Evaluating galectin-3 (LGALS3) +191 gene variant and serum galectin-3 levels in Egyptian children with familial Mediterranean fever

Samia S E. Mahmoud; Huda M. Mohamed; Yomna M. Farag; Mona M. Abdul Salam; Sara I. Falah

doi:10.53730/ijhs.v6nS4.12051

Authors

Samia S E. Mahmoud Department of Pediatrics and Pediatric Rheumatology Faculty of Medicine, Cairo University, Cairo, Egypt
Huda M. Mohamed Department of Pediatrics and Pediatric Rheumatology Faculty of Medicine, Cairo University, Cairo, Egypt
Yomna M. Farag Department of Pediatrics and Pediatric Rheumatology Faculty of Medicine, Cairo University, Cairo, Egypt
Mona M. Abdul Salam Department of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt
Sara I. Falah
sarahfalah40@gmail.com
Department of Pediatrics and Pediatric Rheumatology Faculty of Medicine, Cairo University, Cairo, Egypt

Keywords:

FMF, galectin-3, proteinuria, renal affection, single nucleotide polymorphism

Abstract

Background: The most important and devastating complications of Familial Mediterranean fever (FMF) is renal amyloidosis, usually affecting the kidneys leading to end stage renal failure. FMF- related renal amyloidosis needed to be diagnosed early. Optimal colchicine dose is effective in prevention and reversing renal amyloidosis. Aim of the work: to evaluate serum galectin-3 level and its gene polymorphism (LGALS3 191 C>A) as a marker of proteinuria and subclinical inflammation in Egyptian children and adolescents with FMF. Methods: Fifty FMF patients in attack free period and 40 healthy children were included as a control group. Serum levels of galectin-3 were measured, Galectin-3 (LGALS3) c.191 C>A (rs4644) gene variant was investigated and morning spot urine was collected for determination of albumin / creatinine ratio (ACR). Results: Serum Galectin-3 levels were significantly higher in FMF patients than control group, P < 0.03. Regarding genotype and allele distribution of (LGALS3) c. 191 C>A polymorphism there was statistical significant difference between cases and control, 13 patients (42%) had CC and the remaining 37 patients (63%) were CA. The control had 18 child (58%) with CC compared to 22 child with CA (37%) and BUN level was higher among CC type of Galectin-3 (LGALS3) c.191 C>A.

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References

Chawla N, Deshmukh M, Sharma A, Patole S (2016): Strategies for medical management of pediatric eosinophilic esophagitis—a systematic review. Journal of Pediatric Gastroenterology and Nutrition. 2016;63(6):e152–e7.

Chen SS, Sun LW, Brickner H, Sun PQ (2015): Down-regulating galectin-3 inhibits pro-inflammatory cytokines production by human monocytes derived dendritic cells via RNA interference . Cell Immunol, 294(1)-44-53.

de Oliveira F, Gatto M, Luisetto R, Ghirardello A, Punzi L and Doria A (2015) : Galectin-3 in autoimmunity and autoimmune diseases. Experimental Biology and Medicine ;0:1-10.

Desmedt V, Desmedt S, Delanghe JS, Speeckaert R, Speeckaert MM (2016): Galectin-3 in renal pathology:than an innocent bystand.AM JNephrol ;43:305-17 .

Dong R, Zhang M, Hu Q, Zheng S, Soh A, Zheng Y, Yuan H (2018) : Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review). Int. J. Mol. Med., 41, 599–614.

Kaur T, Sodhi A, Singh J, Arora S, Kamboj SS and Kaur M (2015): Evalution of Galectin-3 Genetic Variants and its Serum levels in Rheumatoid Arthritis in North India. Int J Hum Genet, 15(3) 131-8.

Mastunaga N, Anan I, Rosenberg P, Nagai R, Lundstrom O,Horiuchi S, Ando Y,Suhr OB (2005): Advanced glycation end products is implicated in amyloid-related kidney complication. Scand J Clin Lab Invest.;65(4):263-72.

Mohamed, M., Elhariri, H. M., Elsheikh, M. S., Atti, M. A., Belawo, H. M., & Adel, A. (2022). Effect of COVID-19 quarantine on caregivers of Egyptian children with autistic spectrum disorder. International Journal of Health Sciences, 6(S4), 1000–1007. https://doi.org/10.53730/ijhs.v6nS4.5901

Mor A, Shinar Y, Zaks N, Lagevitz P, Chetrit A, Shtrasburg S, Rabinovitz E, Livneh A (2005): Evaluation of disease severity in Familial Mediterranean Fever. Semin Arthritis Rheum; 35: 57-64.

Mordechai Shohat (2016): Familial Mediterranean fever. GeneReviews. December 15; http:// www.ncbi.nlm. nih.gov/booksl NBK 1227/.

O'Seaghdha CM, Hwang SJ, Ho JE, Vasan RS, Levy D, Fox CS (2013): Elevated galectin-3 precedes the development of CKD. J Am Soc Nephrol 2013;24:1470-7.

Ozen S, Demirkaya E, Duzova A, Erdogan O, Erken E, Glu A, Kasapcopur O, Kasifoglu T, Kisacik B, Ozdogan H, Tunca M, Acikel C (2014): FMF50 : a score for assessing outcome in familial Mediterranean fever . Ann Rheum Dis, 7 (5):897-901 . doi: 10.1136.

Rohani P, Najafi Sani M, Ahmadi M, Ziaee V. (2017): A Case of Eosinophilic Esophagitis Accompanying Familial Mediterranean Fever.Case Rep Gastrointest Med.6863921. doi: 10.1155/6863921.

Sciacchitano S, Lavra L, Morgante A, Ulivieri A, Magi F, De Francesco, G Bellotti C, Salehi L and Ricci A. (2018): Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z Int. J. Mol. Sci., 19, 379; doi:10-3390.

Suryasa, I. W., Rodríguez-Gámez, M., & Koldoris, T. (2022). Post-pandemic health and its sustainability: Educational situation. International Journal of Health Sciences, 6(1), i-v. https://doi.org/10.53730/ijhs.v6n1.5949

Suryatika, I. B. M., Anggarani, N. K. N., Poniman, S., & Sutapa, G. N. (2020). Potential risk of cancer in body organs as result of torak CT-scan exposure. International Journal of Physical Sciences and Engineering, 4(3), 1–6. https://doi.org/10.29332/ijpse.v4n3.465

Yalcinkaya F, Cakar N, Acar B, Tutar E, Guriz H,Elhan AH, Qzturk S,Kansu A, Ince E, Atalay S,Girgin N, Dogru U, Aysev D, Ekim M (2007): The value of acute phase reactant for the prediction of Familial Mediterranean fever associated amyloidosis a case control study.Rheumatol Int.; 27(6):517-22.

Yilmaz H, Inan O, Darcin T, Bilgic MA, Akcay A (2015): Serum galectin-3 levels were associated with proteinuria in patients with familial Mediterranean fever. Clin Exp Nephrol 2015;19:436-42.