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Protein families are groups of homologous proteins; that is, they have similarities in amino acid sequences and three-dimensional structures. Protein families usually occur because of gene duplication, where an additional copy of a gene is inserted into the genome of an organism. Mutations that change the amino acids but still allow the protein to be properly synthesized, will lead to new protein family members. If these new proteins contain similar amino acids in key...

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Related Experiment Video

Updated: Feb 13, 2026

Ultrafast Lignin Extraction from Unusual Mediterranean Lignocellulosic Residues

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Published on: March 9, 2021

[Familial Mediterranean fever].

S Georgin-Lavialle¹, V Hentgen², K Stankovic Stojanovic¹

¹Service de médecine interne, centre de référence des maladies auto-inflammatoires et de l'amylose inflammatoire (CEREMAIA), hôpital Tenon, 4, rue de la Chine, 75020 Paris, France; Inserm UMRS_933, hôpital Trousseau, 26, avenue du Dr-Arnold-Netter, 75012 Paris, France; Université Paris 6, Pierre-et-Marie-Curie (UPMC), Assistance publique-Hôpitaux de Paris (AP-HP), Paris, France.

La Revue De Medecine Interne

|March 13, 2018

Summary

This summary is machine-generated.

Familial Mediterranean Fever (FMF) is a common auto-inflammatory disease caused by MEFV gene mutations. Colchicine effectively prevents FMF attacks and severe complications like amyloidosis.

Keywords:

Colchicine Familial Mediterranean fever Fièvre méditerranéenne familiale Interleukine 1 Interleukin 1 MEFV Pyrin Pyrine

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Area of Science:

Genetics
Immunology
Rheumatology

Background:

Familial Mediterranean Fever (FMF) is the most prevalent monogenic auto-inflammatory disorder.
It is an autosomal recessive condition linked to MEFV gene mutations impacting pyrin protein function.
Pyrin activation leads to increased interleukin-1 secretion by immune cells.

Purpose of the Study:

To provide a comprehensive overview of Familial Mediterranean Fever (FMF).
To discuss the diagnosis, treatment, and pathophysiology of FMF.
To include recent findings on dominant forms of MEFV-associated auto-inflammatory diseases.

Main Methods:

This article is a state-of-the-art review.
It synthesizes current knowledge on FMF pathophysiology, diagnosis, and treatment.
It incorporates recent genetic findings related to MEFV mutations.

Main Results:

FMF presents with recurrent attacks of serositis (abdomen, chest, joints) and fever.
Attacks are typically short-lived (1-3 days) and self-limiting.
Daily colchicine (1-2mg) is highly effective in preventing FMF attacks and amyloidosis.

Conclusions:

Colchicine is the cornerstone treatment for FMF, preventing disease flares and severe complications.
Understanding MEFV gene mutations is crucial for FMF diagnosis and management.
Emerging research highlights new auto-inflammatory conditions associated with MEFV, including dominant forms.