vitamin K deficiency

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Fatal Intracranial Hemorrhage in a Normal Infant Secondary to Vitamin K Deficiency

Fatal Intracranial Hemorrhage in a Normal Infant Secondary to Vitamin K Deficiency

Fatal Intracranial Hemorrhage in a Normal Infant Secondary to Vitamin K Deficiency.. Since the initiation of routine vitamin K prophy-.[r]

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Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases?

Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases?

Vitamin K has an excellent safety profile, and no tox- icity has been observed even with very high-doses [35]. Vitamin K is obligatory to maturate clotting factors in the liver, however, it is also necessary for the activation of anticlotting factors (i.e. protein C and S). Whereas protein C is solely produced in the liver, about 50% of protein S is synthesized hepatically and the other half in the vascular wall [36]. Protein S production in the vascu- lar system seems to be of key importance in local throm- bosis prevention [36]. The triage theory posits that in case of scarcity, nature will provide nutrients first to places in the body where shortage leads to an immediate treat to short-term survival at the expense of places where shortage only has long-term consequences (Fig. 3) [37]. Regarding vitamin K deficiency, increased bleeding tendency is the biggest short-term threat for survival, and the limited supply of vitamin K will therefore be preferentially used for the synthesis of clotting factors with the sacrifice of protein S maturation in the vascular wall [37]. Therefore, counterintuitively, vitamin K sup- plementation does not increase the risk of thrombo- embolism and might even decrease it by fully activating the anti-thrombosis activity [37]. The triage theory also
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Vitamin K deficiency: a case report and review of current guidelines

Vitamin K deficiency: a case report and review of current guidelines

Recently Witt et al. evaluated whether a prophylactic regimen of 1 mg vitamin K orally at birth followed by 150 μg daily during weeks 2 to 13 sufficiently prevented VKDB in breastfed infants. Their data in high-risk group, for example undiagnosed children with biliary atresia, showed that this regimen does not successfully prevent VKDB in these children, in contrast to a regi- men consisting of a single intramuscular injection of 2 mg vitamin K at birth. They concluded that a prophy- lactic regimen for breastfed infants consisting of 1 mg vitamin K orally at birth, followed by either 25 μg or 150 μg daily during weeks 2 to 13, does not sufficiently prevent VKDB in breastfed infants with still undiag- nosed biliary atresia. They assumed that this insufficient prevention is also present in infants with yet undiag- nosed others forms of neonatal cholestasis. In their study efficient prevention was obtained by regimen consisting of single intramuscular injection of 2 mg vitamin K at birth [23].
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Vitamin K Deficiency After the Newborn Period

Vitamin K Deficiency After the Newborn Period

oral vitamin K intakes, expressed as K, activity,. were 0.0 to 8.4 sg/kg/day.[r]

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Dietary induced subclinical vitamin K deficiency in normal human subjects

Dietary induced subclinical vitamin K deficiency in normal human subjects

The PT and APTT remained constant throughout the study period and did not increase in response to the vitamin K depletion even though plasma levels of vitamin K, fell below the normal ra[r]

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Abetalipoproteinemia Presenting as Severe Vitamin K Deficiency

Abetalipoproteinemia Presenting as Severe Vitamin K Deficiency

at Viet Nam:AAP Sponsored on September 7, 2020. www.aappublications.org/news[r]

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Are Pediatricians Complicit in Vitamin K Deficiency Bleeding?

Are Pediatricians Complicit in Vitamin K Deficiency Bleeding?

patient-driven end of the spectrum, the physician presents factual information and available options, leaving parents to decide. This would be appropriate when there is more than one option with comparable effectiveness, not the case in our vitamin K scenario. At the physician- driven end of the spectrum, care is provided without discussion, as in life-threatening situations. Our vitamin K scenario falls somewhere in the middle, which leads to the next question: When a family declines the recommended care, how far can a clinician ethically go to promote a low-risk option with clear health benefit?
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Vitamin K Deficiency in Newborns: A Case Report in α-1-Antitrypsin Deficiency and a Review of Factors Predisposing to Hemorrhage

