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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Willow ptarmigan chicks raised on a diet containing 265 mg ascorbic acid/kg develop scury-like symptoms and die by 4 weeks of age. If blueberry plants are given as an ad libitum supplement to this diet, the malady is prevented. We have described the clinical, pathological and histological changes which accompany this malnutrition and conclude that they are in accord with the description of scurvy in guinea pig and man. Biochemical determination of ascorbic acid synthesis in the kidney of ptarmigan chicks indicated a rate of synthesis five times that found in livers of growing white rats. Blueberry plants and many other plants found in the natural diet of ptarmigan chicks contain 2,000 to 5,000 mg ascorbic acid/kg dry weight. Feeding experiments showed that the pathological signs were avoided and that already afflicted chicks recovered if the vitamin C content of the diet was raised to 750 mg/kg dry weight of food. Since the food intake of the chicks was 5 to 8 g/day the daily requirement of external vitamin C is about 150 mg/kg body weight. To our knowledge this is the first example of an animal which, while producing vitamin C itself, requires substantial amounts of external vitamin C to survive.
J Nutr 1979 Dec
PMID:Vitamin C deficiency in growing willow ptarmigan (Lagopus lagopus lagopus). 51 12

Increasing knowledge concerning the molecular structure of collagen and the steps involved in its biosynthesis provides the basis for a new look at the collagen diseases. Some, like the Ehlers-Danlos syndrome, are now known to be the expression of primary molecular defects; others, such as scurvy and scleroderma, appear to be secondary to some process that disrupts normal controls over collagen synthesis or deposition.
Hosp Pract 1977 Dec
PMID:Collagen diseases and the biosynthesis of collagen. 92 26

Scurvy is rarely diagnosed in our society today. The authors describe the case of a 31-year-old man with weakness, gingival pain, and a rash over the lower extremities. He had a history of poor nutritional intake, no alcohol consumption, and a 13 pack-year history of cigarette smoking. Laboratory studies revealed an extremely deficient serum ascorbic acid level. Treatment was begun with oral ascorbic acid tablets and, within 3 days after discharge, all clinical symptoms of scurvy had resolved. Scurvy is an easily treated disease and should be considered when there is an appropriate history and classic clinical findings. Because vitamin C deficiency can be seen in many chronic disease states, it is important to recognize some of the early features and clinical manifestations of such nutritional deficiencies.
J Am Osteopath Assoc 1992 Dec
PMID:Scurvy in a nonalcoholic person in the United States. 148 83

Scurvy is caused by severe deficiency of vitamin C or ascorbic acid, and is usually diagnosed by the overt clinical signs which appear at an advanced stage. Laboratory examinations, and in particular ascorbic acid assays, do not yet enable subclinical vitamin C deficiency to be reliably detected; hence the importance of knowing the situation which expose to this deficiency.
Presse Med 1991 Dec 07
PMID:[Vitamin C. From scurvy to the ideal vitamin balance]. 183 66

The clinical findings of scurvy have been known for well over 3,000 years. In 1753, Sir James Lynd demonstrated the efficiency of citrus fruit in the prevention of this condition. Scurvy still occurs from time to time in this country, notably in the elderly, particularly in bachelors who live alone and eat a poor diet. Scurvy has been associated with gastrointestinal malignancy, but, as far as we know, it has not been reported in association with carcinoma of the caecum. We report the case of an elderly female patient who presented with features of scurvy and was also found to have carcinoma of the caecum.
Br J Clin Pract 1990 Dec
PMID:Carcinoma of the caecum in a scorbutic patient. 196 14

Recently, a new type of skeletal lesions has been described in Cooley's anemia as a possible complication secondary to therapy. In 12 children affected with thalassemia major, who received an intensive transfusional regimen combined with continuous iron chelation therapy (desferoxamine-B: 50-80 mg/kg/day), some radiological abnormalities of the long bones were observed similar to those described in rickets and scurvy. These rickets and/or scurvy-like lesions had never been reported before the introduction of high-dose desferoxamine therapy. The pathogenesis of these lesions is uncertain, but the toxic effect of desferoxamine probably plays an important role in their development. The association of growth retardation and rickets and/or scurvy-like skeletal lesions in Cooley's anemia patients may be used as a valuable clinical criterion in long-term chelation management.
Radiol Med 1990 Dec
PMID:[Rickets- and/or scurvy-like bone lesions in beta-thalassemia major]. 228 Nov 61

