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Journal articles on the topic 'Gemfibrozilo'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Maguiña, Elbis, Fernando Nuevo V., and Jesús Rumiche B. "Análisis costo-efectividad del uso de estatinas frente a gemfibrozilo en pacientes de consultorios externos del Centro Médico Naval: "Cirujano Mayor Santiago Tavara"." Ciencia e Investigación 9, no. 1 (June 19, 2006): 33–40. http://dx.doi.org/10.15381/ci.v9i1.5090.

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El objetivo de la investigación fue determinar y comparar el costo-efectividad de Atorvastatina 20 mG y Pravastatina 20m mG trente a Gemfibrozilo 600mG, en el tratamiento de hiperlipidemia, e identificar los factores de riesgo. Fue un estudio transversal, descriptivo y retrospectivo, realizado en el Centro Médico Naval, en el período de enero de 2002 a julio de 2005. Se revisaron historias clínicas de 64 pacientes hiperlipidémicos, entre 40 y 64 años, que acuden a los consultorios externos de Cardiología, Endocrinología, Geriatría y Medicina Interna a quienes se les prescribió: Estatinas 20 mg/ día o Gemfibrozilo 600 mg/ día. La efectividad se determinó según el National Cholesterol Education Program (NCEP2001). Se aplicó una encuesta para conocer problemas de cumplimiento de terapia. Según el análisis costo-efectividad (reducción del nivel sérico de LDL-c), las Estatinas reportan una relación costo-efectiva de 13,76 nuevos soles por porcentaje de reducción; y el Gemfibrozilo, no resultó efectivo. Por reducción de nivel de triglicéridos, el Gemfibrozilo presentó una relación cost-efectiva de 1,74 nuevos soles por porcentaje de reducción y las Estatinas no fueron efectivas. Según logro de objetivos terapéuticos, el Gemfibrozilo presentó una relación costo-efectiva menor (361,2 nuevos soles por paciente), debido a su menor costo.

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2

García Llopis, Paula, Alejandra González D’huicque, and Vicente Palop Larrea. "Edema facial por gemfibrozilo." Medicina Clínica 135, no. 8 (September 2010): 384. http://dx.doi.org/10.1016/j.medcli.2009.06.040.

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3

Acuña Elvira, Nerea. "Consulta farmacéutica: intoxicación por gemfibrozilo." Farmacéuticos Comunitarios 9, no. 2 (July 30, 2017): 49–51. http://dx.doi.org/10.5672/fc.2173-9218.(2017/vol9).002.06.

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4

Tormo Molina, J., I. Gázquez Pérez, and A. Matas Hoces. "Cerivastatina y gemfibrozilo: una combinación peligrosa*." Atención Primaria 28, no. 6 (2001): 438–39. http://dx.doi.org/10.1016/s0212-6567(01)70410-6.

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de Arriba Méndez, José-Javier, Elena Gómez Merino, José Antonio Sáez Barcelona, and Lourdes Sáez Méndez. "Rabdomiólisis grave asociada a cerivastatina y gemfibrozilo." Medicina Clínica 117, no. 7 (January 2001): 278–79. http://dx.doi.org/10.1016/s0025-7753(01)72086-6.

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6

Bosch Rovira, T., J. A. Llompart Pou, and J. Forteza-Rey. "Rabdomiólisis asociada al tratamiento combinado con cerivastatina y gemfibrozilo." Revista Clínica Española 201, no. 12 (January 2001): 731–32. http://dx.doi.org/10.1016/s0014-2565(01)70966-6.

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7

Vascónez Espinosa, F., N. Gómez Rodríguez, A. Martín Joven, and F. J. Posada García. "Rabdomiólisis complicada con insuficiencia renal aguda en un paciente tratado con gemfibrozilo y cerivastatina." Revista Clínica Española 201, no. 4 (January 2001): 228–29. http://dx.doi.org/10.1016/s0014-2565(01)70806-5.

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8

Alean Flórez, Joel, Daniela Márquez Méndez, Saudith María Burgos Núñez, Germán Enamorado-Montes, and José Marrugo Negrete. "Productos farmacéuticos y de cuidado personal presentes en aguas superficiales, de consumo humano y residuales en el departamento de Córdoba, Colombia." Revista de Investigación Agraria y Ambiental 12, no. 2 (June 2, 2021): 179–97. http://dx.doi.org/10.22490/21456453.4231.

