Impact of Colchicine on Histology of Testis in Rats
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Colchicine is a drug widely used for the management of many disorders, such as acute gout and Behçet’s disease. It is also prescribed for the treatment of pericarditis, atrial fibrillation coronary artery diseases, and secondary amyloidosis. In case this drug is used at the early stages of coronavirus infection, its anti-inflammatory properties may reduce the severe inflammatory reactions related to a cytokine storm by affecting the inflammasome. The purpose of the present study was to determine the toxicity of Colchicine on testis in rats from different age groups for 10 days. A total of 27 male Wistar rats were divided into three groups. The rats in group I (control group) were administered distilled water by oral gavage. Group II consisted of young rats (5-6 months old) who orally received Colchicine 3 mg/kg body weight. Group III entailed rats of 14-16 months who were orally administered colchicine 3 mg/kg body weight. The testis of the treated groups was dissected and examined for histological changes and morphometrical analysis. The obtained results indicated that high doses of Colchicine (3 mg/kg body weight) could induce tissue damage to the testis, including degeneration and necrosis of both Sertoli and Leydig cells with irregular divisions of germinal epithelium, even when it was used for short periods (10 days). In the elderly treated rats, there were severe tissue damages, including degeneration and necrosis of germinal epithelium with irregular divisions of germ cells, necrosis of Sertoli and Leydig cells with sloughing of germinal epithelium toward the lumen of the tubule. Therefore, there is a need to conduct more studies to investigate the side effect of Colchicine as it is excessively used in the management of coronavirus.Keywords:
Germinal epithelium
Colchicine
Histology
Letters and Corrections1 September 1977Colchicine in Familial Mediterranean FeverRIDA A. FRAYHA, M.D.RIDA A. FRAYHA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-87-3-382_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The cause and pathogenesis of familial Mediterranean fever (FMF) are not clear, hence treatment, by necessity, has been empirical. Prophylactic colchicine therapy has recently been shown to be highly effective in preventing the attacks by suppressing the inflammatory reaction and its symptoms without affecting the basic biorhythm or the underlying excitatory process (1, 2). The mechanism of action of colchicine in FMF remains unclear. Colchicine is known to disrupt the intracellular microtubular structures and to interfere with cellular motility and division. Dinarello and associates (3) have recently shown that patients with FMF on colchicine have significantly fewer...References1. GOLDSTEINSCHWABE RA: Prophylactic colchicine therapy in familial Mediterranean fever. A controlled, double-blind study. Ann Intern Med 81:792-794, 1974 LinkGoogle Scholar2. ZEMERREVACHPRAS DMM: A controlled trial of colchicine in preventing attacks of familial Mediterranean fever. N Engl J Med 291:932-934, 1974 CrossrefMedlineGoogle Scholar3. DINARELLOCHUSIDFAUCI CMA: Effects of prophylactic colchicine therapy on leukocyte function in patients with familial Mediterranean fever. Arthritis Rheum 19:618-622, 1976 CrossrefMedlineGoogle Scholar4. KHACHADURIANARMENIAN AH: The management of familial paroxysmal polyserositis. Experience with low-fat diets and Clofibrate. Leb Med J 25:495-502, 1972 MedlineGoogle Scholar5. STEINSTEIN OY: Colchicine-induced inhibition of very low-density lipoprotein release by rat liver in vivo. Biochem Biophys Acta 306:142-147, 1973 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Internal Medicine American University Hospital Beirut Lebanon PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1977Volume 87, Issue 3Page: 382-382KeywordsColchicineFeversPathogenesis Issue Published: 1 September 1977 PDF DownloadLoading ...
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Background
Familial Mediterranean Fever (FMF) is considered as the prototype of autoinflammatory diseases, and colchicine is the main treatment option for FMF. However, the data on cessation of colchicine treatment in FMF patients is limitedObjectives
To define the characteristics of children with familial Mediterranean fever (FMF) whose colchicine treatment was discontinued and then to compare these features of the patients whose colchicine was restarted with the ones not restarted.Methods
Sixty-four out of 1786 children with FMF whom colchicine was stopped by the physician or patients/parents own decision were enrolled. These patients were grouped into two as: group 1; children whose colchicine was re-started and group 2; children whose colchicine was not re-started. The demographic, clinical and genetic data were collected and compared between group1 and group 2.Results
Colchicine was stopped in 59.4% (38/64) by the physician and 40.6% (26/64) of them had stopped colchicine by patients/parents will. Colchicine was ceased at a median of 10.6 (2.120.5) years of age, and attack- and inflammation-free periods of 18.2 (6-148) months. The median follow-up of 64 patients after colchicine cessation was 37.4 (6.4-154.7) months. It was re-started in seventeen patients due to attacks (n=11) or elevated acute phase reactants (n=6), while remaining 47 patients did not require colchicine. The age at cessation of the colchicine was lower (p= 0.04) and duration of colchicine treatment until its cessation was shorter (p= 0.007) in group 1 than group 2.Conclusion
Even though the results of our study are not satisfactory enough to endorse the hypothesis that colchicine may be discontinued by close follow-up; older age and long duration of colchicine treatment before cessation may be two important features that should be considered in the future studies.References
[1] Sonmez HE, Batu ED, Bilginer Y, Ozen S. Discontinuing colchicine in symptomatic carriers for MEFV (Mediterranean FeVer) variants. Clin Rheumatol. 2017;36(2):421-5. [2] Ben-Zvi I, Krichely-Vachdi T, Feld O, Lidar M, Kivity S, Livneh A. Colchicine-free remission in familial Mediterranean fever: featuring a unique subset of the disease-a case control study. Orphanet J Rare Dis. 2014;9:3.Acknowledgement
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Familial Mediterranean Fever (FMF) is a hereditary autoinflammatory syndrome characterized by recurrent serositis or arthritis attacks and, in some patients, chronic subclinical inflammation that predisposes to secondary amyloidosis. Colchicine is the gold standard of treatment, which reduces attack frequency and amyloidosis risk. However, up to 5% of patients are considered resistant or inadequately respond to colchicine, and some others cannot tolerate the side effects of effective doses of colchicine (colchicine intolerant). We examine how the definition of colchicine resistance has evolved along with various characteristics of colchicine that may help explain unresponsiveness to the drug. Key factors in assessing colchicine resistance include attack frequency and severity, levels of acute phase reactants, colchicine dosage and composition, and treatment compliance. Promising clinical results have been obtained with biologics targeting interleukin-1 in colchicine-resistant or -intolerant patients with FMF. These results underscore the need to identify patients who are not optimally managed with colchicine and who might therefore benefit from additional biologic therapies.
