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Musculoskeletal manifestations of scurvy.

Scurvy occurs in individuals who eat inadequate amounts of fresh fruit or vegetables, often because of dietary imbalances related to advanced age or homelessness. Asthenia, vascular purpura, bleeding, and gum abnormalities are the main symptoms. In 80% of cases, the manifestations of scurvy include musculoskeletal symptoms consisting of arthralgia, myalgia, hemarthrosis, and muscular hematomas. Vitamin C depletion is responsible for structural collagen alterations, defective osteoid matrix formation, and increased bone resorption. Imaging studies may show osteolysis, joint space loss, osteonecrosis, osteopenia, and/or periosteal proliferation. Trabecular and cortical osteoporosis is common. Children experience severe lower limb pain related to subperiosteal bleeding. Laboratory tests show nonspecific abnormalities including anemia and low levels of cholesterol and albumin. The finding of a serum ascorbic acid level lower than 2.5 mg/l confirms the diagnosis. Vitamin C supplementation ensures prompt resolution of the symptoms.

Ascorbic Acid Deficiency↗

[Scurvy: follicular purpura as a diagnostic sign].

Scurvy is a set of clinical manifestations characterized by general weakness, anemia, gingivitis and cutaneous bleeding, caused by a lack of ascorbic acid in the diet. This pathology is currently a clinical rarity, although it can still be seen in cases of malnutrition associated with alcoholism or with dietary deficiencies, especially in childhood and old age. We present the case of a 45-year-old male who consulted his physician because of lower limb edema with follicular purpura, accompanied by asthenia, polyarthralgia and bleeding gums. After treatment with 1 g/day of vitamin C was initiated, the patient's symptoms quickly improved. The diagnosis of scurvy was based on the patient's clinical symptoms, dietary history and the rapid resolution of the symptoms when vitamin C supplements were initiated.

Humans↗

[Scurvy and acquired ichthyosis associated to Whipple's disease].

The skin manifestations, except for hyperpigmentation, are uncommon in Whipple's disease (WD). We present the case of a 48-year-old male with chronic diarrhea and long course general syndrome associated to neurological manifestations. Skin examination revealed lesions in the lower limbs and gums that were clinically consistent with scurvy and were confirmed by histological study and measurement of blood vitamin C levels. Furthermore, he had lesions that were clinically and histologically consistent with acquired ichthyosis. The digestive tract biopsy study showed non-necrotizing epithelioid granulomas without the presence of PAS positive macrophages. The patient was diagnosed of Whipple's disease through the identification of genomic fragments of Tropheryma Whippelii by PCR in duodenal samples. He was treated with antibiotics for two years with resolution of the cutaneous and digestive picture but with partial improvement of the neurological symptoms. In the literature reviewed, we did not find any case of acquired ichthyosis associated to WD and only one of scurvy secondary to this rare disease.

Anti-Bacterial Agents↗

Scurvy.

Scurvy is caused by a deficiency of ascorbic acid. We describe a 31-year-old Hispanic man who had perifollicular hemorrhages, follicular hyperkeratosis, corkscrew hairs, and gingival hemorrhage after consuming a peculiar and restricted diet for 1 year. A diagnosis of scurvy was made and the patient's disease resolved after treatment with vitamin C.

Adult↗

Scurvy: bilateral lower extremity ecchymoses and paraparesis.

A 46-year-old man presented with two weeks of progressive paraparesis and large confluent ecchymoses of both thighs. There was a history of poor dietary intake and daily alcohol use. He had had similar problems each of the past two winters. In 1979 he required hospitalization for "sciatica." In 1980 he was bedridden for two months because of lower extremity weakness. Examination revealed poorly fitting dentures, large confluent ecchymoses of both thighs, perifollicular hemorrhages, and a low serum ascorbic acid concentration. Oral ascorbic acid was begun in the hospital and all clinical symptomatic consequences of scurvy rapidly resolved. We present this case to reiterate the clinical presentation of scurvy and to emphasize the importance of recognizing early signs of nutritional deficiencies that may be confused with more common, but often less treatable, diseases.

Ascorbic Acid↗

[Scurvy in intensive care despite vitamin supplementation].

INTRODUCTION: Scurvy can occur in hospitalized patients despite vitamin supplementation. OBSERVATION: A 63 Year-old patient who had spent several weeks in intensive care developed an unexplained anemia and ecchymoses. Despite daily administration of 130 mg/day of vitamin C since his admission, his ascorbic acid blood levels had collapsed. Administration of 1g/day relieved the symptoms within four weeks. DISCUSSION: Whether a deficiency had existed prior to admission or not, scurvy developed during the week of intensive care despite parenteral nutrition supplying a daily dose of 130 mg of vitamin C. Such deficiencies decompensated in surgical situations remain a reality in developed countries. CONCLUSION: In certain pathological contexts and in all the growing number of cases in elderly patients and many surgical indications, the need for vitamin C supplementation has to be defined. The needs at that particular time must be taken into account and the prior nutritional status.