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Contextualización: gracias al avance de técnicas analíticas sensibles desarrolladas en las últimas décadas, se ha podido identificar y cuantificar la presencia de diversos contaminantes en el medio acuático, dentro de este grupo se encuentran los contaminantes emergentes (CE) conformados por productos de cuidado e higiene personal, antibióticos, hormonas, plastificantes, fármacos y otros que son vertidos a las fuentes de agua alterando el equilibrio de estos ecosistemas. Vacío de investigación: diversas investigaciones muestran que los contaminantes emergentes pueden comprometer la vida acuática y la salud humana. A la fecha en la ciudad de montería y en el departamento de Córdoba no se encuentran reportados ningún estudio que permita evidenciar la presencia de contaminantes emergentes en agua superficial, de consumo humano y residual. Propósito del estudio: el presente estudio, tuvo como objetivo evaluar la presencia de cinco contaminantes emergentes comunes: naproxeno, ibuprofeno, gemfibrozilo, cafeína y triclosán en muestras de agua de consumo humano, residual y superficial colectadas al norte del país, representando así uno de los primeros estudios en reportar la presencia de estos compuestos en fuentes hídricas en esta región. Metodología: se empleó extracción en fase sólida (SPE) para el análisis de las muestras de agua, la detección y cuantificación se realizó por cromatografía líquida de alta eficacia con detector de arreglo de diodo y fluorescencia molecular (HPLC-DAD-FLD). Resultados y conclusiones: el ibuprofeno fue el compuesto que se encontró con mayor frecuencia en las muestras de agua, caso contrario al triclosán, que fue el menos detectado (2.25 µg/L); se halló cafeína en un máximo de 43.38 µg/L mientras que las concentraciones de naproxeno e ibuprofeno estuvieron entre 0.047 y 10.21 µg/L, resaltando la presencia de ibuprofeno y gemfibrozilo en agua de consumo humano. Estos resultados manifiestan la presión antropogénica ejercida sobre los compartimientos acuáticos, convirtiéndose en un problema ambiental que compromete la dinámica y servicios ecosistémicos. Se encontró que las plantas de abastecimiento de agua no tienen en cuenta la presencia de estos compuestos en sus sistemas de potabilización, lo cual podría constituirse un problema de salud pública en un futuro.

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Jiménez-Bambague, Eliana M., Carlos A. Madera-Parra, and Enrique J. Peña-Salamanca. "Eliminación de compuestos farmacéuticos presentes en el agua residual doméstica mediante un tratamiento primario avanzado." INGENIERÍA Y COMPETITIVIDAD 22, no. 1 (January 29, 2020): 10. http://dx.doi.org/10.25100/iyc.v22i1.8794.

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Se evaluó la presencia de compuestos farmacéuticos de los grupos terapéuticos antiepilépticos, agentes hipolipemiantes, analgésicos antiinflamatorios y tranquilizantes en tres jornadas de muestreo, además se estimó la eficiencia de eliminación mediante un tratamiento primario avanzado (TPA) con procesos de coagulación, floculación y sedimentación en la planta de tratamiento de agua residual de la ciudad de Cali (Colombia). De los compuestos medidos, 10 estuvieron por encima del límite de detección de la técnica analítica usada: carbamazepina, 10,11-Dihidro-10,11-dihidroxicarbamazepina, gabapentina, ácido fenofíbrico, gemfibrozilo, diclofenaco, ibuprofeno, ketoprofeno, naproxeno y paracetamol, en concentraciones que oscilaron entre 0.15 y 10 µgL-1 en el afluente. Después del tratamiento, la mayoría de compuestos tuvieron eficiencias de eliminación inferiores al 30%, siendo el paracetamol y naproxeno los que obtuvieron los mejores porcentajes de 98.1 y 57.1%, respectivamente. Estas eficiencias de eliminación se relacionaron no solo al proceso de coagulación floculación, el cual es favorable para compuestos lipofílicos, sino también a la biodegradación por la acción de las bacterias presentes en la matriz de agua residual.

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Martín-Navarro, Juan Antonio, Vladimir Petkov-Stoyanov, María José Gutiérrez-Sánchez, and Luis Pedraza-Cezón. "Fracaso renal agudo por nefritis intersticial aguda con síndrome de Fanconi en relación con metamizol y gemfibrozilo." Nefrología 36, no. 3 (May 2016): 321–23. http://dx.doi.org/10.1016/j.nefro.2015.06.022.

