitamin K supplementation might contribute to preventing bone loss in postmenopausal women. Evidence on the relationship between serum undercarboxylated osteocalcin (ucOC) levels and bone parameters of quantitative ultrasound (QUS) is limited. We examined the correlation between serum ucOC concentrations and bone status as measured by QUS among middle-aged and older Japanese men and women. METHODS: The subjects were community-dwelling men (n = 358) and women (n = 503) aged ≥ 40 years in Japan. Heel QUS parameters, including the stiffness index, speed of sound, and broadband ultrasound attenuation, were measured. Serum ucOC concentrations were measured by electrochemiluminescence immunoassay. Grip strength was measured in the dominant hand. Information on alcohol drinking, current smoking, exercise, and menopause in women was collected. RESULTS: Serum ucOC concentrations were significantly associated with age in both sexes. Serum ucOC concentrations in men were higher at ≥ 80 years than those in the age groups of 40-49, 50-59, and 60-69 years. Serum ucOC concentrations in women were higher in the age groups of 50-59 and 60-69 years than those at 40-49 years. Partial correlation analysis adjusting for covariates (age, body mass index, grip strength, alcohol drinking, current smoking, and exercise in men; age, body mass index, grip strength, alcohol drinking, current smoking, exercise, and menopause in women) showed that serum ucOC concentrations were negatively significantly correlated with all QUS parameters in women. Serum ucOC concentrations were not correlated with them in men. CONCLUSIONS: Vitamin K deficiency, evaluated with higher serum ucOC, was correlated with poor bone status in women.
Asunto(s)
Densidad Ósea , Osteocalcina/sangre , Ultrasonografía , Deficiencia de Vitamina K/diagnóstico , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Japón , Masculino , Persona de Mediana Edad , Factores SexualesRESUMEN
Vitamin K is required for the É£-carboxylation of specific glutamic acid residues within the Gla domain of the 17 vitamin K-dependent proteins (VKDPs). The timely detection and correction of vitamin K deficiency can protect against bleeding. Vitamin K also plays a role in bone metabolism and vascular calcification. Patients at increased risk of vitamin K deficiency include those with a restricted diet or malnutrition, lipid malabsorption, cancer, renal disease, neonates and the elderly. Coagulation assays such as the prothrombin time have been used erroneously as indicators of vitamin K status, lacking sufficient sensitivity and specificity for this application. The measurement of phylloquinone (K1) in serum is the most commonly used marker of vitamin K status and reflects abundance of the vitamin. Concentrations <0.15 µg/L are indicative of deficiency. Disadvantages of this approach include exclusion of the other vitamin K homologues and interference from recent dietary intake. The cellular utilisation of vitamin K is determined through measurement of the prevalence of undercarboxylated VKDPs. Most commonly, undercarboxylated prothrombin (Protein Induced by Vitamin K Absence/antagonism, PIVKA-II) is used (reference range 17.4-50.9 mAU/mL (Abbott Architect), providing a retrospective indicator of hepatic vitamin K status. Current clinical applications of PIVKA-II include supporting the diagnosis of vitamin K deficiency bleeding of the newborn, monitoring exposure to vitamin K antagonists, and when used in combination with α-fetoprotein, as a diagnostic marker of hepatocellular carcinoma. Using K1 and PIVKA-II in tandem is an approach that can be used successfully for many patient cohorts, providing insight into both abundance and utilisation of the vitamin.
