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Nutritional Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Chelsea Kesty, Madeline Hooper, Erin McClure, Emily Chea, Cynthia Bartus
Overview: All neonates are born with low levels of vitamin K. Approximately 8–31% of healthy adults are vitamin K deficient. Severe deficiencies with clinically significant bleeding are limited to individuals taking vitamin K antagonists, such as warfarin, and those with malabsorption syndromes. Adults can acquire vitamin K deficiency through diseases of fat malabsorption (e.g., celiac disease and cystic fibrosis), inadequate dietary intake (typically seen in vegans), antibiotic regimens (that decrease gut bacteria responsible for vitamin K production), or vitamin K–inhibiting anticoagulation therapy.
Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Like dietary lipids and other fat-soluble vitamins, ingested vitamin K is incorporated into mixed micelles via the action of bile and pancreatic enzymes, and it is absorbed by enterocytes of the small intestine (82). Vitamin K is rapidly metabolized and excreted. This rapid metabolism accounts for vitamin K’s relatively low blood levels and tissue stores compared to those of the other fat-soluble vitamins (82). Vitamin K deficiency is rare because vitamin K is present in dietary foods, mostly in leafy green foods, and the bacteria in human intestines can make vitamin K (3, 9, 33, 82–86). Sometimes taking antibiotics can kill the bacteria and lead to a temporary mild deficiency. Vitamin K deficiency can lead to bleeding and hemorrhage, such as oozing in the nose, gums, and intestines. Other diseases may lead to vitamin K deficiency such as celiac disease, Crohn’s disease, liver disease, bleeding disorders, gallbladder or biliary disease, cystic fibrosis, long-term hemodialysis, treatment by warfarin (an anticoagulant drug), and serious burns (33, 82–86). Because vitamin K is required for the carboxylation of osteocalcin in bone, vitamin K deficiency could also reduce bone mineralization and contribute to osteoporosis, and is associated with a higher risk of osteoarthritis (82–84). Allergic reaction to vitamin K supplementation is possible.
The vitamins
Published in Geoffrey P. Webb, Nutrition, 2019
Vitamin K deficiency leads to a reduced efficiency of the blood clotting system and thus to a tendency to bleed. Primary dietary deficiency of vitamin K is almost never seen but malabsorption for example in untreated coeliac disease can precipitate deficiency and lead to bleeding. The coumarin group of anticoagulant drugs (e.g. warfarin) exert their effect by blocking the effects of vitamin K and lead to reduced levels of clotting factors in blood. Therapeutic overdosage of these drugs or accidental overdose from warfarin-containing rodent poisons leads to bleeding and vitamin K acts as an antidote to warfarin.
Life-threatening massive upper gastrointestinal bleeding in a term and healthy baby
Published in Baylor University Medical Center Proceedings, 2023
Serdar Alan, Sevde Nur Vural, Hacer Fulya Gulerman, Meryem Albayrak, Didem Aliefendioglu
Upper gastrointestinal (UGI) bleeding involves a hemorrhage originating from the proximal part of the ligament of Treitz in the distal duodenum and presenting with hematemesis or melena.1 The most common cause of hematemesis or the presence of blood in the stomach contents in newborns in the first days of life is usually maternal blood swallowed during delivery or sucking from a cracked nipple.2 Vitamin K deficiency bleeding (VKDB) of the newborn, previously known as hemorrhagic disease of the newborn, has decreased considerably in the era of vitamin K prophylaxis.3 The common reported causes of UGI bleeding in newborns are stress gastritis, gastric/duodenal ulcers, esophagitis, nasogastric tube trauma, vascular malformations, gastrointestinal duplications, coagulopathy, congenital coagulation defects, and milk protein allergy.4 Massive UGI hemorrhage is very rare in healthy term infants and is commonly seen in sick or premature infants and infants with asphyxia.5 Here we report a previously healthy newborn admitted to the neonatal intensive care unit (NICU) due to life-threatening severe UGI hemorrhage.
Calciphylaxis-as a drug induced adverse event
Published in Expert Opinion on Drug Safety, 2019
Ignacio Portales-Castillo, Daniela Kroshinsky, Cindy K. Malhotra, Roberta Culber-Costley, Mario Gennaro Cozzolino, Shelly Karparis, Charles L. Halasz, Jeremy Goverman, Harold J. Manley, Rajeev Malhotra, Sagar U. Nigwekar
Calciphylaxis can be classified based on the presence or absence of renal disease as uremic and non-uremic and the distribution of the lesions can be described as central (trunk and extremities proximal to elbow and knees) or peripheral. Although they have similar histopathologic patterns, the risk factors and clinical characteristics associated with each classification may differ [13,14]. Patients with uremic calciphylaxis often have elevated levels of the calcium-phosphate product and/or PTH. These parameters however are commonly normal in non-uremic cases. In non-uremic patients, calciphylaxis is more commonly associated with the use of medications such as corticosteroids and warfarin and these patients more often have other conditions associated with vitamin K deficiency like liver disease, obesity and gastric bypass [14,15].
The pathophysiology and management of vascular calcification in chronic kidney disease patients
Published in Expert Review of Cardiovascular Therapy, 2023
Mehmet Kanbay, Sidar Copur, Cem Tanriover, Furkan Yavuz, Andrea Galassi, Paola Ciceri, Mario Cozzolino
Lastly, vitamin K deficiency is a prevalent issue among CKD patients that may be attributable to malnutrition or anticoagulant medications. Two inhibitors of VC, namely matrix Gla protein (MGP) and Gla-rich protein (GRP), require vitamin K-dependent posttranslational gamma carboxylation while their deficiency or inactivity have been linked to increased risk for VC in both in vitro and in vivo studies [23–27]. MGP is produced by VSMCs and chondrocytes and can inhibit as well as reverse the calcification process [28]. In a detailed review on MGP, Roumeliotis et al. have classified the different forms of MGP and decreased vitamin K2 (especially menaquinone-7) levels can lead to the development of several inactive forms of MGP, based on the degree of carboxylation and/or phosphorylation: the uncarboxylated MGP (ucMGP), carboxylated but dephosphorylated MGP (dpcMGP), phosphorylated but uncarboxylated (pucMGP), and the completely inactive, uncarboxylated and dephosphorylated MGP (dpucMGP), whereas the fully active form is phosphorylated and carboxylated [28]. Circulating dpucMGP has been suggested as a powerful indicator of vitamin K status as well as an important contributor to the pathogenesis of VC with circulatory dpucMGP reported to be elevated in CKD patients and even more exacerbated in dialysis patients [28–32]. Circulating dpucMGP has also been related to mortality and decreased renal function in diabetic CKD patients, in 66 diabetic CKD patients, Roumeliotis et al. reported that elevated plasma dpucMGP levels were linked to all-cause mortality (HR 2.63, 95% CI 1.17 to 5.94, p = 0.02), cardiovascular mortality (HR 2.82, 95% CI 1.07 to 7.49, p = 0.037) and progression of CKD (HR 4.02, 95% CI 1.20 to 13.46, p = 0.024) [33] (Figure 1).