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11

Rotllan, Noemí, Joan Carles Escolà-Gil, Laura Calpe-Berdiel, and Francisco Blanco Vaca. "Efecto de la expresión de la PTEC, el gemfibrozilo y la rosiglitazona en el transporte inverso de colesterol desde macrófagos a heces in vivo." Clínica e Investigación en Arteriosclerosis 21, no. 5 (September 2009): 232–39. http://dx.doi.org/10.1016/s0214-9168(09)72685-3.

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12

Estrela, Gabriel Rufino, Adriano Cleis Arruda, Heron Fernandes Vieira Torquato, Leandro Ceotto Freitas-Lima, Mauro Sérgio Perilhão, Frederick Wasinski, Alexandre Budu, Ricardo Ambrósio Fock, Edgar Julian Paredes-Gamero, and Ronaldo Carvalho Araujo. "Gemfibrozil Induces Anemia, Leukopenia and Reduces Hematopoietic Stem Cells via PPAR-α in Mice." International Journal of Molecular Sciences 21, no. 14 (July 17, 2020): 5050. http://dx.doi.org/10.3390/ijms21145050.

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Hypercholesterolemia, also called high cholesterol, is a form of hyperlipidemia, which may be a consequence of diet, obesity or diabetes. In addition, increased levels of low-density lipoprotein (LDL) and reduced levels of high-density lipoprotein (HDL) cholesterol are associated with a higher risk of atherosclerosis and coronary heart disease. Thus, controlling cholesterol levels is commonly necessary, and fibrates have been used as lipid-lowering drugs. Gemfibrozil is a fibrate that acts via peroxisome proliferator-activated receptor alpha to promote changes in lipid metabolism and decrease serum triglyceride levels. However, anemia and leukopenia are known side effects of gemfibrozil. Considering that gemfibrozil may lead to anemia and that gemfibrozil acts via peroxisome proliferator-activated receptor alpha, we treated wild-type and peroxisome proliferator-activated receptor alpha-knockout mice with gemfibrozil for four consecutive days. Gemfibrozil treatment led to anemia seven days after the first administration of the drug; we found reduced levels of hemoglobin, as well as red blood cells, white blood cells and a reduced percentage of hematocrits. PPAR-alpha-knockout mice were capable of reversing all of those reduced parameters induced by gemfibrozil treatment. Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2α) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2α and erythropoietin mRNA levels in the kidneys. We analyzed bone marrow and found that gemfibrozil reduced erythrocytes and hematopoietic stem cells in wild-type mice but not in PPAR-alpha-knockout mice, while increased colony-forming units were observed only in wild-type mice treated with gemfibrozil. Here, we show for the first time that gemfibrozil treatment leads to anemia and leukopenia via peroxisome proliferator-activated receptor alpha in mice.

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13

Ni, Yu-Fei, Hao Wang, Qiu-Yan Gu, Fei-Ying Wang, Ying-Jie Wang, Jin-Liang Wang, and Bo Jiang. "Gemfibrozil has antidepressant effects in mice: Involvement of the hippocampal brain-derived neurotrophic factor system." Journal of Psychopharmacology 32, no. 4 (March 14, 2018): 469–81. http://dx.doi.org/10.1177/0269881118762072.

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Major depressive disorder has become one of the most serious neuropsychiatric disorders worldwide. However, currently available antidepressants used in clinical practice are ineffective for a substantial proportion of patients and always have side effects. Besides being a lipid-regulating agent, gemfibrozil is an agonist of peroxisome proliferator-activated receptor-α (PPAR-α). We investigated the antidepressant effects of gemfibrozil on C57BL/6J mice using the forced swim test (FST) and tail suspension test (TST), as well as the chronic unpredictable mild stress (CUMS) model of depression. The changes in brain-derived neurotrophic factor (BDNF) signaling cascade in the brain after CUMS and gemfibrozil treatment were further assessed. Pharmacological inhibitors and lentivirus-expressed short hairpin RNA (shRNA) were also used to clarify the antidepressant mechanisms of gemfibrozil. Gemfibrozil exhibited significant antidepressant actions in the FST and TST without affecting the locomotor activity of mice. Chronic gemfibrozil administration fully reversed CUMS-induced depressive-like behaviors in the FST, TST and sucrose preference test. Gemfibrozil treatment also restored CUMS-induced inhibition of the hippocampal BDNF signaling pathway. Blocking PPAR-α and BDNF but not the serotonergic system abolished the antidepressant effects of gemfibrozil on mice. Gemfibrozil produced antidepressant effects in mice by promoting the hippocampal BDNF system.

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14

&NA;. "Gemfibrozil see Lovastatin/gemfibrozil." Reactions Weekly &NA;, no. 291 (March 1990): 8. http://dx.doi.org/10.2165/00128415-199002910-00028.

