Case Presentation: A 62-year-old female presented with one month of progressive bilateral lower extremity pain, weakness, and functional decline. Her medical history was significant for cirrhosis secondary to hepatitis C (treated), chronic pancytopenia, and hypothyroidism. Her medications included atorvastatin, levothyroxine, omeprazole, spironolactone, tiotropium, venlafaxine, and quetiapine. She was a current smoker with a 20-pack year history. Her initial exam revealed tachycardia; petechial, purpuric rash over posteromedial aspect of left thigh; right knee effusion; and a tender, distended abdomen. She was severely anemic and received two transfusions. The rash, arthralgia, and pancytopenia raised concern for vasculitis, for which rheumatology and dermatology were consulted. Initial labs showed elevated myeloperoxidase (MPO) and proteinase-3 (PR-3) antibodies and increased perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) immunofluorescence suggestive of a small-vessel vasculitis. Arthrocentesis of the right knee demonstrated a noninflammatory hemarthrosis, a computed tomography scan noted hyperdense ascites, and colonoscopy/endoscopy were negative. A punch biopsy of the rash showed a dermal hemorrhage (bruise). During week 2, a paracentesis revealed hemoperitoneum but was complicated by the development of a large ecchymoses on the abdomen. Hematology and gastroenterology were consulted to assist in working up the apparent coagulopathy and hemoperitoneum. Throughout the admission the patient underwent extensive laboratory workup with normal partial thromboplastin time (PTT), international normalized ratio (INR), ristocetin assay, and synthetic liver function. She had an elevation in non-specific inflammatory markers, elevated immunoglobulins, and elevation in the gamma interregion initiating a skeletal survey. During week 3, after considering underlying connective tissue dysfunction as the etiology of the apparent coagulopathy, we considered scurvy, and a subsequent vitamin C level resulted as undetectable. A dietary history revealed her diet consisted mostly of Cheetos. She was started on 500 mg daily of vitamin C for 1 month, was then to start a multivitamin, and follow-up with hematology.
Discussion: Vitamin C plays a vital role in hydroxylation of proline and lysine residues during collagen fiber generation. With collagen fiber dysfunction, the coagulation cascade can be disrupted with normal PTT and INR. Previous case reports have shown scurvy can mimic vasculitis on physical exam, however, this patient also had lab evidence of vasculitis with elevated MPO Ab, PR-3 Ab, and p-ANCA immunofluorescence. Furthermore, the patient’s cirrhosis served as an explanation for the coagulopathy. The presentation underwent workup and received consultation from multiple subspecialty teams, resulting in increased length of stay with an expensive diagnostic workup and significantly delayed intervention. A dietary history on admission and early involvement of the inpatient nutrition team could have significantly decreased the resources used while improving the patient outcome.
Conclusions: Scurvy can cause poor wound healing, hemarthrosis, petechiae, perifollicular hemorrhages, and nonspecific myalgias. These findings can be consistent with vasculitis, but scurvy typically lacks the laboratory evidence for vasculitis. This case mimicked vasculitis with both physical exam and lab findings which led to a delayed diagnosis and high resource expenditure.
