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PubMed2002

An unusual presentation of scurvy following head injury.

We report an unusual clinical presentation of scurvy in a one and half year old child. The child presented with abrupt onset of peri-orbital ecchymoses and scalp hemorrhage following head injury. The child also had a history of temper tantrums and head banging. Our case did not have any of the typical clinical features of scurvy. The diagnosis was eventually confirmed radiologically and by observing a dramatic response to vitamin C therapy. It is important to remember that scurvy can present atypically i.e. without bleeding gums, painful limbs, pseudo-paralysis or scorbutic rosary. Scurvy should be kept as a differential diagnosis in a young child presenting with bleeding manifestations. Taking a detailed dietary history is of utmost importance in pediatric practice.

Craniocerebral Trauma↗
PubMed2003

Scurvy in pediatric patients: a review of 28 cases.

OBJECTIVE: To study the dietary factors, clinical findings, plasma vitamin C level and post-treatment outcome of scurvy in pediatric patients at Queen Sirikit National Institute of Child Health. STUDY DESIGN: A retrospective study. METHOD: The medical and radiographic records of pediatric patients, diagnosed with scurvy at Queen Sirikit National Institute of Child Health from 1995 to 2002 were reviewed. RESULTS: Twenty-eight pediatric patients were diagnosed with scurvy. Their ages ranged between 10 months-9 years 7 months (median age of 29 months). 93 per cent of the cases were between 1-4 years of age. All were fed with well-cooked foods and small amounts or no vegetables and fruits. Supplementation with ultra heat temperature (UHT) milk was found in 89 per cent, average 5.8 boxes/day and 14.3 months in duration. Eighty-six per cent of cases were misdiagnosed previously. Clinical manifestations involved limp or inability to walk (96%), tenderness of lower limbs (86%), bleeding per gum (36%), fever (18%), and petechial hemorrhage (3.6%). All cases had abnormal radiographic findings compatible with scurvy and 2 cases had epiphyseal separation. All had clinical improvement within the first week after vitamin C supplementation. CONCLUSION: Vitamin C deficiency was found in the children's intake of small amounts or no vegetables and fruits together with UHT-milk. Frequent manifestations were limping and inability to walk and pain in the lower limbs. Response to vitamin C treatment was dramatic.

Ascorbic Acid↗
PubMed1985

Adult scurvy.

Scurvy is a disease that can mimic other more serious disorders such as deep vein thrombosis, vasculitis, and systemic bleeding disorders. Because the clinical features of scurvy are no longer well appreciated, scorbutic patients are often extensively evaluated for other disorders. Familiarity with the risk factors for and clinical manifestation of scurvy can facilitate earlier diagnosis. We report three patients who highlight the epidemiology, clinical features, and differential diagnosis of scurvy.

Adult↗
PubMed1994

Scurvy resembling cutaneous vasculitis.

Various conditions can imitate cutaneous vasculitis. Scurvy is a less appreciated cause of rash that can resemble vasculitis. Three patients were referred to our rheumatology service for "vasculitis," who subsequently were found to have scurvy. Findings included a purpuric skin rash, myalgias, and malaise. The patients had low vitamin C levels and findings on skin biopsy specimens indicative of scurvy. The three patients were on idiosyncratic diets deficient in vitamin C, and the two patients who allowed us to administer vitamin C therapy improved clinically. We emphasize the importance of a careful dietary history. Early recognition of scurvy is important because it can be treated specifically, and toxic treatment of vasculitis can be avoided.

Adult↗
PubMed1993

Scurvy--a forgotten disease.

A four-year-old male child was reported with sudden inability to stand walk of 10 days duration. Acute paralytic poliomyelitis was diagnosed in the presence of fever, respiratory infection, muscle tenderness, and weakness in lower extremity in an unimmunized child. Reevaluation after a week showed swelling, thickening, and tenderness of left femur. Plain x-ray of the left thigh was advised to exclude underlying osteomyelitis of the femur. X-ray showed features of scurvy. The child responded well to parenteral vitamin C therapy and resumed normal walking with in two weeks. Scurvy can present as pseudoparalysis of acute onset without any other signs even in older children. It emphasized the need for an index of suspicion of scurvy in a case of suspected paralysis. Dramatic response to vitamin C therapy can be used to confirm the diagnosis in the absence of laboratory support. Health education can be accelerated to prevent a disease like scurvy.

Ascorbic Acid↗
PubMed2002

Scurvy in a patient with presumptive oral lichen planus.

Scurvy is a disease caused by vitamin C deficiency. In this study, a patient with scurvy is presented with soreness and ulcerations of the mouth that were previously diagnosed as oral lichen planus. This disease is relatively more common than scurvy in the United States. Physicians should be aware that even in developed countries, soreness of the mouth and ulceration can be seen in patients with scurvy and potentially be misdiagnosed as oral lichen planus.

Journal Article↗
PubMed2001

Evidence of probable scurvy in subadults from archeological sites in North America.