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15

Song, Danjun, Min Luo, Manyun Dai, Shizhong Bu, Weihua Wang, Burong Zhang, Frank J. Gonzalez, and Aiming Liu. "PPARα-dependent increase of mouse urine output by gemfibrozil and fenofibrate." Canadian Journal of Physiology and Pharmacology 95, no. 2 (February 2017): 199–205. http://dx.doi.org/10.1139/cjpp-2016-0140.

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While gemfibrozil and fenofibrate are prescribed for anti-dyslipidemia treatment, a rational basis for the use of these drugs for treatment of dyslipidemia with concurrent metabolic syndrome has not been established. In this study, wild-type and Pparα-null mice were fed gemfibrozil- or fenofibrate-containing diets for 14 days. Urine output (24 h) was monitored, and urine, serum, and liver and kidney tissues were subjected to toxicity assessment. A 2-month challenge followed by a 2-week wash-out was performed for gemfibrozil to determine urine output and the potential toxicity. A therapeutically equivalent dose of gemfibrozil was more effective than fenofibrate in increasing urine output. This regulatory effect was not observed in Pparα-null mice. In contrast, hepatomegaly induced by fenofibrate was more pronounced than that of gemfibrozil. No significant toxicity was observed in liver or kidney in the 2-month treatment with gemfibrozil. These data demonstrated PPARα mediates the increased urine output by fibrates. Considering the relative action on hepatomegaly and the regulatory effect on urine output, gemfibrozil may be the preferable drug to increase urine output. These results revealed a new pharmacodynamic effect of clinically prescribed PPARα agonists and suggested the potential value of gemfibrozil in modification of blood pressure.

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16

Hari, Rosida. "PROFIL KADAR TRIGLISERIDA PASIEN HIPERTRIGLISERIDEMIA SETELAH PENGGUNAAN GEMFIBROZIL 300 mg DI POLIKLINIK PRATAMA POLITEKNIK NEGERI JEMBER." JURNAL ILMIAH FARMASI AKADEMI FARMASI JEMBER 4, no. 1 (August 12, 2021): 32–37. http://dx.doi.org/10.53864/jifakfar.v4i1.44.

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Penyakit kardiovaskular merupakan penyebab kematian utama didunia dan jumlah kasus penyakit ini telah mengalami peningkatan selama satu decade terakhir. Salah satu penyebabnya adalah hipertrigliserida. Hipertrigliseridemia atau tingginya kadar trigliserida darah merupakan salah satu kelainan fraksi lipid yang berhubungan dengan peningkatan resiko penyakit kardiovaskular Penurunan kadar trigliserida dalam darah dapat dilakukan dengan terapi Gemfibrozil. Gemfibrozil adalah regulator lipid plasma yang dapat menurunkan kadar kolesterol total, kolesterol LDL, kolesterol VLDL dan trigliserida serta meningkatkan kolesterol HDL. Penelitian ini bertujuan untuk mengetahui efektivitas gemfibrozil 300 mg terhadap kadar trigliserida pada pasien hipertrigliseridemia di Poliklinik Pratama Negeri Jember (periode Mei-Juli 2020). Jenis penelitian yang digunakan adalah deskriptif observasional dengan metode pendekatan cross sectional. Teknik pengambilan sampel menggunakan total sampling. Pengukuran kadar trigliserida dilakukan pada 60 pasien sebelum dan sesudah menggunakan gemfibrozil 300 mg. Hasil penelitian menunjukkan, persentase penurunan setelah menggunakan gemfibrozil 300 mg terendah sebesar 10,27 ± 8,64% dan tertinggi sebesar 40,40 ± 12,38%. Rata-rata kadar trigliserida sebelum penggunaan gemfibrozil 300 mg sebesar 295,35 ± 35 mg / dl dan rata-rata kadar trigliserida setelah penggunaan gemfibrozil 300 mg adalah 196,75 ± 49,59 mg / dl.

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17

Bröijersén, Anders, Anders Hamsten, Angela Silveira, Kamaran Fatah, Alison H. Goodall, Sabina Eriksson, Bo Angelin, and Paul Hjemdahl. "Gemfibrozil Reduces Thrombin Generation in Patients with Combined Hyperlipidaemia, without Influencing Plasma Fibrinogen, Fibrin Gel Structure or Coagulation Factor VII." Thrombosis and Haemostasis 76, no. 02 (1996): 171–76. http://dx.doi.org/10.1055/s-0038-1650548.

