Topical Steroid Rebound Phenomena as Bioenergetic Blockade: Urinary Organic Acid Profiling Reveals Localized Scurvy, Not Mitochondrial Overdrive

Urinary organic acid profiles from five patients with topical steroid rebound phenomena (TSRP/TSW) are evaluated against the metabolic predictions of a Krebs cycle blockade model centred on α-ketoglutarate dehydrogenase (α-KGDH) impairment under glucocorticoid-induced pericyte calcium lock. The cohort demonstrates near-universal urinary ascorbate depletion, selective succinate elevation in a subset of patients, universally spared glycolytic endpoints, and evidence of electron transport chain congestion via the ETF-QO pathway. This pattern discriminates between two competing interpretive frameworks: it is consistent with a specific enzymatic blockade at α-KGDH and inconsistent with the generalised mitochondrial overactivation model advanced by Shobnam et al. (2025) to explain NAD⁺ excess in TSW skin biopsies. The data reframe the observed NAD⁺ accumulation as a consequence of impaired TCA flux rather than overdrive, and propose a staging hierarchy — from isolated ascorbate depletion through SDH-dependent succinate accumulation to decompensated metabolic crisis with lactate elevation — that accounts for the clinical heterogeneity of TSRP within a single mechanistic continuum. Urinary ascorbic acid is identified as the most consistent metabolic signal across the cohort and is proposed as a candidate biomarker warranting formal investigation. The mechanistic framework additionally identifies a basis for caution regarding metformin use in this population, given its established inhibition of thiamine transport via THTR-2. Observational case series; hypothesis-generating. Controlled validation with tissue-level metabolite quantification and paired plasma/intracellular vitamin C measurements is indicated.