Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous follicles that affects nearly 90% of teenagers; half of them continue to experience symptoms as adults. There have been several reports of monomorphic acneiform eruptions in patients treated with intramuscular cobalamin injections. The eruptions resolved after the cessation of the therapy. Cyanocobalamin, pyridoxine (B₆), and riboflavin (B₂) have been reported to exacerbate existing acne. Moreover, it was reported that in acne patients, the serum level of vitamin B₁₂ was significantly decreased after treatment, but no explanation was given. We propose a vitamin B₁₂-mediated bacterial mechanism for acne pathogenesis on the evidence mentioned above. One hundred twenty AV patients were recruited.
     Our results proved that vitamin B₁₂ was involved in the pathogenesis of AV; in vivo, it proved that AV patients had significantly higher serum levels of the vitamin than controls and showed a positive correlation to the disease duration and severity. In vitro, it proved that vitamin B₁₂ supplementation to p. acnes cultures significantly raised the porphyrins produced in these cultures when compared to the non-supplemented ones. It also proved that this shift in the metabolism is secondary to inhibition of the cbiL gene of the vitamin B₁₂ synthesis in the bacteria; as porphyrins and vitamin B₁₂ share the same precursors, vitamin B₁₂ does has a role in either elicitation or aggravation of AV.