• gastroenterology
• internal medicine
• minerals/trace elements
• scurvy
• vitamins

• Humans
• Ascorbic Acid/therapeutic use
• Ascorbic Acid/administration & dosage
• Ascorbic Acid/blood
• Ascorbic Acid Deficiency/diagnosis
• Ascorbic Acid Deficiency/complications
• Crohn Disease/diagnosis
• Crohn Disease/complications
• Diagnosis, Differential
• Malnutrition/complications
• Scurvy/diagnosis
• Scurvy/etiology
• Scurvy/complications
• Scurvy/drug therapy

• nutritional deficiency
• pellagra
• schizophrenia
• scurvy

• Dermatology
• Exposure
• UV
• Wilderness medicine
• Xerosis

• Humans
• Arctic Regions/epidemiology
• Skin Diseases/etiology
• Skin Diseases/epidemiology
• Skin Diseases/therapy
• Skin Diseases/diagnosis
• Antarctic Regions/epidemiology
• Dermatology
• Skin/pathology

• Vietnam
• agricultural transition
• demography
• osteological paradox
• survivorship

• Humans
• Scurvy/epidemiology
• Adult
• Male
• Prevalence
• Middle Aged
• Female
• Vietnam/epidemiology
• Young Adult
• History, Ancient
• Adolescent
• Child
• Survivorship
• Child, Preschool
• Aged
• Infant

• DP110101097 Australian Research Council
• FT120100299 Australian Research Council
• EC-54332R-18 National Geographic Society

• Bariatric
• Malnutrition
• Micronutrients
• Minerals
• Vitamins

• Humans
• Micronutrients/deficiency
• Dietary Supplements
• Antioxidants
• Zinc/deficiency
• Critical Illness
• Risk Factors

• Dental anthropology
• Human dentition
• Middle ages
• Oral pathologies
• Tooth wear

• Humans
• History, Medieval
• Male
• Female
• Adult
• Paleodontology
• Switzerland
• Germany
• Middle Aged
• Rural Population
• Adolescent
• Oral Health
• Dental Caries/history
• Dental Caries/epidemiology
• Tooth Wear/history
• Tooth Loss
• Child
• Cemeteries
• Diet/history
• Dental Enamel Hypoplasia/history
• Life Style

• Humans
• Malnutrition/prevention & control
• Micronutrients

• alcoholic
• high-risk group
• solitary skin lesion
• uncommon scurvy manifestation
• vitamin c deficiency

• alcohol use disorder (aud)
• diagnose
• intracerebral hemorrhage
• scurvy
• vitamin c deficiency

• pediatric dermatology
• pseudoscleroderma
• scurvy
• vitamin C deficiency

• continuous renal replacement therapy
• critical care
• intensive care unit
• vitamin C

• Female
• Humans
• Continuous Renal Replacement Therapy
• Critical Illness/therapy
• Ascorbic Acid Deficiency/complications
• Ascorbic Acid/therapeutic use
• Renal Replacement Therapy
• Acute Kidney Injury/therapy

• anemia
• prison
• scurvy
• vitamin C
• vitamin deficiency

• No specific grant from funding organization

• Scurvy
• autism spectrum disorder
• history of medicine
• vitamin C deficiency

• Child
• Infant
• Adolescent
• Humans
• Child, Preschool
• Animals
• Scurvy/complications
• Scurvy/diagnosis
• Autism Spectrum Disorder/complications
• Ascorbic Acid/therapeutic use
• Diet
• Milk

• dietary patterns change
• lower extremities pain
• scurvy
• staying indoors
• vitamin C deficiency

• National Natural Science Foundation of China

• ascorbic acid deficiency
• clinical case report
• hemorrhagic disorders
• malabsorption
• malnutrition
• purpura
• scurvy
• vitamin c
• vitamin c supplementation
• vitamin deficiency

• scurvy
• food preferences
• ascorbic acid
• feeding and eating disorders
• child
• adverse childhood experiences