Asunto(s)
Análisis Químico de la Sangre , Deficiencia de Vitamina K/diagnóstico , Vitamina K/sangre , Biomarcadores/sangre , Análisis Químico de la Sangre/normas , Pruebas de Coagulación Sanguínea , Humanos , Valor Predictivo de las Pruebas , Precursores de Proteínas/sangre , Protrombina , Reproducibilidad de los Resultados , Vitamina K 1/sangre , Deficiencia de Vitamina K/sangre , Sangrado por Deficiencia de Vitamina K/sangre , Sangrado por Deficiencia de Vitamina K/diagnósticoRESUMEN
The cardinal biological role of vitamin K is to act as cofactor for the carboxylation of a number of vitamin K-dependent proteins, some of which are essential for coagulation, bone formation and prevention of vascular calcification. Functional vitamin K deficiency is common and severe among dialysis patients and has garnered attention as a modifiable risk factor in this population. However, no single biochemical parameter can adequately assess vitamin K status. For each biological function of vitamin K, the degree of carboxylation of the relevant vitamin K-dependent protein most accurately reflects vitamin K status. Dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP) is the best biomarker for vascular vitamin K status when cardiovascular endpoints are studied. Dp-ucMGP levels are severely elevated in haemodialysis patients and correlate with markers of vascular calcification and mortality in some but not all studies. The aetiology of vitamin K deficiency in haemodialysis is multifactorial, including deficient intake, uraemic inhibition of the vitamin K cycle and possibly interference of vitamin K absorption by phosphate binders. The optimal vitamin K species, dose and duration of supplementation to correct vitamin K status in dialysis patients are unknown. Dp-ucMGP levels dose-proportionally decrease with supraphysiological vitamin K2 supplementation, but do not normalize even with the highest doses. In the general population, long-term vitamin K1 or K2 supplementation has beneficial effects on cardiovascular disease, bone density and fracture risk, and insulin resistance, although some studies reported negative results. In haemodialysis patients, several trials on the effects of vitamin K on surrogate markers of vascular calcification are currently ongoing.
Asunto(s)
Suplementos Dietéticos , Diálisis Renal/efectos adversos , Deficiencia de Vitamina K , Vitamina K/uso terapéutico , Vitaminas/uso terapéutico , Biomarcadores/sangre , Humanos , Estudios Longitudinales , Factores de Riesgo , Vitamina K/análisis , Vitamina K 1/uso terapéutico , Vitamina K 2/análisis , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/terapiaRESUMEN
OBJECTIVE: To compare the prevalence of vitamin K deficiency after intramuscular vitamin K or no treatment in neonates with sepsis on prolonged (>7 days) antibiotic therapy. STUDY DESIGN: Open label randomized controlled trial. SETTING: Level 3 Neonatal Intensive Care Unit (NICU). PARTICIPANTS: Neonates with first episode of sepsis on antibiotics for ≥7 days were included. Neonates with clinical bleeding, vitamin K prior to start of antibiotic therapy (except the birth dose), cholestasis or prenatally diagnosed bleeding disorder were excluded. INTERVENTIONS: Randomized to receive 1 mg vitamin K (n=41) or no vitamin K (n=39) on the 7th day of antibiotic therapy. MAIN OUTCOME MEASURES: Vitamin K deficiency defined as Protein Induced by Vitamin K Absence (PIVKA-II) >>2 ng/mL after 7 ± 2 days of enrolment. RESULTS: The prevalence of vitamin K deficiency was 100% (n=80) at enrolment and it remained 100% even after 7 ± 2 days of enrolment in both the groups. CONCLUSIONS: Neonates receiving prolonged antibiotics have universal biochemical vitamin K deficiency despite vitamin K administration on 7th day of antibiotic therapy.
Asunto(s)
Antibacterianos/uso terapéutico , Cuidado Intensivo Neonatal/métodos , Síndrome de Lemierre/tratamiento farmacológico , Deficiencia de Vitamina K/prevención & control , Vitamina K/uso terapéutico , Vitaminas/uso terapéutico , Femenino , Estudios de Seguimiento , Humanos , Recién Nacido , Inyecciones Intramusculares , Unidades de Cuidado Intensivo Neonatal , Síndrome de Lemierre/complicaciones , Masculino , Prevalencia , Resultado del Tratamiento , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/epidemiología , Deficiencia de Vitamina K/etiologíaAsunto(s)
Enfermedades Cardiovasculares/epidemiología , Deficiencia de Vitamina K/epidemiología , Vitamina K/sangre , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/mortalidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pronóstico , Medición de Riesgo , Factores de Riesgo , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/mortalidadRESUMEN
Although there are several reports of intracranial hemorrhage associated with vitamin K deficient bleeding, there are few reported cases of extracranial manifestations, specifically involving the thymus. Here, we discuss the unique case of a 4-week-old infant presenting with scrotal discoloration, respiratory distress, and widened mediastinum, found to have thymic hemorrhage related to confirmed coagulopathy secondary to late-onset vitamin K deficiency bleeding of the newborn.