Ascorbic Acid↗

Scurvy: forgotten but not gone.

Scurvy is still seen sporadically in the developed world. At a time when subclinical vitamin C deficiency in the general population is being recognized increasingly, the need for clinicians to be aware of this disease remains. We present the case of a 9-year-old boy admitted to hospital with musculoskeletal pain, weakness and changes in the skin and gums. After extensive investigation, he was found to have vitamin C deficiency resulting from a restricted eating pattern. Musculoskeletal complaints are a common mode of presentation of scurvy in children. Failure to appreciate this fact and the risk factors for poor vitamin C intake in the paediatric age group can result in unnecessary and invasive investigations for apparent 'multisystem' disease.

Ascorbic Acid↗

Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.

Previous studies showed that administration of ascorbate to glutathione (GSH)-deficient newborn rats and guinea pigs prevented toxicity and mortality and led to increased tissue and mitochondrial GSH levels; ascorbate thus spares GSH. In the present work, we tried to answer the converse question: Does administration of GSH spare ascorbate? Because administered GSH is not well transported into most cells, we gave GSH monoethyl ester (which is readily transported and converted into GSH intracellularly) to guinea pigs fed an ascorbate-deficient diet. We found that treatment with GSH ester significantly delays appearance of the signs of scurvy and that this treatment spares ascorbate; thus, the decrease of tissue levels of ascorbate was delayed. The findings support the conclusions that (i) GSH is essential for the physiological function of ascorbate because it is required in vivo for reduction of dehydroascorbate and (ii) there is metabolic redundancy and overlap of the functions of these antioxidants. The sparing effect of GSH in scurvy may be mediated through an increase in the reduction of dehydroascorbate (which would otherwise be degraded) and to antioxidant effects of GSH that are also produced by ascorbate. Other studies indicate that GSH deficiency in adult mice stimulates ascorbate synthesis in liver. During this work we found that administration of GSH itself is highly toxic to ascorbate-deficient guinea pigs when given in divided i.p. doses totaling 3.75 mmol/kg daily.

Animals↗

Human T-cell function in experimental ascorbic acid deficiency and spontaneous scurvy.

Studies in animal models suggest that ascorbic deficiency impairs T-cell-mediated immunity. We studied five normal volunteers hospitalized on a metabolic unit and consuming a strictly controlled diet deficient in ascorbic acid I) after a 5-wk control period of ascorbic acid supplementation (75 mg/day) and 2) after a 9-wk period of no supplementation. Three of the subjects were restudied after a 5-wk period of ascorbic acid supplementation after the deficient period. At the end of both control periods ascorbic acid levels in plasma ranged from 0.9 to 1.3 mg/dl and in leukocytes from 19 to 30 microgram/10(8) cells. At the end of the deficient period levels of ascorbic acid in plasma ranged from 0.09 to 0.15 mg/dl and in leukocytes from 6.2 to 10 microgram/10(8) cells, levels at or below those frequently found in frank scurvy. None of the T-cell parameters tested including mitogen responsiveness to phytohemagglutinin and percentage of T-cells bearing receptors for IgM (helper cells) and IgG (suppressor cells) was different in the deficient period compared to the control periods. One patient with spontaneous scurvy (plasma ascorbic acid 0.07 mg/dl, leukocytic ascorbic acid 4.9 microgram/10(8) cells) was studied at the time of admission and after vigorous ascorbic acid repletion. All T-cell parameters after repletion were unchanged from admission. We conclude that in man ascorbic acid deficiency, even at the scorbutic level, does not alter T-cell numbers or impair in vitro T-cell function.

Adult↗

Scurvy occurring in a teenager.

Scurvy is now an uncommon condition in the western world. We report a case of scurvy in a 14-year-old female with an inadequate diet who developed a purpuric rash affecting her trunk and legs. The rash resolved dramatically with ascorbic acid therapy.

Adolescent↗

Scurvy in the British Mercantile Marine in the 19th century, and the contribution of the Seamen's Hospital Society.

When long voyages in sailing vessels were commonplace, scurvy was a major health hazard in mariners of all nations. The observations of James Lind (1716-94) and others indicated that citrus fruits had both a preventive and curative role in this disease. In the light of this work, by 1800 the disease had been virtually eliminated from Britain's Royal Navy. However, it continued in the merchant navies of all nations until the latter half of the 19th century. In 1867, the Merchant Shipping Amendment Act was passed by the British Parliament largely as a result of a concerted effort by the Seamen's Hospital Society (SHS), one of whose physicians, Harry Leach (1836-79) was the major proselytiser for improved conditions in the merchant service. Examination of the SHS records before and after this event demonstrate a marked reduction in the prevalence of scurvy in the Port of London. Although other factors-such as the introduction of steam ships, which resulted in faster voyages-were clearly important, the compulsory administration of genuine lime juice under supervision in the merchant service seems to have exerted a significant effect.