• Male
• Child
• Humans
• Scurvy/complications
• Scurvy/diagnosis
• Autism Spectrum Disorder
• Brazil
• Malnutrition
• Diagnosis, Differential

• Female
• Humans
• Myalgia
• Hemorrhage/diagnosis
• Hemorrhage/etiology

• vitamin A deficiency
• vitamin B deficiency
• vitamin C deficiency
• vitamin D deficiency
• vitamin E deficiency
• vitamin K deficiency

• Scurvy
• biosocial
• gold fields
• medical history
• nutrition

• Gut microbiota
• Vitamin C
• Vitamin E
• β-carotene

• Humans
• Leg
• Purpura/diagnosis
• Purpura/etiology
• Lower Extremity
• Exanthema/etiology

• ascorbic acid
• gingivitis
• nutrition
• scurvy
• vitamin C
• vitamin C deficiency

• gastrointestinal bleeding
• mucosal ooze
• scurvy
• vitamin C deficiency
• vitamin C supplementation

• chatgpt
• food insecurity
• malnutrition
• psychosocial factors
• scurvy
• vitamin c deficiency

• Male
• Humans
• Child
• Leg
• Pain
• Malnutrition/complications
• Malnutrition/diagnosis
• Exanthema/etiology

• T32 DK007673 NIDDK NIH HHS

• Antarctica
• Scott
• Scurvy
• Shackleton
• beriberi
• cardiac
• expedition
• nutrition
• polar
• thiamine

• Humans
• Scurvy/diagnosis
• Expeditions
• Antarctic Regions

• ascorbic acid
• malnutrition
• petechial rash
• scurvy
• vitamin c

Vitamin C (VC) is an indispensable antioxidant and co-factor for optimal function and development of eukaryotic cells. In animals, VC can be synthesized by the organism, acquired through the diet, or both. In the single VC synthesis pathway described in animals, the penultimate step is catalysed by Regucalcin, and the last step by l-gulonolactone oxidase (GULO). The GULO gene has been implicated in VC synthesis only, while Regucalcin has been shown to have multiple functions in mammals.

Both GULO and Regucalcin can be found in non-bilaterian, protostome and deuterostome species. Regucalcin, as here shown, is involved in multiple functions such as VC synthesis, calcium homeostasis, and the oxidative stress response in both Deuterostomes and Protostomes, and in insects in receptor-mediated uptake of hexamerin storage proteins from haemolymph. In Insecta and Nematoda, however, there is no GULO gene, and in the latter no Regucalcin gene, but species from these lineages are still able to synthesize VC, implying at least one novel synthesis pathway. In vertebrates, SVCT1, a gene that belongs to a family with up to five members, as here shown, is the only gene involved in the uptake of VC in the gut. This specificity is likely the result of a subfunctionalization event that happened at the base of the Craniata subphylum. SVCT-like genes present in non-Vertebrate animals are likely involved in both VC and nucleobase transport. It is also shown that in lineages where GULO has been lost, SVCT1 is now an essential gene, while in lineages where SVCT1 gene has been lost, GULO is now an essential gene.

The simultaneous study, for the first time, of GULO, Regucalcin and SVCTs evolution provides a clear picture of VC synthesis/acquisition and reveals very different selective pressures in different animal taxonomic groups.

The online version contains supplementary material available at 10.1186/s12862-022-02040-7.

• TBI
• antioxidants
• inflammation
• oxidative stress
• reactive nitrogen species
• reactive oxygen species
• synapse

• Humans
• Antioxidants/therapeutic use
• Antioxidants/pharmacology
• Oxidative Stress
• Brain Injuries, Traumatic/drug therapy
• Lipid Peroxidation
• Reactive Oxygen Species/pharmacology
• Brain

