Introduction Porphyria and Wilson’s disease are genetically inherited metabolic diseases that can show multisystem involvement. Hereditary coproporphyria (HCP) can manifest itself with a wide range of symptoms such as abdominal pain, diarrhea, blisters on the skin, neuropathy, psychosis, and paraplegia as a result of the mutation of coproporphyrinogen oxidase (CPOX), one of the heme biosynthesis enzymes. Wilson’s disease, which is transmitted in an autosomal recessive manner, is characterized by the accumulation of copper (Cu2+) in the tissue as a result of inadequate excretion into plasma and bile owing to a mutation in the ATP7B gene. Depending on the organ where copper accumulates, the patient may present with tremors, jaundice, cirrhosis, early osteoporosis, heart failure, renal tubular dysfunction, Kayser-Fleischer ring, and behavioral disorders. In this study, a case report was compared with the literature, and the effect of copper accumulation on HCP was investigated.

Clinical Findings Our 26-year-old male patient was found compatible with the CPOX gene mutation as s result of the genetic test requested upon suspicion of Wilson’s Disease. The dry copper weight in the patient’s tissue was recorded as 609 μg/g. Through literature review it was established that copper (Cu2+) suppresses the heme pathway, and this suppression is especially pronounced in the performance of ATP7B. In the Wilson’s disease where the copper accumulation in the tissue is excessive, it is expected that the heme pathway will be suppressed and the CPOX enzyme will be decreased. Thus in line with this thought, our hypothesis based on the synergistic progression of our patient’s Wilson and HCP diseases was supported; and the existence of a pathophysiological condition in which Wison’s disease, where both the heme pathway and the CPOX enzyme are suppressed, and HCP exacerbate each other has been revealed.

Conclusion The association of hHCP and Wilson, which has not been previously reported in the literature to the best of our knowledge, is discussed in terms of liver mechanisms and common pathophysiology. Although the effects of Wilson and HCP diseases on each other are not yet known, the mechanism of this synergistic relationship can be explained through biochemical and pathological studies in future studies. The existence of patients diagnosed with Wilson’s disease, which resembles porphyria, and experimental studies are strong evidence that heme metabolism should be investigated in Wilson’s disease.