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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.
Scurvy developed in a 56-year-old man with poor dietary intake and was associated with knee hemarthroses and synovial thickening. The synovial membrane showed interstitial hemorrhage and many large fibroblasts but little collagen and some disarray of vascular basement membrane. Hemarthroses and all knee symptoms completely resolved on a normal diet. To our knowledge, these are the first electron-microscopic studies of synovial membrane in human scurvy, and our findings support a defect in collagen synthesis as a factor in etiology.
A five year old girl presented with short femora, cupped distal metaphyses and flexion deformity of the knees suggesting previous epiphyseo-metaphyseal damage. The aetiology was suggested by finding a history of previous infantile scurvy with separated distal femoral epiphyses. The rarity of this complication and possible contributing factors are discussed.
This communication advances the proposal that all the diverse manifestations of scurvy can be attributed to depolymerisation of ground substance glycosaminoglycans brought about by exposure to uninhibited cellular hyaluronidase. It suggests that ascorbic acid exerts its prime biological function indirectly by incorporation into a glycosaminoglycan residue to form the physiological hyaluronidase inhibitor. The therapeutic implications of this working hypothesis are briefly discussed.
L-Gulono-gamma-lactone oxidase (L-gulono-gamma-lactone:oxygen 2-oxidoreductase, EC 1.1.3.8) is the enzyme that catalyzes the terminal step of L-ascorbic acid biosynthesis in mammalian liver. The absence of the oxidase activity in primates and guinea pigs is the reason why these animals are subject to scurvy, which must be considered an inborn error of metabolism. Attempts were made to determine if a protein immunologically crossreactive with L-gulono-gamma-lactone oxidase is present in these animals. Detergent-solubilized microsomal preparations from guinea pig and African green monkey liver did not precipitate the antisera directed to either rat or goat enzyme, nor did any of the other cell fractions obtained from guinea pig liver react with either antiserum. No crossreactive protein was detectable in guinea pig microsomes even with the sensitive procedure or micro-complement fixation. On the other hand, extracts of all 10 other mammalian (4 orders) liver microsomes tested were shown to contain L-gulono-gamma-lactone oxidase activity that did crossreact with antibodies to the rat and goat enzymes. One explanation of these findings is that, in the guinea pig, and perhaps in primates too, the structural gene for L-gulono-gamma-lactone oxidase is not expressed.
A case of scurvy presenting in a patient with Crohn's disease is reported. A normal response to replacement therapy is seen. Vitamin C (ascorbic acid) deficiency was found in 7 out of 10 patients with clinically quiescent Crohn's disease, 4 of whom had an adequate oral intake of vitamin C. There was no significant difference in oral intake between patients with Crohn's disease and matched controls but there was a significant difference (P less than 0.001) in leucocyte ascorbic acid levels. It is recommended that patients with Crohn's disease be screened for vitamin C deficiency and receive prophylactic vitamin C supplements daily.
The endothelial and sub-endothelial lesions during early stages of experimental atherogenesis and scurvy have been studied by means of scanning EM and transmission EM, making use also of the Con-A reaction. The surface coat modifications were accompanied by formation of vacuoles in the endothelial cells and by sub-endothelial 'oedema', not only in rabbits fed a hypercholesterolic diet but also in scorbutic guinea pigs. The endothelial lesions were sometimes found even before clear modifications of the Con-A surface reactive layer were apparent.
The authors report the case a 11-month-old baby girl admitted by the "Mother and Child Welfare" doctor. On admission, she was very hypotrophic, febrile and pale. Furthermore, she had anaemia complicated with painful invalidating oedema of both thighs. X-ray film show moderate lesions of the metaphysis, but very rapidly, there was a hugh bilateral sub-periosteal hematoma. They insist on the value of periosteal hematoma as a characteristic sign of scurvy. This was later confirmed by laboratory investigations and by the finding of urinary infection due to bilateral reflex on cystography and to right uretero-hydronephrosis on I.V.P. This case is singular because it associates three findings: severe vitamin deficiency by dietetic error due to modern industrial alimentation and a major urinary tract malformation with refractory urinary tract infection.
The translation form Latin of a XVIIth century medical document concerning scurvy is reported. Stress is laid on the importance of historical research of this type as an intellectual exercise and as a historical curiosity.
Scintigraphic bone changes in two cases of scurvy are described, the cause being subperiosteal hematoma. Generalized increased uptake was shown in the affected femur at an early state of the disease. At a late stage, marked uptake both in the femoral shaft and surrounding tissue was seen causing scintigraphic appearance of widened ("club-shaped") femur.
Microsomes from livers of scorbutic guinea-pigs showed a reduced rate of acetanilide hydroxylation. The response of "scorbutic" liver microsomes to the inhibitor Metyrapone (2-methyl-1,2 di (3-pyridyl) propan-1-one) was different from that of liver microsomes from non-scorbutic guinea-pigs.
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