• UL1 TR001863 NCATS NIH HHS

Although scurvy, the severe form of vitamin C deficiency, has been almost eradicated, the prevalence of subclinical vitamin C deficiency is much higher than previously estimated and its impact on human health might not be fully understood. Vitamin C is an essential molecule, especially in the central nervous system where it performs numerous, varied and critical functions, including modulation of neurogenesis and neuronal differentiation. Although it was originally considered to occur only in the embryonic brain, it is now widely accepted that neurogenesis also takes place in the adult brain. The subventricular zone (SVZ) is the neurogenic niche where the largest number of new neurons are born; however, the effect of vitamin C deficiency on neurogenesis in this key region of the adult brain is unknown. Therefore, through BrdU labeling, immunohistochemistry, confocal microscopy and transmission electron microscopy, we analyzed the proliferation and cellular composition of the SVZ and the lateral ventricle (LVE) of adult guinea pigs exposed to a vitamin-C-deficient diet for 14 and 21 days. We found that neuroblasts in the SVZ and LVE were progressively and significantly decreased as the days under vitamin C deficiency elapsed. The neuroblasts in the SVZ and LVE decreased by about 50% in animals with 21 days of deficiency; this was correlated with a reduction in BrdU positive cells in the SVZ and LVE. In addition, the reduction in neuroblasts was not restricted to a particular rostro–caudal area, but was observed throughout the LVE. We also found that vitamin C deficiency altered cellular morphology at the ultrastructural level, especially the cellular and nuclear morphology of ependymal cells of the LVE. Therefore, vitamin C is essential for the maintenance of the SVZ cell populations required for normal activity of the SVZ neurogenic niche in the adult guinea pig brain. Based on our results from the guinea pig brain, we postulate that vitamin C deficiency could also affect neurogenesis in the human brain.

• adult neurogenesis
• ascorbic acid
• lateral ventricle extensions
• subventricular zone
• vitamin C

Patients with inflammatory bowel disease (IBD) are prone to several nutritional deficiencies. However, data are lacking on vitamin C deficiency in Crohn’s disease (CD) and ulcerative colitis (UC) patients, as well as the impact of clinical, biomarker and endoscopic disease severity on the development of vitamin C deficiency.

To determine proportions and factors associated with vitamin C deficiency in CD and UC patients.

In this retrospective study, we obtained clinical, laboratory and endoscopic data from CD and UC patients presenting to the IBD clinic at a single tertiary care center from 2014 to 2019. All patients had an available plasma vitamin C level. Of 353 subjects who met initial search criteria using a cohort discovery tool, 301 ultimately met criteria for inclusion in the study. The primary aim described vitamin C deficiency (≤ 11.4 μmol/L) rates in IBD. Secondary analyses compared proportions with deficiency between active and inactive IBD. Multivariate logistic regression analysis evaluated factors associated with deficiency.

Of 301 IBD patients, 21.6% had deficiency, including 24.4% of CD patients and 16.0% of UC patients. Patients with elevated C-reactive protein (CRP) (39.1% vs 16.9%, P < 0.001) and fecal calprotectin (50.0% vs 20.0%, P = 0.009) had significantly higher proportions of deficiency compared to those without. Penetrating disease (P = 0.03), obesity (P = 0.02) and current biologic use (P = 0.006) were also associated with deficiency on univariate analysis. On multivariate analysis, the objective inflammatory marker utilized for analysis (elevated CRP) was the only factor associated with deficiency (odds ratio = 3.1, 95% confidence interval: 1.5-6.6, P = 0.003). There was no difference in the presence of clinical symptoms of scurvy in those with vitamin C deficiency and those without.

Vitamin C deficiency was common in IBD. Patients with elevated inflammatory markers and penetrating disease had higher rates of vitamin C deficiency.