Vitamin K Deficiency in Newborns: A Case Report in α-1-Antitrypsin Deficiency and a Review of Factors Predisposing to Hemorrhage

Vitamin K, and fresh frozen plasma returned the prothrombin time and partial thromboplastin time to normal values within 18 hours, suggesting that the infant ad severe vitamin K deficien[r]

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Fatal Intramuscular Bleeding Misdiagnosed as Suspected Nonaccidental Injury

Fatal Intramuscular Bleeding Misdiagnosed as Suspected Nonaccidental Injury

Fatal intracranial hemorrhage in a normal infant secondary to vitamin K deficiency. Nagi NA, Al-Dubooni HM, Al-Shirkat SAR[r]

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The importance of the analysis of vitamins a, d and k in the pediatric population in the intensive care unit: commentary on clinical research and literature review

The importance of the analysis of vitamins a, d and k in the pediatric population in the intensive care unit: commentary on clinical research and literature review

Since 1961, the efficacy of neonatal vitamin K prophylaxis (oral or parenteral) in the prevention of early vitamin K deficiency bleeding is firmly established (American Academy of Pediatrics, 1961). In the literature, there are several manuscript on intracranial bleeding due to vitamin K deficiency (Yilmaz et al., 2009; Demirören et al., 2004; Matsuzaka et al. 1989; Gopakuma et al., 2010). In the Netherlands, it is proposed to use of pediatric intensive care registries to assess the efficacy of national vitamin K prophylactic regimens. The Pediatric Intensive Care Evaluation registry allows ongoing monitoring of the incidence of late intracranial vitamin K deficiency bleeding (Visser et al., 2011). Bleeding is a common occurrence in intensive-care-unit (ICU) patients. All newborns require phylloquinone after birth to prevent vitamin K deficiency bleeding (Clarke et al., 2015). However, little is known about the impact of genetic variants in the vitamin K-dependent coagulation system on the development of intraventricular hemorrhage (IVH) in premature infants (Schreiner et al., 2014). According to Parker, (2013), bleeding in patients in pediatric intensive care units is associated with an increased risk of mortality. For Parker, (2013), interventions directed toward correcting the abnormal coagulation test results are generally either not warranted (in the case of liver disease) or not fully successful (in the case of disseminated intravascular coagulation). According to McNinch et al., (1985), in life- threatening bleeds, fresh frozen plasma should be administered prior to VK. In preterm infants born of a mother with Crohn disease, careful observation for coagulation is warranted even after vitamin K administration (Fujioka et al., 2017).
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Vitamin K as a regulator of benzo(a)pyrene metabolism, mutagenesis, and carcinogenesis  Studies with rat microsomes and tumorigenesis in mice

Vitamin K as a regulator of benzo(a)pyrene metabolism, mutagenesis, and carcinogenesis Studies with rat microsomes and tumorigenesis in mice

Vitamin K3 inhibits the conversion of benzo(a)pyrene to its more polar metabolites in an in vitro rat liver microsomal system. Vitamin K3 also inhibits benzo(a)pyrene metabolism in rat liver fragments and reduces its mutagenicity in the Ames test. Higher concentrations of vitamin K3 are required to comparably reduce benzo(a)pyrene metabolism when the microsomal system has been induced with 3-methylcholanthrene. High pressure liquid chromatography analysis of the products of benzo(a)pyrene metabolism shows a uniform reduction of all the metabolic products. When tumors were induced in ICR/Ha female mice by the intraperitoneal injection of benzo(a)pyrene, those mice given vitamin K3 before or both before and after benzo(a)pyrene had a slower rate of tumor appearance and tumor death rate as compared with those receiving benzo(a)pyrene alone. However, vitamin K1 increased the rate of tumor death while vitamin K deprivation and warfarin decreased the rate of tumor appearance and death in benzo(a)pyrene-injected mice. These studies indicate that vitamin K3 is an inhibitor of aryl hydrocarbon hydroxylase and reduces the carcinogenic and mutagenic metabolites in vitro, and inhibits benzo(a)pyrene tumorigenesis in vivo. That vitamin K1 enhances the benzo(a)pyrene effect while warfarin and vitamin K deficiency inhibit benzo(a)pyrene tumorigenesis indicates that vitamin K1, vitamin K deprivation, or possibly blockade of its metabolic cycle also modulates benzo(a)pyrene metabolism in vivo but by a mechanism or at a […]
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Hereditary combined deficiency of the vitamin K-dependent clotting factors

