Scurvy in the present times: vitamin C allergy leading to strict fast food diet.

Scurvy results from a deficiency of vitamin C, a nutrient otherwise known as ascorbic acid. Today, scurvy is rare yet emerges in select patients. The patient reported herein developed scurvy secondary to deliberate avoidance of vitamin C-rich foods. Classic cutaneous manifestations of scurvy include follicular hyperkeratosis and perifollicular hemorrhage encompassing coiled "corkscrew" hairs and hairs bent into "swan-neck" deformities. Ecchymoses, purpura, and petechiae are also characteristically prominent. Classic oral abnormalities include erythematous, swollen gingivae that hemorrhage from subtle microtrauma.Subungual linear splinter hemorrhages may also manifest as a sign of the disease. To establish the diagnosis requirements include characteristic physical exam findings, evidence of inadequate dietary intake, and rapid reversal of symptoms upon supplementation. Although unnecessary for diagnosis, histological findings demonstrate perifollicular inflammation and hemorrhage, fibrosis, and hyperkeratosis, amongst dilated hair follicles and keratin plugging. Although citrus fruit allergies have been historically documented, ascorbic acid has not been previously reported as an allergen. Although lacking absolute certainty, this report suggests a presumed case of ascorbic acid allergy based on patient history and favorable response to ascorbic acid desensitization therapy.

A colonization of basal cell carcinoma by malignant melanoma in situ resembling a malignant basomelanocytic tumor.

We report a case of colonization of basal cell carcinoma (BCC) by malignant melanoma in situ (MIS) simulating a malignant basomelanocytic tumor. A biopsy of a pigmented lesion present on an 83-year-old man's scalp displayed intimate admixing of basaloid and melanocytic cells. This seemingly inseparable combination of BCC and neoplastic melanocytes has been referred to as a malignant basomelanocytic tumor. However, our case also displays an adjacent component of MIS, thus favoring colonization of BCC by MIS as the etiology. To our knowledge, this is the third case report of colonization of BCC by MIS resembling a malignant basomelanocytic tumor.

A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis.

Cutaneous small-vessel vasculitis (CSVV) is a disorder characterized by neutrophilic inflammation predominantly limited to the superficial cutaneous postcapillary venules. CSVV may be idiopathic or may have a defined cause such as infection, medication, connective tissue disease, or malignancy. CSVV may also be associated with extracutaneous disease or systemic vasculitis. The most common clinical presentation of CSVV consists of symmetrically distributed palpable purpura of the lower extremities. In general, lesional skin biopsy samples should be examined with light microscopy and direct immunofluorescence for adult patients with suspected CSVV. A complete history, review of systems, physical examination, and selected laboratory studies also should be performed to assess for inciting causes or extracutaneous involvement of CSVV. Treatment varies and depends on the chronicity of CSVV, the severity of cutaneous involvement, and the presence or absence of both an underlying cause and extracutaneous involvement of CSVV. An isolated episode of CSVV associated with a known inciting factor may be managed by removal or treatment of the trigger, along with symptomatic measures. First-line systemic treatments for chronic, idiopathic CSVV include colchicine or dapsone, used singly or in combination. Recurrent, chronic, or severely symptomatic CSVV that does not respond to the aforementioned therapies may require initiation of an immunosuppressive agent such as azathioprine, mycophenolate mofetil, methotrexate, cyclosporine, or rituximab.