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SummaryA double-blind, placebo-controlled, cross-over study was conducted in 21 men with combined hyperlipoproteinaemia to examine if lipid-lowering treatment with gemfibrozil (10-12 weeks) affects blood coagulation and fibrin gel structure at rest or during mental stress. Gemfibrozil lowered plasma triglycerides by 57 ± 4%, whereas high density lipoprotein (HDL) cholesterol increased by 22 ± 5%. Gemfibrozil lowered the triglyceride content of low density lipoprotein (LDL). Gemfibrozil reduced the plasma concentrations of thrombin-antithrombin complex (TAT) and prothrombin fragment F1+2 (F1+2), both at rest and during mental stress. However, there were no effects of gemfibrozil treatment on the plasma concentrations of fibrinogen, factor VII antigen, activated factor VII (Vila) or activated factor XII (XIIa), or on fibrin gel structure. Acute mental stress per se did not influence coagulation factors, reaction products or fibrin gel structure, or their responses to the study drug. Thus, gemfibrozil reduces thrombin generation in men with combined hyperlipoproteinaemia, without influencing the plasma levels of fibrinogen, Vila and XIIa, or fibrin gel structure. Attenuation of thrombin generation may contribute to the primary-preventive effects of gemfibrozil on coronary heart disease.

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Andersen, P., P. Smith, I. Seljeflot, S. Brataker, and H. Arnesen. "Effects of Gemfibrozil on Lipids and Haemostasis after Myocardial Infarction." Thrombosis and Haemostasis 63, no. 02 (1990): 174–77. http://dx.doi.org/10.1055/s-0038-1645040.

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SummaryThe effects of gemfibrozil on haemostatic variables were studied in 43 survivors of myocardial infarction with serum triglycerides (TG) ≥2 mmol/1 2 weeks prior to randomization. The study was double-blind, placebo-controlled and stratified for chronic betablockade. Twenty-two individuals were given gemfibrozil 600 mg twice daily and 21 individuals received matching placebo. After 8 weeks the TG level was unchanged in the placebo group, whereas a 44% reduction was noted in the gemfibrozil group (p <0.0001). Fibrinogen increased in both groups, while bleeding time and platelet count were unchanged. Clotting factor VH-phospholipid complex decreased in both groups, but the change was more marked and attained statistical significance only in the gemfibrozil group (60% reduction, p <0.01). By DDAVP-stimulated D-Dimer agglutination test 8 in 21 patients in the placebo group (38%) still had reduced fibrinolytic capacity versus none in the gemfibrozil group (p = 0.001). Thus, in this study, gemfibrozil improved reduced fibrinolytic capacity and may have reduced hypercoagulability by lowering the clotting factor VH-phospholipid complex.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 1323 (October 2010): 23. http://dx.doi.org/10.2165/00128415-201013230-00079.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 437 (February 1993): 7. http://dx.doi.org/10.2165/00128415-199304370-00025.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 443 (March 1993): 9. http://dx.doi.org/10.2165/00128415-199304430-00036.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 856 (June 2001): 9. http://dx.doi.org/10.2165/00128415-200108560-00024.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 314 (August 1990): 7. http://dx.doi.org/10.2165/00128415-199003140-00034.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 317 (September 1990): 5–6. http://dx.doi.org/10.2165/00128415-199003170-00026.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 329 (December 1990): 6. http://dx.doi.org/10.2165/00128415-199003290-00021.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 331 (December 1990): 8. http://dx.doi.org/10.2165/00128415-199003310-00039.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 478 (November 1993): 8. http://dx.doi.org/10.2165/00128415-199304780-00042.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 1291 (March 2010): 26. http://dx.doi.org/10.2165/00128415-201012910-00078.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 1298 (April 2010): 18. http://dx.doi.org/10.2165/00128415-201012980-00053.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 960 (July 2003): 11. http://dx.doi.org/10.2165/00128415-200309600-00036.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 991 (March 2004): 9. http://dx.doi.org/10.2165/00128415-200409910-00024.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 726 (November 1998): 8. http://dx.doi.org/10.2165/00128415-199807260-00025.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 899 (April 2002): 11. http://dx.doi.org/10.2165/00128415-200208990-00035.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 914 (August 2002): 8. http://dx.doi.org/10.2165/00128415-200209140-00025.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 631 (December 1996): 9. http://dx.doi.org/10.2165/00128415-199606310-00025.

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Todd, Peter A., and Alan Ward. "Gemfibrozil." Drugs 36, no. 3 (September 1988): 314–39. http://dx.doi.org/10.2165/00003495-198836030-00004.