Asunto(s)
Contusiones/etiología , Escroto/patología , Timo/patología , Deficiencia de Vitamina K/complicaciones , Antifibrinolíticos/administración & dosificación , Antifibrinolíticos/uso terapéutico , Contusiones/patología , Diagnóstico Diferencial , Enfermedades de los Genitales Masculinos/etiología , Enfermedades de los Genitales Masculinos/patología , Humanos , Recién Nacido , Masculino , Mediastino/diagnóstico por imagen , Mediastino/patología , Síndrome de Dificultad Respiratoria del Recién Nacido/etiología , Síndrome de Dificultad Respiratoria del Recién Nacido/terapia , Escroto/irrigación sanguínea , Timo/irrigación sanguínea , Resultado del Tratamiento , Vitamina K/administración & dosificación , Vitamina K/uso terapéutico , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/patología , Sangrado por Deficiencia de Vitamina K/tratamiento farmacológicoRESUMEN
Patients with primary biliary cholangitis (PBC) are at risk for various harmful consequences of chronic cholestasis. These include fat-soluble vitamin deficiency, even in the setting of macronutrient sufficiency, as well as metabolic bone disease, including osteoporosis with fractures. Hyperlipidemia is often present and less commonly associated with risk of cardiovascular event; however, the long-term effect of new emerging therapies for PBC remains to be determined. Patients with PBC also have infrequent but notable risk of portal hypertension despite early-stage disease. This review discusses the background, evaluation, and practical management of these complications of chronic cholestasis.
Asunto(s)
Avitaminosis/diagnóstico , Carcinoma Hepatocelular/diagnóstico , Hiperlipidemias/diagnóstico , Hipertensión Portal/diagnóstico , Hipertensión Portal/terapia , Cirrosis Hepática Biliar/terapia , Neoplasias Hepáticas/diagnóstico , Osteoporosis/diagnóstico , Absorciometría de Fotón , Avitaminosis/etiología , Avitaminosis/terapia , Conservadores de la Densidad Ósea/uso terapéutico , Enfermedades Óseas Metabólicas/diagnóstico , Enfermedades Óseas Metabólicas/tratamiento farmacológico , Enfermedades Óseas Metabólicas/etiología , Carcinoma Hepatocelular/etiología , Carcinoma Hepatocelular/terapia , Colestasis/complicaciones , Colestasis/terapia , Dieta Saludable , Detección Precoz del Cáncer , Várices Esofágicas y Gástricas/diagnóstico , Várices Esofágicas y Gástricas/etiología , Várices Esofágicas y Gástricas/terapia , Ejercicio Físico , Ácidos Fíbricos/uso terapéutico , Hemorragia Gastrointestinal/diagnóstico , Hemorragia Gastrointestinal/etiología , Hemorragia Gastrointestinal/terapia , Humanos , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Hiperlipidemias/etiología , Hiperlipidemias/terapia , Hipertensión Portal/etiología , Cirrosis Hepática Biliar/complicaciones , Neoplasias Hepáticas/etiología , Neoplasias Hepáticas/terapia , Tamizaje Masivo , Osteoporosis/tratamiento farmacológico , Osteoporosis/etiología , Fracturas Osteoporóticas/prevención & control , Deficiencia de Vitamina A/diagnóstico , Deficiencia de Vitamina A/etiología , Deficiencia de Vitamina A/terapia , Deficiencia de Vitamina D/diagnóstico , Deficiencia de Vitamina D/etiología , Deficiencia de Vitamina D/terapia , Deficiencia de Vitamina E/diagnóstico , Deficiencia de Vitamina E/etiología , Deficiencia de Vitamina E/terapia , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/etiología , Deficiencia de Vitamina K/terapiaRESUMEN
BACKGROUND: Vitamin K (VK) is a co-factor of the γ-glutamyl carboxylase that catalyzes the conversion of glutamate residues to γ-carboxyglutamate in VK-dependent proteins. The carboxylation reaction imparts the essential calcium-binding residues for the biological function of several proteins involved in the process of coagulation and bone metabolism. VK deficiency is frequently encountered in newborns and can lead to fatal hemorrhagic complications. This review describes and discusses the clinical application of VK deficiency testing. METHODS: References and data were researched in PubMed and reviewed. RESULTS: In adults, VK deficiency is associated with uncontrolled bleeding, liver dysfunction, osteoporosis, and coronary diseases. An improved understanding of the role of VK deficiency in health and illness can be achieved by setting a gold-standard in the inter-laboratory estimations of VK. However, conventional methods used to measure the VK deficiency based upon the coagulation time lack sensitivity and specificity. Recently, the alterations in proteins induced by VK absence or antagonism (PIVKA) have proven to be suitable biomarkers for detecting VK deficiency. The measurement of PIVKA-II exhibits an enhanced sensitivity and specificity in comparison to other methods conventionally used for the assessment of VK deficiency in newborns and adults. CONCLUSIONS: PIVKA-II could potentially be employed as an effective biomarker in the diagnosis of VK deficiency.