Our investigations have brought new aspects of the biochemistry of ascorbic acid to light: Ascorbic acid exceeds the functions of a vitamin, since it not only has its known cofactor roles for several enzymes, but also affects the regulation of the levels of the circulating thyroid and adrenal cortical hormones. In guinea-pigs the ability to detoxicate certain drugs, e.g. barbiturates, decreases with a minimal but not yet perilous supply of ascorbic acid. This symptom is connected with high blood levels of cortisol, which are probably also involved in the injuries to connective tissue known in scurvy. Guinea-pigs, which like man are dependent on ascorbic acid as an essential foodstuff, are able to adapt to high doses of ascorbic acid. Under these conditions they catabolize it at an increased rate. However, for a certain period after a sudden drop in the high dosage of ascorbic acid there is a danger that a hypovitaminotic, suboptimal metabolic state will develop. Oral and parenteral applications of ascorbic acid yield different results, since the organism limits the absorption of the physiological oral uptake. When this limit is exceeded, the liver in particular is unprotected and becomes swamped. The harmlessness of high doses of ascorbic acid probably holds true only in the case of oral uptake.
Z Ernahrungswiss 1985 Dec
PMID:[New aspects of the biochemistry of vitamin C]. 391 64

1. The effect of ascorbic acid deficiency on glycosaminoglycans of granulation tissue and cartilage of guinea pigs was investigated by determination of the changes in the glucosamine and galactosamine contents 12 days after tendonectomy. 2. In normal granulation tissue, the glucosamine and galactosamine contents rose to a peak at 5 and 10 days respectively, whereas the hydroxyproline and proline contents continued to rise throughout the 20 days after tendonectomy. 3. The galactosamine in scorbutic granulation tissue, but not in that of pair-fed controls, decreased significantly in absolute amount and relatively to glucosamine, which remained practically unchanged; the cartilage galactosamine did not decrease during the 22 days of deficiency owing to the presence of excess of preformed galactosaminoglycans, which masked the small amount of newly formed glycosaminoglycans. 4. The chemical results were confirmed by radioactivity studies in vivo of incorporation of [U-(14)C]glucose into galactosamine and glucosamine of scorbutic granulation tissue and cartilage. The incorporation of (14)C into galactosamine decreased significantly in scurvy in both tissues. 5. The results indicated in both tissues a decreased formation of galactosamine during scurvy, although an increased degradation of polymerized glycosaminoglycans could not be entirely ruled out. It is concluded that, if lack of ascorbic acid causes an impaired galactosamine formation, the most likely position for the block may be in the UDP-N-acetylglucosamine 4-epimerase reaction.
Biochem J 1968 Dec
PMID:The effect of scurvy on glycosaminoglycans of granulation tissue and costal cartilage. 423 17

1. Guinea-pigs kept on a diet deficient in ascorbic acid lost weight and became moribund in about 24 days.2. The adrenal ascorbic acid concentration fell rapidly during the first 2 weeks, and the plasma corticosteroid concentration and 17-oxogenic steroid excretion rose sharply in the third week of ascorbic acid deficiency.3. Both histamine and corticotrophin increased the plasma corticosteroid concentration when injected during the second week but failed to change the pre-existing high concentration of the steroid in the third week of ascorbic acid deficiency.4. The observations confirm that ascorbic acid is not involved in corticoidogenesis and that scurvy is a severe stress which increases adrenocortical activity to such an extent that the rate of synthesis of corticosteroids is incapable of matching the rate of their release.
Br J Pharmacol 1970 Dec
PMID:Ascorbic acid deficiency and pituitary adrenocortical activity in the guinea-pig. 432 49

A 54-year-old woman was admitted for evaluation of palpable purpura, arthralgias, and myalgias. An unusual dietary history was noted. This finding, along with follicular hyperkeratoses and corkscrew hairs, suggested scurvy, which was confirmed by results of laboratory evaluation, examination of biopsy specimens, and response to therapy. Scurvy, though unusual in developed countries, should be considered in the differential diagnosis of palpable purpura.
Cutis 1984 Dec
PMID:Scurvy: a clinical mimic of vasculitis. 651 17


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