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Scurvy As Cause of Purpura in the XXI Century: a Review on This “Ancient” Disease

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Scurvy As Cause of Purpura in the XXI Century: a Review on This “Ancient” Disease European Review for Medical and Pharmacological Sciences 2018; 22: 4355-4358 Scurvy as cause of purpura in the XXI century: a review on this “ancient” disease M. ANTONELLI1, M.L. BURZO1, G. PECORINI1,2, G. MASSI3, R. LANDOLFI1, A. FLEX1,2 1Institute of Internal Medicine, Catholic University of the Sacred Heart, A. Gemelli, Hospital Foundation, School of Medicine, Rome, Italy 2Laboratory of Vascular Biology and Genetics, Catholic University of the Sacred Heart, A. Gemelli, Hospital Foundation, School of Medicine, Rome, Italy 3Institute of Pathology, Catholic University of the Sacred Heart, A. Gemelli, Hospital Foundation, School of Medicine, Rome, Italy Abstract. – OBJECTIVE: Scurvy is defined as it is re-emerging in Western Countries popula- a deficiency of ascorbic acid, which is an essen- tion with unusual eating habits2. Ascorbic acid tial exogenous vitamin in humans. Vitamin C is is a reversible biologic reductant that involves a involved in collagen synthesis and its deficit can great number of biochemical reactions and meta- cause disorders of connective tissue. The most frequent symptoms are weakness, arthralgias, bolic processes. Particularly, it provides electrons anorexia and depression, commonly associated needed to reduce molecular oxygen, functioning with follicular hyperkeratosis and perifollicular as an anti-oxidant factor capable of stabilizing a hemorrhage, with purpura. number of other compounds, including vitamin E PATIENTS AND METHODS: A young woman, and folic acid. In addition, it functions as a co- with a history of malnutrition, manifested purpu- factor for hydroxylation reactions of mono- and ra and hematoma of the left lower limb. The lab- oratory tests didn’t detect alterations either in di-oxygenase enzyme iron and copper depen- coagulation, the platelet count or in the autoim- dent. In fact it acts like an enzyme complement munity. The total body TC scan didn’t show neo- for lysil- and prolyl-hydroxylase that catalyzes plasia or other suspected lesions. Excluding the formation of hydroxyproline and hydroxylysine most important causes of purpura, in consider- in collagen synthesis3. The failure in this step re- ation of malnutrition, scurvy was suspected. sults in impaired wound healing and deficient os- RESULTS: A skin biopsy confirmed the diag- teoblast and fibroblast function. Ascorbic acid is nosis. Accordingly to this finding, a treatment with a daily intravenous infusion of vitamin C also an enzymatic cofactor of dopamine-beta-hy- was started with consequent improvement of droxylase. Hence it is involved in the synthesis of hematoma and purpura. cathecolamines and in biosynthesis of carnitine, CONCLUSIONS: Scurvy is a re-emerging dis- necessary for the long-chain fatty acids transport ease, also in western countries. When purpura across the mitochondrial membrane4. appears in young adults, scurvy has to be inves- For these reasons the vitamin C deficit can in- tigated, especially when a history of malnutri- tion is present. The treatment with vitamin C in- duce different and various clinical presentations. fusions should be started as soon as possible in They are preceded from weakness, malaise, ar- order to prevent any complications. thralgias, anorexia and depression. Then, follicu- lar hyperkeratosis and perifollicular hemorrhage Key Words: with petechiae (typically on the skin of lower Scurvy, Purpura, Vitamin C, Ascorbic acid. limbs) and coiled hairs appear. Other common symptoms include subungual multiple hemor- rhages (more extensive than in bacterial endocar- Introduction ditis), ecchymosis, gingivitis with bleeding and receding gums, edema, and anemia5. Moreover, Scurvy is a clinical syndrome linked to ascor- muscle-skeletal pain can develop, caused by hem- bic acid deficiency, largely due to impaired col- orrhages in the muscles or periosteum6. lagen synthesis with consequent disorder of con- At present, because of the variety of clinical nective tissue1. Although scurvy is considered a manifestations, the diagnosis of scurvy is fre- disease of the era of great maritime expeditions, quently misunderstood with both clinical evalu- Corresponding Author: Mariangela Antonelli, MD; e-mail: [email protected] 4355 M. Antonelli, M. L. Burzo, G. Pecorini, G. Massi, R. Landolfi, A. Flex ation and diagnostic imaging7. Imaging studies could detect osteolysis, joint space loss, osteo- necrosis, osteopenia or osteoporosis, periosteal proliferation and/or subperiostial bleeding8. Bi- ological signs are represented by abnormalities including anemia and low levels of cholesterol and albumin. Finally, a serum ascorbic acid level lower than 2.5 mg/l allows to diagnose scurvy9. When