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Familial Mediterranean fever (FMF) is the most common hereditary autoinflammatory syndrome. FMF is caused by mutations in the MEFV gene which encodes the pyrin protein. FMF is characterized by sporadic, paroxysmal attacks of fever and serosal inflammation, lasting 1-3 days. Patients may develop renal amyloidosis. Colchicine prevents attacks and renal amyloidosis.5% to 10% of the patients with FMF are resistant or intolerant to colchicine. Colchicine resistant patients may receive biological therapies. Anti-interleukin-1 drugs are the most important agents of biological treatments. In this review, colchicine resistance and treatment options will be evaluated. Keywords: Colchicine resistance, Familial Mediterranean fever, therapy.
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Фамилната средиземноморска треска (FMF) е автозомно-рецесивно заболяване, характеризиращо се с повтарящи се епизоди на фебрилитет и серозит. При 5-10% от пациентите лечението с Colchicine не е ефективнo за предотвратяване на възпалителните атаки. Други 5-10% от пациентите са с непоносимост към ефективните дози Colchicine и имат сериозни нежелани реакции. Лечението с антиинтерлевкин-1 (IL-1) може да бъде алтернатива за тези пациенти, въпреки че в много държави тази индикация не се реимбурсира от Националната здравноосигурителна система. Представеният клиничен случай демонстрира трудния и дълъг процес на поставянето на диагнозата FMF при млада пациентка с оплаквания от юношеска възраст. Молекулярно-генетичният анализ доказва мутация в MEFV гена, унаследен от майката и бащата. При болната не се установи родствена връзка с лица от Средиземноморския регион. След започване на лечение с Colchicine се наблюдава разреждане на епизодите на фебрилитет (по-малко от един годишно) и значително подобрение в състоянието на пациентката. Въпреки че Colchicine е стандартната терапия за предотвратяване на атаките и потискане на възпалението, 5-10% от пациентите са Colchicine-резистентни, поради което в тези случаи се препоръчва терапия с анти-IL1.
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Introduction: Familial Mediterranean fever (FMF) is a monogenic auto-inflammatory disease characterized by recurrent attacks of fever and serositis. Although colchicine prevents the recurrence of FMF attacks and the development of secondary amyloidosis, the major long-term complication of FMF in most of the patients; 5 – 10% of patients may have inadequate symptom control despite good adherence to colchicine in maximally tolerated doses.Areas covered: In this review, we summarize the treatment approaches for FMF patients to prevent and treat acute attacks, control chronic inflammation, and treat special manifestations and complications.Expert opinion: Colchicine remains the gold standard treatment of FMF. Although colchicine prevents the recurrence of FMF attacks and the development of secondary amyloidosis, 5 – 10% of patients do not respond to conventional colchicine treatment in maximally tolerated doses. Based on the findings of hypersecretion of IL-1β in auto-inflammatory diseases as FMF, IL-1 inhibitors have been proposed as a treatment for crFMF. Attack treatment is mainly supportive and biologic drugs such as anti-IL-1 and anti-IL-6 are added to colchicine therapy in secondary amyloidosis.
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Abstract Background Familial Mediterranean Fever (FMF), an autoinflammatory disease, is characterized by self-limited inflammatory attacks of fever and polyserositis along with high acute phase response. Although colchicine remains the mainstay in treatment, intolerance and resistance in a certain portion of patients have been posing a problem for physicians. Main body Like many autoimmune and autoinflammatory diseases, many colchicine-resistant or intolerant FMF cases have been successfully treated with biologics. In addition, many studies have tested the efficacy of biologics in treating FMF manifestations. Conclusion Since carriers of FMF show significantly elevated levels of serum TNF alpha, IL-1, and IL-6, FMF patients who failed colchicine were successfully treated with anti IL-1, anti IL-6, or TNF inhibitors drugs. It is best to use colchicine in combination with biologics.
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