Autopsy↗

Subclinical scurvy in the guinea pig.

Twenty-eight guinea pigs from nine episodes of subclinical scurvy had diarrhea, weight loss and dehydration. The classical signs of scurvy were not seen. Microscopically the epiphyses were attenutated and irregular. The amount of osteoid was less than normal. Many guinea pigs had acute enteritis. In some there were many hemosiderin-laden macrophages in the intestinal lamina propria. All episodes were associated with either autoclaving food without adequate supplementation or other inadequate feed management practices.

Animals↗

Early settlements in Newfoundland and the scourge of scurvy.

Two important archeological investigations currently underway in the Avalon Peninsula of Newfoundland, at Cupids (established 1610) and Ferryland (1621), help to focus questions on health and health care in early seventeenth-century English settlements. This review looks at one aspect only, the problem of scurvy and what treatments were tried. In adding to our understanding of early colonial settlements and on how new medicinal plants were "discovered," the Newfoundland story reveals a considerable interest in local plants as substitutes for scurvy grass. Suggestions are offered on how they may have been chosen and the rationales behind their use.

Archaeology↗

Scurvy in capybaras bred in captivity in Argentine.

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.

Animals↗

[Scurvy presenting with ecchymotic purpura and hemorrhagic ulcers of the lower limbs].

INTRODUCTION: The risk of vitamin C deficiency is underestimated in industrialized countries and is only disclosed in rare cases of severe scurvy. CASE REPORT: We report three cases of scurvy presenting with ecchymotic purpura and hemorrhagic ulcerations of the lower limbs. Vitamin C supplementation led to rapid improvement of the skin lesions. DISCUSSION: Clinical diagnosis of low-grade deficiency can be difficult. Biological diagnosis requires special care in sample taking and transport.

Aged↗

[Scurvy and adrenal insufficiency].

We describe a case of scurvy in a 32-year-old woman. The disease was associated with bilateral tumours of the quadriceps muscles and malignancy was considered. Adrenal insufficiency was also diagnosed. All abnormalities subsided in response to vitamin C therapy. It is unknown whether there is a causal link between the two diseases, but evaluation of adrenal function seems justified in future cases of scurvy.

Adrenal Insufficiency↗

[A case of scurvy with alveolar hemorrhage].

A 53-yr-old man with a history of chronic renal failure was admitted to the hospital of Hyogo College of Medicine on March 24th, 1999, because of severe continuous hemoptysis. On February 14th, 1999, the patient had undergone a cadaveric kidney transplantation in the urology department of another hospital. He did not experience any immunological reactions due to tissue rejection. On admission, subcutaneous bleeding at the site of an injection received 1 month before was noticed on his left arm. Petecheae of the extremities and a conjunctival hemorrhage were also noted. However, coagulation and fibrinolysis tests were essentially normal. These findings indicated that the hemorrhages were due to vessel weakness. Scurvy was diagnosed since his serum vitamin C was extremely low (0.2 microgram/ml). The patient was given ascorbic acid (1 g/day), and his condition improved dramatically. Ten years ago, the patient had had renal failure, which had been treated with chronic maintenance dialysis and dietary restriction. It has been postulated that a diet lacking in vitamin C or the steroid treatment he received after kidney transplantation may have induced the scurvy.

Hemorrhage↗

Royal naval physician Sir John Jamison (1776-1844), Scurvy and Sweden's medico-surgical institute.

As a direct consequence of Sweden's devastating losses in its war with Russia in 1808-9, an institute for the training of military surgeons was established in Stockholm in December 1810. This establishment soon became known as the Karolinska Institute and is the forerunner of today's eponymous institution. This paper records the nature of the British assistance that led indirectly to the founding of this institute. This aid took the form of a report into the high morbidity and mortality rates due to scurvy which were sustained by the Swedish Fleet in Carlscrona in the summer of 1808. This report, written by John Jamison, Fleet Physician to the Baltic Command of Sir James Saumarez, was used by the Stockholm medical authorities as part of their campaign for improved training of military medical personnel. Whilst Jamison's report did not in itself lead to the establishment of the Stockholm medico-surgical institute, it was undoubtedly important, and serves both as an example of Anglo-Swedish relations during the Napoleonic era and a reminder of the ravages of scurvy.

Academies and Institutes↗