• Inflammatory bowel disease
• Crohn’s disease
• Ulcerative colitis
• Vitamin C deficiency
• Scurvy
• Malnutrition

• Ascorbic Acid
• Ascorbic Acid Deficiency/complications
• Ascorbic Acid Deficiency/epidemiology
• Biological Products
• Biomarkers
• C-Reactive Protein/analysis
• Chronic Disease
• Colitis, Ulcerative/complications
• Crohn Disease/diagnosis
• Crohn Disease/epidemiology
• Humans
• Inflammatory Bowel Diseases/complications
• Inflammatory Bowel Diseases/epidemiology
• Leukocyte L1 Antigen Complex/metabolism
• Prevalence
• Retrospective Studies
• Scurvy/complications
• Vitamin D Deficiency

• ascorbic acid
• dermatology
• nutrition
• skin
• vitamin C
• wounds

• Ascorbic Acid/therapeutic use
• Humans
• Scurvy/complications
• Scurvy/diagnosis
• Skin

• boiled vegetables
• scurvy
• vitamin C deficiency

• Ascorbic Acid/therapeutic use
• Diet
• Humans
• Male
• Middle Aged
• Musculoskeletal Pain
• Scurvy/diagnosis
• Scurvy/etiology
• Vegetables
• Vitamins/therapeutic use

• Dialysis
• Haematology (incl blood transfusion)
• Malnutrition
• Vitamins and supplements

• Anemia
• Ascorbic Acid/therapeutic use
• Gastrointestinal Hemorrhage/complications
• Gastrointestinal Hemorrhage/therapy
• Hematoma/complications
• Humans
• Male
• Renal Dialysis
• Scurvy/complications
• Scurvy/diagnosis
• Vitamins

• Anemia
• Hemolysis
• Scurvy
• Transfusion-Dependent
• Vitamin C

Scurvy is a nutritional disorder caused by vitamin C deficiency. It was a notorious disease in the ancient world, especially among the sailors, and is of rare occurrence in contemporary, developed countries due to increased access and advancement in nutrition services. Scurvy primarily affects the skin and soft tissue, presenting with a myriad of clinical manifestations ranging from musculoskeletal to bleeding-related complaints and even sudden death in later stages. In this article, we present the case of an elderly female with scurvy-related weakness and gait instability leading to mechanical falls, easy bruising, fatigue, and petechial rash. She had improvement in her constitutional symptoms after the initiation of vitamin C supplements. This case reinforces the need to consider scurvy as one of the differentials for petechial rash and easy bruising apart from bleeding diathesis and vasculitis in the contemporary world, especially in at-risk populations.

• clock drawing test
• cognitive impairment
• geriatric patients
• mini mental state examination
• older hospitalised patients
• vitamin C deficiency

• Aged
• Humans
• Male
• Scurvy/diagnosis

• alopecia
• malnutrition
• medical dermatology
• minerals
• nutrition
• skin disease
• vitamins

• Humans
• Scurvy/complications
• Scurvy/diagnosis

• adult
• burns
• critical care
• pulmonary disease
• sepsis
• vitamins
• wound healing

Scurvy is a disease caused by vitamin C deficiency, historically associated with long sea voyages, periods of famine and war. Currently, it is often misdiagnosed and underreported, as physicians tend to consider it a disease of the past.

We present the case of a 79-year-old female who was admitted to the Emergency Department complaining of pruritus. The patient lived alone and in poor hygiene conditions. Diet was scarce. One week before admission she was in contact with flea-ridden stray dogs. Sometime later she noted several fleas and multiple pruritic small papules, crusts, and excoriations on her torso, limbs, palms, soles, and scalp. Physical examination showed the patient to be pale, emaciated, and poorly groomed. Laboratory analysis showed microcytic anemia. Flea bites were treated with oral antihistamines and prednisolone. Follow-up one month later showed weight gain and partial resolution of skin lesions. However, multiple small ecchymosis on both lower and upper limbs, and occasional perifollicular petechias on her lower extremities, were noted. Additional workup showed undetectable serum vitamin C levels. A diagnosis of scurvy was made. The patient was treated with 1000 mg per day of oral vitamin C for one month leading to complete recovery.

We present this case to remind that early recognition of vitamin C deficiency and appropriate supplementation are essential in patients with scurvy. Physicians should be aware of classic signs, symptoms, and social factors associated with this forgotten disease.

• avitaminosis
• flea infestations
• malnutrition
• scurvy
• social determinants of health