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Spencer, Caroline M., and Lee B. Barradell. "Gemfibrozil." Drugs 51, no. 6 (June 1996): 982–1018. http://dx.doi.org/10.2165/00003495-199651060-00009.

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Ahmad, Saeed. "Gemfibrozil." Southern Medical Journal 84, no. 1 (January 1991): 102. http://dx.doi.org/10.1097/00007611-199101000-00027.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 394 (March 1992): 7. http://dx.doi.org/10.2165/00128415-199203940-00026.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 374 (October 1991): 5. http://dx.doi.org/10.2165/00128415-199103740-00019.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 421 (October 1992): 8. http://dx.doi.org/10.2165/00128415-199204210-00033.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 1383 (January 2012): 21. http://dx.doi.org/10.2165/00128415-201213830-00072.

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&NA;. "Gemfibrozil." Reactions Weekly &NA;, no. 1390 (February 2012): 18–19. http://dx.doi.org/10.2165/00128415-201213900-00067.

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Atmaca, Hulusi, Hayriye Sayarlıoğlu, Eyüp Külah, Nejat Demircan, and Tekin Akpolat. "Rhabdomyolysis Associated with Gemfibrozil—Colchicine Therapy." Annals of Pharmacotherapy 36, no. 11 (November 2002): 1719–21. http://dx.doi.org/10.1345/aph.1c028.

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OBJECTIVE: To report a case of rhabdomyolysis possibly due to combination therapy with colchicine and gemfibrozil. CASE SUMMARY: A 40-year-old man with amyloidosis and hepatitis B virus—related chronic liver disease was admitted to the university hospital because of fatigue, lack of appetite, dark brownish urine, and myalgia for 2 weeks. The patient was receiving colchicine and gemfibrozil. Elevations of serum creatine kinase, lactate dehydrogenase, and aspartate aminotransferase concentrations with myalgia were compatible with the diagnosis of rhabdomyolysis. DISCUSSION: To our knowledge, myopathy and rhabdomyolysis due to a combination of colchicine and gemfibrozil therapy have not been previously reported. Preexisting mild renal failure, hepatitis B—related chronic liver disease, and amyloidosis may be contributing risk factors for the development of rhabdomyolysis in this patient. An objective causality assessment revealed that the adverse drug event was possible. CONCLUSIONS: Patients receiving combination therapy with colchicine and gemfibrozil, especially those with renal and hepatic dysfunction, should be monitored for rhabdomyolysis, and concomitant colchicine and gemfibrozil therapy should be considered in the differential diagnosis of rhabdomyolysis.

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Werremeyer, Amy B., Ji M. Koo, and Justin M. Welch. "A Comparison of Adverse Effects of Simvastatin plus Gemfibrozil and Atorvastatin plus Gemfibrozil." Hospital Pharmacy 42, no. 7 (July 2007): 631–36. http://dx.doi.org/10.1310/hpj4207-631.

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Background The manufacturer of simvastatin recommends a dose limitation of 10 mg daily when used in combination with gemfibrozil, due to increased risk of myopathy and rhabdomyolysis. Little information is available regarding the risk of adverse effects of atorvastatin when used in combination with gemfibrozil. Purpose To compare the rate of discontinuation or dose reduction due to adverse effects with simvastatin and gemfibrozil versus atorvastatin and gemfibrozil. Methods Retrospective review of patients taking gemfibrozil in combination with simvastatin 10 mg, simvastatin 80 mg, or atorvastatin 40 mg for at least 6 months. Results A total of 166 patients were included; 59 were taking simvastatin 10 mg (S10), 47 were taking simvastatin 80 mg (S80), and 60 were taking atorvastatin 40 mg (A40). There was no significant difference in the rate of discontinuation or dose reduction due to adverse effects among the groups (10.2% for S10, 21.2% for S80, and 10% for A40, P = 0.159). A paired comparison of discontinuation or dose reduction due to adverse effects between the simvastatin 80 mg and atorvastatin 40 mg groups approached a trend toward a difference ( P = 0.104). Severe adverse effects occurred in the simvastatin 80 mg and atorvastatin 40 mg groups. Conclusion Our results did not show a significant difference in discontinuation or dose reduction due to adverse effects between patient groups taking gemfibrozil in combination with simvastatin 10 mg, simvastatin 80 mg, or atorvastatin 40 mg. However, the rate of this outcome in the S80 group was approximately double that for the S10 and A40 groups. Further studies are needed to compare the safety of these statin-gemfibrozil combinations.