Asunto(s)
Biomarcadores/sangre , Precursores de Proteínas/sangre , Deficiencia de Vitamina K/sangre , Adulto , Enfermedad Coronaria/sangre , Enfermedad Coronaria/complicaciones , Hemorragia/sangre , Hemorragia/complicaciones , Humanos , Recién Nacido , Hepatopatías/sangre , Hepatopatías/complicaciones , Osteoporosis/sangre , Osteoporosis/complicaciones , Protrombina , Deficiencia de Vitamina K/complicaciones , Deficiencia de Vitamina K/diagnósticoRESUMEN
BACKGROUND: Matrix Gla protein (MGP) is an extrahepatic protein that is dependent on glutamate carboxylation, a vitamin K-dependent process. Its dysfunctional form, desphospho-uncarboxylated-MGP, has been associated with increased arterial calcification and stiffness. The aim of this study was to measure the degree of postoperative carboxylation of MGP and two other Gla proteins in patients scheduled for abdominal or orthopaedic surgery. METHODS: Forty patients undergoing abdominal or orthopaedic surgery were included. Blood samples were collected preoperatively and four days after the surgery. Desphospho-carboxylated MGP (dp-cMGP), desphospho-uncarboxylated MGP (dp-ucMGP), carboxylated osteocalcin (OC) (cOC), uncarboxylated OC (ucOC), and uncarboxylated prothrombin (PIVKA-II) were analysed. RESULTS: Preoperatively, 29 patients had dp-ucMGP levels above the reference values. Patients with pre-existing cardiovascular comorbidities had higher dp-ucMGP preoperatively compared with patients with no record of cardiovascular disease. Postoperatively, this number increased to 36 patients, and median dp-ucMGP levels increased (p < 0.0001) and correlated to a PIVKA-II increase (r = 0.44). On the other hand, dp-cMGP levels did not significantly alter. Decreased levels of ucOC and cOC were seen after surgery (p = 0.017 and p = 0.0033, respectively). Comorbidities, possible nutritional defects, and complications affecting Gla protein activity and function were identified. CONCLUSIONS: Dp-ucMGP was high preoperatively, and had further increased postoperatively. This pattern was linked to several comorbidities, possible nutritional defects, and postoperative complications, which motivates further research about potential interactions between perioperative corrective treatments with vitamin K supplements, cardiovascular biomarkers, and incidents of stroke and myocardial infarction events.
