Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case is reported of a 29-year-old previously healthy female patient who developed the typical clinical picture of scurvy eight months after changing to a diet exclusively containing cooked cereals. Serum levels of B12, folic acid, and calcium were lowered and the alkaline phosphatase was slightly raised due to the dietary lack of vitamins A, D, B12 and folic acid. No clinical signs of these deficiencies could be observed. Addition of vitamin C to this diet resulted in complete cure in a matter of days. Signs and symptoms of scurvy are discussed in the light of the recent literature. This rare disease is particularly worth considering if one of the following situations is encountered: hemorrhages in the skin, muscles, joints or mucous membranes without apparent cause; therapy-resistant ulcers of mucous membranes in elderly patients; Sicca syndrome and/or wounds exhibiting poor healing.
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PMID:[Scurvy in an adult]. 91 80

The effect of vitamin C deficiency on the digestive and absorptive functions of the gut has been investigated in guinea pigs. The absorption of D-glucose was significantly elevated, but that of L-leucine, L-alanine and L-lysine considerably depressed in the intestine of scorbutic guinea pigs compared to controls. The intestinal transport of vitamin B12 was also diminished. Activities of sucrase and alkaline phosphatase on the brush border were enhanced, but that of leucine aminopeptidase markedly reduced in scorbutic animals compared to controls. Maltase activity was unaffected in vitamin C deficient animals. Chemical analysis of the brush borders isolated from scorbutic animals revealed a considerable decrease in membrane protein, total lipids, phospholipids, and free cholesterol contents compared to control animals. In vivo 2-(14)C-acetate incorporation into membrane lipids suggested that the observed decrease in lipid components of the scorbutic membranes is due to reduced synthesis. Administration of ascorbic acid to scorbutic animals ameliorated the intestinal aberrations observed in scurvy.
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PMID:Effect of vitamin C deficiency in guinea pigs on intestinal functions and chemical composition of brush border membrane. 730 86

Four cases of scurvy diagnosed within a period of two years are reported. They comprised 2 male patients with heavy nicotine and alcohol abuse, a 35-year-old woman with malnutrition due to food supplements phobia, and a 69-year-old woman with malnutrition due to dementia and social isolation. All four patients were adynamic and anemic. Three patients showed typical dermatologic signs with hemorrhagic hyperceratosis, suffusions or cork-screw hair. Two patients complained of parodontol disorders. Other symptoms were gastrointestinal bleeding, sicca syndrome, retinal bleeding, subdural hematoma, edema and arthralgia. Associated disorders were folic acid and vitamin B12 depletion in two cases, and nephropathy and pneumonia with pneumothorax in one case each. In all cases the serum asorbic acid concentration was below the scorbutic level of 11 mumol/l. Historical data, pathogenesis, incidence, clinical presentation, diagnosis and therapy of scurvy are discussed. We conclude that scurvy can be observed even in a developed country such as Switzerland at the end of the 20th century. The real incidence may be underestimated because symptoms are not well known and disappear rapidly after admission because of sufficient vitamin C content in normal diet. Patients at risk are socially isolated alcoholics, old people, psychiatric patients and diet enthusiasts. Usually scurvy occurs in conjunction with other deficiencies. Smoking and acute illness enhance ascorbic acid depletion. With a knowledge of the symptomatology of scurvy, it is easy to diagnose and treatment is simple and effective.
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PMID:[Scurvy--a mistakenly forgotten disease]. 809 Nov 64

Nutritional deficiencies result in many distinctive cutaneous manifestations. Vitamin C deficiency, or scurvy, produces follicular hyperkeratosis, perifollicular hemorrhages, gingival hypertrophy, and bleeding (1). We report here a case of malnutrition who suddenly developed extensive eccymoses on the lower extremities sharing morphological similarities with purpura fulminans. Although the patient did not have the characteristic dermatological features of scurvy, serum levels of vitamins C, K, B12, and E were decreased.
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PMID:Confluent ecchymoses on the lower extremities of a malnourished patient. 1040 89

Diet as a key factor in determining genomic stability is more important than previously imagined because we now know that it impacts on all relevant pathways, namely exposure to dietary carcinogens, activation/detoxification of carcinogens, DNA repair, DNA synthesis and apoptosis. Current recommended dietary allowances for vitamins and minerals are based largely on the prevention of diseases of deficiency such as scurvy in the case of vitamin C. Because diseases of development, degenerative disease and aging itself are partly caused by damage to DNA it seems logical that we should focus better our attention on defining optimal requirements of key minerals and vitamins for preventing damage to both nuclear and mitochondrial DNA. To date, our knowledge on optimal micronutrient levels for genomic stability is scanty and disorganised. However, there is already sufficient evidence to suggest that marginal deficiencies in folate, vitamin B12, niacin and zinc impact significantly on spontaneous chromosome damage rate. The recent data for folate and vitamin B12 in humans with respect to micronucleus formation in blood and epithelial cells provide compelling evidence of the important role of these micronutrients in maintenance of genome integrity and the need to revise current RDAs for these micronutrients based on minimisation of DNA damage. Appropriately designed in vitro studies and in vivo placebo controlled trials with dose responses using a complementary array of DNA damage biomarkers are required to define recommended dietary allowances for genomic stability. Furthermore these studies would have to be targeted to individuals with common genetic polymorphisms that alter the bioavailability of specific micronutrients and the affinity of specific key enzymes involved in DNA metabolism for their micronutrient co-factor. That there is a need for an international collaborative effort to establish RDAs for genomic stability is self-evident.
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PMID:Micronutrients and genomic stability: a new paradigm for recommended dietary allowances (RDAs). 1206 72

Immune support by micronutrients is historically based on vitamin C deficiency and supplementation in scurvy in early times. It has since been established that the complex, integrated immune system needs multiple specific micronutrients, including vitamins A, D, C, E, B6, and B12, folate, zinc, iron, copper, and selenium, which play vital, often synergistic roles at every stage of the immune response. Adequate amounts are essential to ensure the proper function of physical barriers and immune cells; however, daily micronutrient intakes necessary to support immune function may be higher than current recommended dietary allowances. Certain populations have inadequate dietary micronutrient intakes, and situations with increased requirements (e.g., infection, stress, and pollution) further decrease stores within the body. Several micronutrients may be deficient, and even marginal deficiency may impair immunity. Although contradictory data exist, available evidence indicates that supplementation with multiple micronutrients with immune-supporting roles may modulate immune function and reduce the risk of infection. Micronutrients with the strongest evidence for immune support are vitamins C and D and zinc. Better design of human clinical studies addressing dosage and combinations of micronutrients in different populations are required to substantiate the benefits of micronutrient supplementation against infection.
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PMID:A Review of Micronutrients and the Immune System-Working in Harmony to Reduce the Risk of Infection. 3196 93