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Cao, Suzanne, NhuChi Dao, Kristina Roloff, and Guillermo Valenzuela. "Pregnancies Complicated by Familial Hypertriglyceridemia: A Case Report." American Journal of Perinatology Reports 08, no. 04 (October 2018): e362-e364. http://dx.doi.org/10.1055/s-0038-1676832.

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Background Although rare, familial hypertriglyceridemia can cause acute and life-threatening complications in pregnancy. Cases The first patient's pregnancy was complicated by multiple admissions for pancreatitis due to hypertriglyceridemia and noncompliance with gemfibrozil. In her second pregnancy, she was compliant with gemfibrozil and only experienced pancreatitis episodes toward the end of pregnancy. The second patient had diabetes mellitus and familial hypertriglyceridemia. She required multiple hospitalizations for diabetic ketoacidosis secondary to insulin noncompliance. In both pregnancies, she was compliant with gemfibrozil and had no complications related to hypertriglyceridemia. Conclusion Treatment with gemfibrozil in pregnancies complicated by hypertriglyceridemia may prevent complications without adverse maternal or fetal effects and could be considered in treating pregnant patients with severe hypertriglyceridemia. These cases also demonstrate the importance of medication compliance in the prevention of poor outcomes.

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Chakkarwar, Vishal Arvind, and Pravin Kawtikwar. "EFFECT OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-ALPHA-AGONISTS ON DIABETES-INDUCED ACUTE KIDNEY INJURY: ROLE OF OXIDATIVE STRESS AND HYPERLIPIDEMIA." Asian Journal of Pharmaceutical and Clinical Research 12, no. 1 (January 7, 2019): 143. http://dx.doi.org/10.22159/ajpcr.2018.v12i1.29397.

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Objective: The present study investigated the possible effect of fenofibrate and gemfibrozil peroxisome proliferator-activated receptor-alpha agonist in diabetes-induced acute kidney injury (AKI) in rats.Methods: Rats were administered streptozotocin (STZ) (50 mg/kg, i.p., single dose) to induce experimental diabetes mellitus. The development of diabetic AKI was assessed biochemically and histologically. In addition, the diabetes-induced lipid profile and renal oxidative stress were assessed. The single dose of STZ produced diabetes, which induced renal oxidative stress, altered the lipid profile and subsequently produced kidney injuryAKI in 7 weeks by increasing serum creatinine, blood urea nitrogen (BUN), proteinuria, and glomerular damage. Treatment with fenofibrate and gemfibrozil (30 mg/kg p.o, 7 weeks) normalized the altered lipid profile by decreasing serum cholesterol, triglycerides, and increasing serum high-density lipoprotein in diabetic rats. Lisinopril (1 mg/kg, p.o., 7 weeks, reference compound) prevents lipid alteration and development of diabetic AKI.Result: Fenofibrate and gemfibrozil, besides hyperglycemia, significantly prevented the development of diabetic AKI by reducing (serum and tissue) oxidative stress, hyperlipidemia, serum BUN, creatinine, and urinary protein. Further, fenofibrate, but not gemfibrozil, considerably reduced renal structural and functional abnormalities in diabetic rats. The fenofibrate was more effective in attenuating the diabetes-induced AKI and renal oxidative stress as compared to treatment with and gemfibrozil.Conclusion: The fenofibrate and gemfibrozil treatment markedly prevented the diabetes-induced AKI. In comparison, the fenofibrate is found to be a superior approach to attenuate the diabetic AKI than gemfibrozil.

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Chakkarwar, Vishal Arvind, and Pravin Kawtikwar. "EFFECT OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-ALPHA-AGONISTS ON DIABETES-INDUCED ACUTE KIDNEY INJURY: ROLE OF OXIDATIVE STRESS AND HYPERLIPIDEMIA." Asian Journal of Pharmaceutical and Clinical Research 12, no. 1 (January 7, 2019): 143. http://dx.doi.org/10.22159/ajpcr.2019.v12i1.29397.