Hereditary combined deficiency of the vitamin K-dependent clotting factors

Clinical symptoms of VKCFD vary according to procoag- ulant protein levels which depend on the availability of vitamin K. The severity of the bleeding pattern is there- fore influenced by both dietary intake of vitamin K and functional status of the gut microflora, as well as by the penetrance of the genetic defect which is widely variable. Accordingly, in the most severe cases, onset of symptoms occurs in newborns while a delayed recognition of the disorder is possible in milder cases. Despite a modest propensity to thrombosis hypothesized in milder cases due to the deficiency of natural anticoagulants, VKCFD is characterized by a cluster of different, often life threaten- ing, bleeding symptoms occurring both spontaneously and in a surgical setting. Reviewing the scientific litera- ture on this disease, the spectrum of bleeding symptoms appears to range from mild to severe and usually involves skin and mucosae. Easy bruising is common. Muco-cuta- neous bleeding, such as gastrointestinal bleeding, may also appear spontaneously or after antibiotic therapy, because of the decreased vitamin K production by gut bacteria. Bleeding from the umbilical cord is reported [6,8]. Hemarthrosis is rarely described [8]. VKCFD can sometimes cause fatal intracranial haemorrhage in the first weeks of life, which is similar to the haemorrhagic disease the newborns that results form acquired vitamin K deficiency [6,7,16]. The case of a woman with persis- tent menorrhagia, but whose worst bleeding episodes occurred mainly in a surgical scenario, such as post-par- tum haemorrhage and haemoperitoneum following ovar- ian cyst rupture, has been described [17]. Antibiotic and anticonvulsivant therapy administration must be care- fully evaluated as these drugs can worsen the bleeding pattern [8].
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A review of Warfarin woes and non Vitamin k dependent anticoagulants benefits

A review of Warfarin woes and non Vitamin k dependent anticoagulants benefits

Other side effects of warfarin use include; warfarin necrosis in patients deficient in protein C (Chan et al., 2000), purple toe syndrome (Talmadge and Spyropoulos, 2003), osteoporosis has also been seen to likely be a result of the warfarin side effect. as seen in three studies in 1999 (Caraballo et al., 1999), 2002 (Pilon et al., 2004) and 2006 (Gage et al., 2006). Several studies have implicated warfarin use in vascular and valvularcalcification (Palaniswamy et al., 2011). A rarely talked about side effect is calcification of cartilages, blood vessels and even heart valves. Any suggestion that warfarin might be associated with vascularcalcification raises the question as to why so many people, when placed on warfarin, do not develop vascularcalcification. Perhaps the complexity of the vitamin K-dependent carboxylation process might explain why some patients may be at higher risk for the development of associated vascularcalcification. Ultimately, these observations raise questions about whether the risk of vascularcalcification should be added to the risk of bleeding when considering whether to initiate certainpatients on warfarin. Interestingly, patients anticoagulated for peripheralvascular disease had an almost 10 times higher risk of bleeding than those anticoagulated for other reasons (Anand et al., 2007). It is intriguing to wonder whether certainpatients have global underactivity of their carboxylation processes, such as those with undetected vitamin K deficiency, and if suchpatients develop premature vascular disease and/or higher rates of bleeding complications when placed on warfarin. Although this is purely speculative at this point, it raises interesting questions about whether there might be certainidentifiablepopulations that are particularly at risk
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FACTORS THAT CAN LEAD TO THE DEVELOPMENT OF SKELETAL
DEFORMITIES IN FISHES: A REVIEW