Asunto(s)
Abdomen/cirugía , Proteínas de Unión al Calcio/sangre , Enfermedades Cardiovasculares/etiología , Proteínas de la Matriz Extracelular/sangre , Procedimientos Ortopédicos/efectos adversos , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/diagnóstico , Comorbilidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estado Nutricional , Osteocalcina/sangre , Fosforilación , Estudios Prospectivos , Precursores de Proteínas/sangre , Protrombina , Medición de Riesgo , Factores de Riesgo , Factores de Tiempo , Resultado del Tratamiento , Regulación hacia Arriba , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/etiología , Proteína Gla de la MatrizAsunto(s)
Anticonvulsivantes/efectos adversos , Epilepsia/tratamiento farmacológico , Fenitoína/efectos adversos , Sepsis/sangre , Deficiencia de Vitamina K/inducido químicamente , Adolescente , Anorexia/sangre , Anorexia/etiología , Anorexia/metabolismo , Cistitis/complicaciones , Discapacidades del Desarrollo/complicaciones , Humanos , Masculino , Tiempo de Protrombina , Sepsis/etiología , Sepsis/terapia , Vitamina K/administración & dosificación , Vitamina K/sangre , Vitamina K/metabolismo , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/tratamiento farmacológicoRESUMEN
INTRODUCTION: Zellweger spectrum disorders (ZSDs) are caused by an impairment of peroxisome biogenesis, resulting in multiple metabolic abnormalities. This leads to a range of symptoms, including hepatic dysfunction and coagulopathy. This study evaluated the incidence and severity of coagulopathy and the effect of vitamin K supplementation orally and IV in ZSD. METHODS: Data were retrospectively retrieved from the medical records of 30 ZSD patients to study coagulopathy and the effect of vitamin K orally on proteins induced by vitamin K absence (PIVKA-II) levels. Five patients from the cohort with a prolonged prothrombin time, low factor VII, and elevated PIVKA-II levels received 10 mg of vitamin K IV. Laboratory results, including thrombin generation, at baseline and 72 h after vitamin K administration were examined. RESULTS: In the retrospective cohort, four patients (13.3%) experienced intracranial bleedings and 14 (46.7%) reported minor bleeding. No thrombotic events occurred. PIVKA-II levels decreased 38% after start of vitamin K therapy orally. In the five patients with a coagulopathy, despite treatment with oral administration of vitamin K, vitamin K IV caused an additional decrease (23%) of PIVKA-II levels and increased thrombin generation. CONCLUSION: Bleeding complications frequently occur in ZSD patients due to liver disease and vitamin K deficiency. Vitamin K deficiency is partly corrected by vitamin K supplementation orally, and vitamin K administered IV additionally improves vitamin K status, as shown by further decrease of PIVKA-II and improved thrombin generation.
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Trastornos de la Coagulación Sanguínea/tratamiento farmacológico , Coagulación Sanguínea/efectos de los fármacos , Suplementos Dietéticos , Hemorragia/tratamiento farmacológico , Deficiencia de Vitamina K/tratamiento farmacológico , Vitamina K/administración & dosificación , Síndrome de Zellweger/tratamiento farmacológico , Administración Intravenosa , Administración Oral , Adolescente , Biomarcadores/sangre , Trastornos de la Coagulación Sanguínea/sangre , Trastornos de la Coagulación Sanguínea/diagnóstico , Trastornos de la Coagulación Sanguínea/epidemiología , Niño , Femenino , Hemorragia/sangre , Hemorragia/diagnóstico , Hemorragia/epidemiología , Humanos , Incidencia , Masculino , Países Bajos/epidemiología , Proyectos Piloto , Prueba de Estudio Conceptual , Estudios Prospectivos , Precursores de Proteínas/sangre , Protrombina , Estudios Retrospectivos , Índice de Severidad de la Enfermedad , Resultado del Tratamiento , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/epidemiología , Adulto Joven , Síndrome de Zellweger/sangre , Síndrome de Zellweger/diagnóstico , Síndrome de Zellweger/epidemiologíaAsunto(s)
Hematoma Subdural/complicaciones , Hematoma Subdural/diagnóstico por imagen , Complicaciones del Embarazo/diagnóstico , Ultrasonografía Prenatal/métodos , Deficiencia de Vitamina K/complicaciones , Adulto , Femenino , Humanos , Recién Nacido , Madres , Embarazo , Complicaciones del Embarazo/terapia , Pronóstico , Vitamina K/uso terapéutico , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/terapia , Vitaminas/uso terapéuticoRESUMEN
