Cureus
Atopic Dermatitis or Subacute Cutaneous Lupus: Resolving a Diagnostic Challenge Through Clinicopathologic Correlation
By Ana Sophia Ortiz Robles, Norma Edith Torres Gudiño, Flavio Antonio Sarabia Alba and 2 others.
Abstract
This report presents a 44-year-old Mexican woman with hypothyroidism and atopic dermatitis who developed severe mixed-pattern hepatotoxicity after a 10-day course of an over-the-counter joint supplement (Ismerely FTX Plus) of incompletely disclosed composition.A public US Food and Drug Administration (FDA) Medication Health Fraud Notification confirmed the product was adulterated with undeclared dexamethasone phosphate and diclofenac.The clinical course was complicated by probable secondary hemophagocytic syndrome, with a peak ferritin of 19,114.9ng/mL (93 times the upper reference limit), resolving spontaneously without immunosuppression after discontinuation of the causative agent.The rarity of this case lies in the convergence of an unconventional trigger, a hemophagocytic lymphohistiocytosis (HLH)-like response, and spontaneous resolution in a host with pre-existing autoimmune vulnerability.The patient presented with five days of intermittent fever up to 39.4°C and severe right upper quadrant pain, followed by fatigue, hair changes, and cutaneous lesions of the right upper extremity and face.Outpatient studies showed negative viral hepatitis serologies and splenomegaly.Hospital evaluation demonstrated severe mixed-pattern transaminasemia (alanine aminotransferase (ALT) 899 IU/L, aspartate aminotransferase (AST) 1,063 U/L, R factor 4.8), mild bilineage cytopenia (leukopenia 2.96 × 10³/µL, driven by lymphopenia rather than neutropenia, and mild thrombocytopenia 118 × 10³/µL, with normal hemoglobin), elevated inflammatory markers, and hypertriglyceridemia. Autoimmune testing showed a true-positive antinuclear antibody (ANA) titer of 1:80 (homogeneous/nuclear) and borderline anti-smooth muscle antibodies (1:100), with all other lupus-specific antibodies negative.Examination revealed periarticular papulosquamous lesions with mild edema on the right arm and elbow and bilateral malar erythema sparing the nasolabial folds.Skin biopsy showed spongiotic dermatitis with interface vacuolar degeneration and a subcorneal blister pattern, without vasculitis or tissue eosinophilia.Absent eosinophilia argued against drug reaction with eosinophilia and systemic symptoms (DRESS), while negative lupus-specific serologies and unmet classification criteria argued against subacute cutaneous lupus erythematosus (SCLE) or systemic lupus erythematosus (SLE).The most coherent interpretation was drug-or supplement-induced interface dermatitis with idiosyncratic hepatotoxicity, plausibly mediated by cytotoxic T-cell activity against keratinocytes and hepatocytes modified by undisclosed corticosteroid and nonsteroidal anti-inflammatory drug (NSAID) metabolites.Transaminases, ferritin, and cytopenias improved progressively: ALT and AST declined approximately 43% and 62% within five days, with ALT reaching a 70% decline by discharge (hospital day 9), and ferritin declining 93% to 1,309.7 ng/mL at last determination (outpatient follow-up, day 17), in parallel with resolution of cutaneous lesions after supplement discontinuation alone.This case underscores the importance of clinicopathologic correlation over isolated findings and highlights adulterated supplements as an underrecognized trigger of combined hepatic, hematologic, and cutaneous immune-mediated injury.