The authors surveyed subadult human skeletons from Native American archeological sites in the United States for evidence of skeletal lesions associated with scurvy. Geographic regions surveyed include the Midatlantic area, the Southeast (Florida), the Southwest, and the Plains. The prevalence of probable subadult scurvy ranged from zero in the Plains samples to 38% in a small sample from Florida. These data indicate the likelihood that scurvy was a significant childhood disease in many Native American groups. Reasons for variation in prevalence remain speculative but include regional and seasonal variation in food types and abundance, cultural patterns of storage and utilization, periodic food shortages, and the relative importance of corn in the diet. These factors are part of a nutritional complex that is related to disease prevalence which can be studied through evidence seen in archeological human remains.

Adolescent↗
PubMed1983

Scurvy: old disease--new insight.

Scurvy was once the number one killer of seafarers on long voyages. One early theory with widespread acceptance was that rancid fat caused scurvy. I propose to show that rancid fat did, indeed, predispose seafarers to scurvy. I propose to show that Captain Cook's successful voyages in the latter half of the eighteenth century were in part due to removal of rancid fat from the diet of his crew and in part due to dietary anti-scorbutic factors.

Dietary Fats↗
PubMed1999

Adult scurvy.

UNLABELLED: Unlike most animals, which form ascorbic acid by metabolizing glucose, humans require an exogenous source. Vitamin C occurs primarily in fruits and vegetables, and scurvy develops from inadequate consumption of these sources, usually because of ignorance about proper nutrition, psychiatric disorders, alcoholism, or social isolation. The earliest symptom of scurvy, occurring only after many weeks of deficient intake, is fatigue. The most common cutaneous findings are follicular hyperkeratosis, perifollicular hemorrhages, ecchymoses, xerosis, leg edema, poor wound healing, and bent or coiled body hairs. Gum abnormalities, which occur only in patients with teeth, include gingival swelling, purplish discoloration, and hemorrhages. Pain in the back and joints is common, sometimes accompanied by obvious hemorrhage into the soft tissue and joints. Syncope and sudden death may occur. Anemia is frequent, leukopenia occasional. Treatment with vitamin C results in rapid, often dramatic, improvement. (J Am Acad Dermatol 1999;41:895-906.) LEARNING OBJECTIVE: At the conclusion of this learning activity, participants should be familiar with the history, pathogenesis, clinical features, and treatment of scurvy in adults.

Adult↗
PubMed1996

Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis.

Latent scurvy is characterized by a reversible atherosclerosis that closely resembles the clinical form of this disease. Acute scurvy is characterized by microvascular complications such as widespread capillary hemorrhaging. Vitamin C (ascorbate) is required for the synthesis of collagen, the protein most critical in the maintenance of vascular integrity. We suggest that in latent scurvy, large blood vessels use modified LDL--in particular lipoprotein(a)--in addition to collagen to maintain macrovascular integrity. By this mechanism, collagen is spared for the maintenance of capillaries, the sites of gas and nutrient exchange. The foam-cell phenotype of atherosclerosis is identified as a mesenchymal genetic program, regulated by the availability of ascorbate. When vitamin C is limited, foam cells develop and induce oxidative modification of LDL, thereby stabilizing large blood vessels via the deposition of LDL. The structural similarity between vitamin C and glucose suggests that hyperglycemia will inhibit cellular uptake of ascorbate, inducing local vitamin C deficiency.

Animals↗
PubMed2003

Scurvy: historical review and current diagnostic approach.

Scurvy, a deficiency of vitamin C, now most often occurs in disadvantaged groups seen frequently in EDs: alcoholics with poor nutrition, the isolated elderly, and the institutionalized. Its prominent clinical features are lethargy; purpuric lesions, especially affecting the legs; myalgia; and, in advancing disease, bleeding from the gums with little provocation. Common misdiagnoses are vasculitis, blood dyscrasias, and ulcerative gingivitis. Untreated, scurvy is inevitably fatal as a result of infection or sudden death. Fortunately, individuals with scurvy, even those with advanced disease, respond favorably to administration of vitamin C.

Aged↗
PubMed2001

Scurvy identified in the emergency department: a case report.

Scurvy, caused by a lack of Vitamin C in the diet, is thought to occur only sporadically in developed countries. The signs and symptoms are diverse but generally follow a predictable progression most striking for their hemorrhagic component, particularly of the skin, gums, and joints. We report a case of scurvy in an elderly, alcoholic woman. The diagnosis was contemplated based on dermatologic findings and a dietary history. All symptoms resolved within 10 days of oral ascorbic acid supplementation. Patients most at risk for developing scurvy include food faddists, the isolated elderly, and the mentally ill.

Aged↗
PubMed1989

Scurvy--the eternal masquerader.

Osseous involvement in scurvy is unusual in older children even though classical bony changes are well recognized in the infantile variety. This report describes two children with scurvy, aged 6 and 8 years, both of whom presented with bone pains and associated swelling. One child also had a pathological telescoping diaphyseal fracture--a complication not previously described in association with scurvy.

Child↗
PubMed2005

Scurvy leads to endoplasmic reticulum stress and apoptosis in the liver of Guinea pigs.

