Early and severe amyloidosis in a patient with concurrent familial Mediterranean fever and pseudoxanthoma elasticum
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Updated: Jul 26, 2026

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
Published on: June 9, 2018
D Cattan1, B Bouali, N Chassaing
1Department of Hepatogastroenterology, Centre Hospitalier, 94195 Villeneuve-Saint-Georges, France.
Insights
Familial Mediterranean Fever (FMF) and pseudoxanthoma elasticum (PXE) in a young patient were linked to homozygous mutations. ABCC6 deficiency may worsen FMF-related amyloidosis.
Area of Science:
- Genetics
- Rare diseases
- Biochemistry
Background:
- Familial Mediterranean Fever (FMF) is an autoinflammatory disorder characterized by recurrent fevers and serositis.
- Pseudoxanthoma elasticum (PXE) is a genetic disorder affecting connective tissue, leading to characteristic skin, eye, and vascular changes.
- Amyloidosis is a condition where abnormal proteins build up in organs.
Observation:
- A young woman presented with early-onset, extensive FMF-related amyloidosis and PXE.
- Genetic analysis revealed homozygous mutations: G1042S in the ABCC6 gene (PXE) and M694I in the MEFV gene (FMF).
- Parental consanguinity was noted, consistent with the homozygous mutations.
Findings:
- The patient carried a novel homozygous G1042S mutation in ABCC6 and a homozygous M694I mutation in MEFV.
- ABCC6 deficiency might exacerbate amyloidosis by increasing heparan sulfate deposition.
- ABCC6 deficiency could also reduce the efficacy of colchicine therapy for FMF.
Implications:
- This case highlights a potential gene-gene interaction between ABCC6 and MEFV in disease severity.
- Understanding this interaction could lead to improved diagnostic and therapeutic strategies for patients with co-occurring FMF and PXE.
- Further research into the role of ABCC6 in amyloidogenesis is warranted.
Abstract:
A young woman patient had early and extensive familial Mediterranean fever (FMF)-related amyloidosis and pseudoxanthoma elasticum (PXE). She had the novel G1042S mutation in the ATP-binding cassette subfamily C member 6 (ABCC6) gene, responsible for PXE, and the mutation M694I in MEFV, the FMF gene. Both mutations were homozygous, in agreement with consanguinity in the parents. ABCC6 deficiency may have increased the severity of amyloidosis by increasing the deposition in target tissues of heparan sulphate, which colocalizes spatially and temporally with amyloid proteins, and/or by decreasing the therapeutic activity of colchicine.
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