FACTORS THAT CAN LEAD TO THE DEVELOPMENT OF SKELETAL DEFORMITIES IN FISHES: A REVIEW

Skeletal deformities is an important factor that downgrade hatcheries’ production and have a high economic affect to the producers. Fishes with skeletal deformities live less than the normal ones and are not preferred by the consumers. Deformities are a complex mixture of different bone disorders and are not well understood. Nutritional factors such as phosphorus deficiency, vitamin C deficiency, vitamin K deficiency and hypervitaminosis A can lead to twisted neural and hemal spines, development of soft bones, decreased bone mass, vertebral fusion, lordosis, kyphosis and scoliosis. Environmental factors are also important. Current velocity, water temperature and heavy metal pollution are some of them resulting, among other malformations, reduction of the vertebrae Ca/P ratio, shortening and assimilation of cartilage, eye and otic capsules malformations, head enlargement and bone weakening. Lack of functional swimbladder, gene mutations, bacteria and parasites infections, electrofishing, low dissolved oxygen, radiation and walling behavior induced by the color of the tanks are referred to the literature as possible factors that can lead to skeletal deformities.
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Impact of vitamin D deficiency on maternal and birth outcomes in the Saudi population: a cross sectional study

Impact of vitamin D deficiency on maternal and birth outcomes in the Saudi population: a cross sectional study

In Saudi Arabia, hypovitaminosis D can be considered a major public health problem with a significantly high prevalence especially among women, ranging from to ~80 to 100 % in different studies [9–11]. Vitamin D deficiency can be seen not only in infancy and childhood but also across the other life stages from adolescence, adulthood, until old age [12]. The risk of vitamin D deficiency in- creases during pregnancy due to the increase in maternal and fetal demands [13]. Moreover, vitamin D is postulated to have a potential effect on several pregnancy outcomes including fetal skeletal outcome, hypertensive disorders, and gestational diabetes mellitus (GDM) [14–16]. To our knowledge, there is no published data on the relation of low vitamin D and pregnancy, or fetal development, in the Saudi population. The current study aimed to assess 25(OH)D levels in pregnant females residing in Riyadh, and to correlate the vitamin status to the possible mater- nal and neonatal adverse outcomes.
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RESEARCH ARTICLE Comparison of vitamin D levels with bone density, calcium, phosphate and alkaline phosphatase — an insight from major cities of Pakistan

RESEARCH ARTICLE Comparison of vitamin D levels with bone density, calcium, phosphate and alkaline phosphatase — an insight from major cities of Pakistan

from Karachi. Overall, there were 115(39.5%) males and 176(60.5%) females. Of the total, 245(84%) had insufficient vitamin D. No significant difference for gender, milk intake, BMI, exercise and daily sunlight was found (p>0.05). However, there was a significant difference for age group and skin (p<0.05 each). Overall, 154 (53%) subjects had normal BMD. In normal and reduced BMD group, there was a significant difference for gender, age groups and skin colour (p<0.05 each). No significant difference for use of sunscreen, milk intake, BMI, daily sun exposure and daily exercise was found (Table-1). Among the 147(48%) subjects who had reduced bone density, 98(66.6%) had osteopenia and 34(23%) had osteoporosis. Osteoporosis was more in females 28(19%) than males 6(9%). Calcium was low in 202 (69%) cases, ALP was high in 58(20%) cases, while phosphorous was low in 26(9%) and high in 20(7%).
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Vitamin D deficiency exacerbates bleomycin-induced pulmonary fibrosis partially through aggravating TGF-β/Smad2/3-mediated epithelial-mesenchymal transition