Insufficient ascorbate intake causes scurvy in certain species. Beyond its known functions, it has been suggested that ascorbate participates in oxidative protein folding in the endoplasmic reticulum (ER). Because redox imbalance in this organelle might cause ER stress and apoptosis, we hypothesized that this might contribute to the pathology of scurvy. Guinea pigs were divided into 7 groups: the control group was fed a commercial guinea pig food containing 0.1 g/100 g ascorbate for 4 wk, 5 groups consumed an ascorbate-free food for 0, 1, 2, 3, or 4 wk and 1 group was fed this scorbutic diet for 2 wk and then the commercial food plus 1 g/L ascorbate in drinking water for 2 wk. TBARS generation and the expression of some ER chaperones and foldases were determined in hepatic microsomes. The apoptotic index was assessed in histological sections. Although ascorbate, measured by HPLC, was undetectable in the livers of the guinea pigs after they had consumed the scorbutic diet for 2 wk, the microsomal TBARS level was elevated relative to the initial value only at wk 4. Western blot revealed the induction of GRP78, GRP94, and protein disulfide isomerase at wk 3 and 4. Apoptosis was greater than in the control, beginning at wk 3. None of the alterations occurred in the groups fed the commercial guinea pig food or ascorbate-free food followed by ascorbate supplementation. Therefore, persistent ascorbate deficiency leads to ER stress, unfolded protein response, and apoptosis in the liver, suggesting that insufficient protein processing participates in the pathology of scurvy.

Animals↗
PubMed1982

Bachelor scurvy.

Scurvy occurred in an elderly man with fatigue, dyspnea on exertion, and extensive ecchymoses and brawny edema of the legs. Platelet count, prothrombin time, and partial thromboplastin time were normal, but serum ascorbic acid level was very low. Other signs considered to be classic and almost pathognomonic for were absent: bleeding gums, hyperkeratotic follicles, coiled hairs, and perifollicular hemorrhages. Reliance on these well-known features of scurvy may obscure or delay diagnosis of an easily cured disorder Severe scurvy is most commonly suggested by tenderness, extensive ecchymoses, and brawny edema of the lower extremities.

Aged↗
PubMed1983

Specifically decreased collagen biosynthesis in scurvy dissociated from an effect on proline hydroxylation and correlated with body weight loss. In vitro studies in guinea pig calvarial bones.

The question whether ascorbate regulates collagen production solely through its direct role in proline hydroxylation was investigated. Proteins in calvarial bones from control and scorbutic weanling guinea pigs were labeled in short-term cultures with radioactive proline. Proteins were digested with purified bacterial collagenase to distinguish between effects on collagen polypeptide production and hydroxyproline formation. There was a preferential decrease in the absolute rate of collagen biosynthesis beginning after 2 wk of ascorbate deficiency, and this effect was temporally dissociated from decreased proline hydroxylation. There were no significant changes in the absolute rates of collagen degradation or noncollagen protein production. In vitro inhibition of proline hydroxylation in normal bone with alpha, alpha'-dipyridyl did not affect the relative rate of collagen synthesis, further dissociating these functions. Ascorbate added to scorbutic bone cultures reversed defective proline hydroxylation but not defective collagen synthesis, suggesting that the latter was an indirect effect of scurvy. There was a linear correlation between the extent of body weight lost during the 3rd and 4th wk of scurvy and the rate of collagen synthesis in scorbutic bone. This correlation also applied to control animals receiving ascorbate, but with weight loss induced by food restriction. These studies establish for the first time that ascorbate deficiency in guinea pigs leads to a specific decrease in collagen polypeptide synthesis and suggest that this decrease results from the reduced food intake and/or weight-loss characteristic of scurvy.

Animals↗
PubMed1983

Gingival findings in spontaneous scurvy. A case report.

This case report presents clinical observations of alterations in periodontally diseased soft tissues associated with the development of scurvy. The sudden clinical appearance of the gingival lesions suggested a differential diagnosis of scurvy, acute leukemia and diabetes. Such lesions may develop prior to or simultaneous with extraoral findings. Coordination of systemic and local therapy effectively resolved the disease state. The dentist may be the first source of consultation for the patient with scurvy. An appreciation for this rare but potentially devastating condition is necessary for satisfactory management of the disease.

Gingivitis↗
PubMedDate not supplied

[Changes in the oral caused by scurvy].

This report presents a case of a psychiatric patient with scurvy. Upon the clinical examination of the oral cavity, dry and pale lips were noted. Gingiva was highly edematous, soft, purple blue with ulcerated margins. Bleeding was noted upon slightest provocation. Teeth were also affected by the vitamin C deficiency with multiple caries. The patient was asthenic and adynamic. Petechial bleeding and hematomas were present on the skin of extremities. Therapy consisted of rehydration and vitamin C compensation--2 g daily i.v. during 10 days period, and 1.5 g daily orally during the following 2 months. The patient maintained only partial plaque control, and complete recovery of the oral cavity was not established because the patient didn't comply. Concerning that scurvy is a rare disease nowadays, it is very important to recognize its clinical signs, and to establish a valid and prompt diagnosis, because, when untreated, scurvy can have severe consequences on the entire organism.

Female↗