the vitamin C dose is not available, skin biopsy is a valid alternative to diagnosis10. The aim of this review is to underline the im- portance of recognizing purpura as a clinical manifestation of scurvy, with the purpose to reach Figure 1. Hematoma and purpura of the left lower limb. the diagnosis of ascorbic acid deficiency before the development of complications. In particular, we start describing a case report of scurvy in a middle-aged woman. scan was performed, in the hypothesis of occult neoplasia, but nothing was discovered. Patient Case Report refused to undergo endoscopic examinations. A 51 years old female patient was admitted in Considering the patient malnutrition history, a the Department of Internal Medicine with the di- vitamin deficiency was suggested Vitamin B12 agnosis of purpura of the left leg in association and folate levels were evalueted, resulting lower with hematoma. The patient reported a clinical than reference interval, so parenteral infusions of history of multi-allergies in bronchial asthma, these vitamins were performed. In spite of these recurrent tonsillitis and mitral valve prolapsed. findings, the main suspect remained a vitamin C She denied taking drugs at home. In the last three deficiency. The ascorbic acid dosage was unfortu- years, the patient reported a liquid/semi-liquid nately not available in our laboratory. Therefore, nutrition for a referred disturbance of mastica- a skin biopsy of the lesions was performed and tion and gingivitis, associated with weight loss the parenteral supplementation of vitamin C was of about thirty kilograms. For four months she started. In about a week, the anemia improved, as reported the appearance of purpura in the lower purpura and hematoma of the left limb (Figure 2). limbs with progressive and upward trend. The bruising and swelling of the left lower linb was Diagnosis present at the same time (Figure 1). Histological examination showed specific his- tological changes of the follicular pilifera struc- Blood and instrumental tests ture. In particular, the infundibular and isthmic In the emergency room, the patient underwent ectasia with unusual phenomena of dyskeratosis to arteriovenous Doppler ultrasound of the lower of follicular epithelium were observed, showing limbs with the evidence of not-replenished he- matoma, in the absence of deep vein thrombo- sis. Blood tests showed iron deficiency anemia and increased fibrinogen, in the absence of oth- er prominent alterations, especially in coagula- tion. During hospitalization several blood tests were performed to detect the cause of purpura: research of antiphospholipid and anticardiolipin, anti nuclear, extractable nuclear antigens, an- ti-dsDNA, anti-neutrophil cytoplasmic, anti-liver kidney microsome, anti-smooth muscle, anti-mi- tochondrial, anti-Saccharomyces cerevisiae, anti endomysial, anti transglutaminase and anti glia- din antibodies, IgG, IgM, C3, C4, b2 microglobu- lin, rheumatoid factor, crioglobulin. All these re- Figure 2. Resolution of hematoma and purpura after vita- sults were negative. Furthermore, a total body TC min C infusion. 4356 Scurvy as cause of purpura in the XXI century: a review on this “ancient” disease the lower extremities, due to insufficient fruit and vegetable intake attributed to allergies. Also in this case, the finding of a low vitamin C serum concentration permitted the diagnosis. In all these patients the early recognition of scurvy as cause of the purpura and the conse- quent treatment allowed the resolution of signs and symptoms. In order to establish a correct diagnosis in case of purpura, it is firstly fundamental to distinguish unpalpable purpura (e.g., due to primary cutaneous changes, capillary fragility – including scurvy–, changes in the coagulation) from hyperkeratosis (due to deficit of vitamin A). Hence, the atypical Figure 3. Infundibular and isthmic ectasia of follicular pil- presentations of purpura, not explained by common ifera structure. 10x illnesses, should induce to suspect the vitamin C deficit. Our patient arrived with purpura of lower extremities, hematoma of the left leg, gingivitis and the classic follicular dystrophy caused by vitamin receding gums. The normal plate count, the normal C deficiency (Figures 3 and 4). circulating levels of von Willebrand factor and a negative anamnesis for previous hemorrhagic events (such as easy bruising, epistaxis and menometror- Discussion rhagia) led us to exclude primary haemostasis disor- ders. Liver function was normal, as also Prothrom- This case report underlines the variety of clin- bin time (PT) and Partial Thromboplastin Time ical manifestations in scurvy. In particular, in our (aPTT), excluding coagulation disorders as cause of patient we have investigated purpura, since it was the hemorrhagic skin lesion. Moreover, the screen- the prevalent sign reported. Although the
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