BACKGROUND & AIMS: Vitamin K acts as a coenzyme in the γ-carboxylation of vitamin K-dependent proteins, including coagulation factors, osteocalcin, matrix Gla protein (MGP), and the growth arrest-specific 6 (GAS6) protein. Osteocalcin is a key factor for bone matrix formation. MGP is a local inhibitor of soft tissue calcification. GAS6 activity prevents the apoptosis of vascular smooth muscle cells. Few data on vitamin K intake in chronic kidney disease patients and no data in patients on a Mediterranean diet are available. In the present study, we evaluate the dietary intake of vitamin K1 in a cohort of patients undergoing haemodialysis. METHODS: In this multi-centre controlled observational study, data were collected from 91 patients aged >18 years on dialysis treatment for at least 12 months and from 85 age-matched control subjects with normal renal function. Participants completed a food journal of seven consecutive days for the estimation of dietary intakes of macro- and micro-nutrients (minerals and vitamins). RESULTS: Compared to controls, dialysis patients had a significant lower total energy intake, along with a lower dietary intake of proteins, fats, carbohydrates, fibres, and of all the examined minerals (Ca, P, Fe, Na, K, Zn, Cu, and Mg). With the exception of vitamin B12, vitamins intake followed a similar pattern, with a lower intake in vitamin A, B1, B2, C, D, E, folates, K1 and PP. These finding were confirmed also when normalized for total energy intake or for body weight. In respect to the adequate intakes recommended in the literature, the prevalence of a deficient vitamin K intake was very high (70-90%) and roughly double than in controls. Multivariate logistic model identified vitamin A and iron intake as predictors of vitamin K deficiency. CONCLUSIONS: Haemodialysis patients had a significantly low intake in vitamin K1, which could contribute to increase the risk of bone fractures and vascular calcifications. Since the deficiency of vitamin K intake seems to be remarkable, dietary counselling to HD patients should also address the adequacy of vitamin K dietary intake and bioavailability. Whether diets with higher amounts of vitamin K1 or vitamin K supplementation can improve clinical outcomes in dialysis patients remains to be demonstrated.
Asunto(s)
Dieta , Diálisis Renal , Insuficiencia Renal Crónica/sangre , Vitamina K 1/administración & dosificación , Anciano , Índice de Masa Corporal , Estudios de Casos y Controles , Carbohidratos de la Dieta/administración & dosificación , Grasas de la Dieta/administración & dosificación , Proteínas en la Dieta/administración & dosificación , Femenino , Humanos , Masculino , Micronutrientes/administración & dosificación , Persona de Mediana Edad , Evaluación Nutricional , Estado Nutricional , Prevalencia , Ingesta Diaria Recomendada , Insuficiencia Renal Crónica/tratamiento farmacológico , Estudios Retrospectivos , Vitamina K 1/sangre , Deficiencia de Vitamina K/sangre , Deficiencia de Vitamina K/diagnóstico , Deficiencia de Vitamina K/tratamiento farmacológico , Circunferencia de la CinturaRESUMEN
BACKGROUND: Infants are at risk for vitamin K deficiency bleeding (VKDB) because of limited stores of vitamin K (VK) at birth and a low concentration of VK in human breast milk. Therefore, the administration of intramuscular (IM) VK at birth has been recommended since 1961 in the United States. Infants who do not receive IM VK and who are exclusively breast-fed are at increased risk for VKDB. While VKDB is rare, a common presentation of late onset VKDB is intracranial hemorrhage. CASE REPORT: We report the case of a 4-week-old infant who presented to the emergency department with lethargy and a grossly dilated right pupil. The parents denied trauma. A computed tomography scan revealed a right-sided subdural hematoma with midline shift. The infant's international normalized ratio was >10.9 and his prothrombin time PT was >120 seconds. VK was administered and the child was transferred to a tertiary care center for emergent neurosurgery. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The difficult part of making this critical diagnosis is considering it. Any bleeding in a newborn without trauma should prompt inquiry regarding neonatal VK administration and a serum prothrombin time level. Fortunately, once the diagnosis is made, therapy in the emergency department can be lifesaving and is familiar to emergency physicians. Treatment parallels usual care for the adult with excess anticoagulation caused by warfarin. Prompt intravenous VK is universally accepted. Studies to support fresh frozen plasma or prothrombin complex concentrate are lacking but make good clinical sense for life-threatening bleeding.