Vitamin D deficiency exacerbates bleomycin-induced pulmonary fibrosis partially through aggravating TGF-β/Smad2/3-mediated epithelial-mesenchymal transition

reports indicated that calcitriol, the active form of vitamin D3, suppressed TGF-β1-stimulated EMT in human bronchial epithelial cells [29, 30]. In the present study, we investigated whether vitamin D deficiency aggravates Smad2/3-mediated EMT in BLM-induced lung fibrosis. Our results showed that vitamin D deficiency aggravated pulmonary TGF-β1 upregulation and subsequent Smad3 phosphorylation in BLM-induced lung fibrosis. Moreover, vitamin D deficiency aggravated upregulation of pulmonary ZEB1, a transcription factor for EMT, during BLM- induced lung fibrosis. Finally, vitamin D deficiency ag- gravated BLM-induced downregulation of pulmonary E-cadherin. By contrast, vitamin D deficiency aggra- vated BLM-induced upregulation of vimentin and α- SMA in the lungs. These results suggest that vitamin D deficiency exacerbates BLM-induced pulmonary fi- brosis, at least partially, through aggravating TGF-β/ Smad2/3-mediated EMT.
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Vitamin D deficiency and dyslipidemia in early pregnancy

Vitamin D deficiency and dyslipidemia in early pregnancy

Free/ionic calcium in all the subjects or in the vitamin D-deficient sub-group of pregnant women was signifi- cantly related to vitamin D. The mechanistic basis of ionic calcium homeostasis is still not completely estab- lished. However, the roles of the important individual players of calcium homeostasis aid in hypothesizing that serum levels of free/ionized calcium may be reciprocally regulated by parathyroid hormone (PTH) and 1, 25- dihydroxyvitamin D, with the former one serving to in- crease serum level of calcium and the latter to suppress it. PTH causes net bone loss (resorption) and increases blood calcium levels by stimulating osteoclasts. High levels of vitamin D have been shown to inhibit PTH syn- thesis in vitro and in vivo [27, 28]. Vitamin D deficiency is implicated in reduced serum albumin concentrations [29]. Hence, serum ionic/free calcium, which is non- albumin bound calcium, is expected to be higher in vita- min D deficiency conditions.
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VITAMIN B6-DEPENDENCY AND INFANTILE CONVULSIONS

VITAMIN B6-DEPENDENCY AND INFANTILE CONVULSIONS

In the vitamin B, deficiency state, small amounts of the vitamin cure the convul sions, but larger than normal daily require ments are needed to correct the deficiency state as reflected[r]

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HIGH PREVALENCE OF VITAMIN D DEFICIENCY AMONG PREGNANT WOMEN AND THEIR NEWBORNS

HIGH PREVALENCE OF VITAMIN D DEFICIENCY AMONG PREGNANT WOMEN AND THEIR NEWBORNS

An increasing number of studies suggest that vitamin D deficiency during pregnancy is associated with multiple adverse health outcomes in mothers, neonates, and children. There are no representative country data available on vitamin D status of pregnant women in Europe. The aim of this study was to estimate the prevalence of vitamin D deficiency among Belgian pregnant women and to assess the determinants of vitamin D status in the first and third trimester of pregnancy. The women were selected via a multi-stage proportionate- to-size sampling design. Blood samples were collected and a questionnaire was completed face-to-face. 55 obstetric clinics were randomly selected and 1311 pregnant women participated in the study. The median serum 25-hydroxyvitamin D [25-(OH) D] concentration was significantly lower in the first trimester (20.4 ng/ml) than in third trimester (22.7 ng/ml). Of all women, 74.1% (95%CI = 71.8-76.5%) were vitamin D insufficient (25-(OH)D <30 ng/ml), 44.6% (95%CI = 41.9-47.3%) were vitamin D deficient (25-(OH)D <20 ng/ml), while 12.1% (95%CI = 10.3-13.8%) were severely vitamin D deficient (25-(OH)D <10 ng/ml). Of all women included, 62.0% reported taking vitamin D-containing multivitamins, of which only 24.2% started taking those before pregnancy. The risk of vitamin D deficiency (25-(OH) D <20 ng/ml) was significantly higher for less educated women and women who reported not going on holidays to sunny climates. The risk of severe vitamin D deficiency (25-(OH) D <10 ng/ml) decreased for women who reported alcohol consumption during pregnancy, decreased with more frequent use of sunscreen lotion and increased for smokers and women who reported preference for shadow. In conclusion, vitamin D deficiency is highly prevalent among pregnant women in Belgium and this raises concerns about the health consequences for the mother and the offspring. A targeted screening strategy to detect and
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