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Objective: The present study investigated the possible effect of fenofibrate and gemfibrozil peroxisome proliferator-activated receptor-alpha agonist in diabetes-induced acute kidney injury (AKI) in rats.Methods: Rats were administered streptozotocin (STZ) (50 mg/kg, i.p., single dose) to induce experimental diabetes mellitus. The development of diabetic AKI was assessed biochemically and histologically. In addition, the diabetes-induced lipid profile and renal oxidative stress were assessed. The single dose of STZ produced diabetes, which induced renal oxidative stress, altered the lipid profile and subsequently produced kidney injuryAKI in 7 weeks by increasing serum creatinine, blood urea nitrogen (BUN), proteinuria, and glomerular damage. Treatment with fenofibrate and gemfibrozil (30 mg/kg p.o, 7 weeks) normalized the altered lipid profile by decreasing serum cholesterol, triglycerides, and increasing serum high-density lipoprotein in diabetic rats. Lisinopril (1 mg/kg, p.o., 7 weeks, reference compound) prevents lipid alteration and development of diabetic AKI.Result: Fenofibrate and gemfibrozil, besides hyperglycemia, significantly prevented the development of diabetic AKI by reducing (serum and tissue) oxidative stress, hyperlipidemia, serum BUN, creatinine, and urinary protein. Further, fenofibrate, but not gemfibrozil, considerably reduced renal structural and functional abnormalities in diabetic rats. The fenofibrate was more effective in attenuating the diabetes-induced AKI and renal oxidative stress as compared to treatment with and gemfibrozil.Conclusion: The fenofibrate and gemfibrozil treatment markedly prevented the diabetes-induced AKI. In comparison, the fenofibrate is found to be a superior approach to attenuate the diabetic AKI than gemfibrozil.

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Wilkes, H. C., T. W. Meade, S. Barzega, A. J. Foley, L. O. Hughes, K. A. Bauer, R. D. Rosenberg, and G. J. Miller. "Gemfibrozil Reduces Plasma Prothrombin Fragment F1+2 Concentration, a Marker of Coagulability, in Patients with Coronary Heart Disease." Thrombosis and Haemostasis 67, no. 05 (1992): 503–6. http://dx.doi.org/10.1055/s-0038-1648481.

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SummaryThe effects of gemfibrozil on several indices of haemostatic activity were explored in male patients with coronary heart disease (CHD). Sixty-three of 71 patients completed a crossover study in which gemfibrozil 1,200 mg/day and matching placebo were each taken in randomised order for 2 months in a doubleblind manner, separated by a 2-month washout period. Serum cholesterol decreased by an average (95% confidence interval) of 12 (9 to 15)% and non-fasting triglyceride concentration by 43 (34 to 51)% during active treatment. Plasma prothrombin fragment Fi + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase. Factor VII coagulant activity (VIIC) and antigen concentration, and fibrinopeptide A concentration were not influenced by gemfibrozil in the group overall. However, the VIIC response appeared to be dependent upon the untreated cholesterol level. Hypercholesterolaemic men (cholesterol >6.5 mmol/1) experienced a significant reduction in VIIC averaging 6% of standard during active therapy. Other effects of gemfibrozil were a 5 (2 to 9)% increase in plasma fibrinogen by a gravimetric method, an 11 (8 to 13)% increase in platelet count, and a 6 (2 to 10)% reduction in white cell count. The reduced incidence of CHD following gemfibrozil therapy in hyperlipidaemic patients may arise in part through a reduction in procoagulant activity and thus the risk of an occlusive coronary thrombosis.

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Backes, Jim M., Patrick M. Moriarty, and Cheryl A. Gibson. "The Effect of Micronized Fenofibrate on Lipid Profiles of Patients Converted from Gemfibrozil." Hospital Pharmacy 37, no. 9 (September 2002): 953–56. http://dx.doi.org/10.1177/001857870203700915.

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Although numerous studies have established the efficacy of micronized fenofibrate (MF) and gemfibrozil in improving lipid profiles, there are limited comparative data on the lipid-lowering effects of these two agents. The objective of this study was to evaluate the mean changes in lipid values of hypertriglyceridemic patients crossed over from gemfibrozil to MF. The Medical charts of 21 patients were analyzed retrospectively. Patients were maintained on gemfibrozil 600 mg twice daily for a minimum of 3 months. The patient's last fasting lipid profile on gemfibrozil was compared to the first lipid profile after crossover to MF 200 to 201 mg/day. Patients were excluded if there were alterations in other lipid-lowering therapy during the cross-over or documented non-adherence. The lipid profiles after the crossover showed a significant reduction in triglycerides (56%; P < 0.05) and TC/HDL ratio (38%; P < 0.05) and a significant increase in HDL (22%; P < 0.05). There were nonsignificant changes in other lipid values: TC (-22%; P = 0.058), LDL (+5%; P = 0.866) and LDL/HDL ratio (+6; P = 1.0). The results show that MF had additional favorable effects on triglycerides, HDL, and TC/HDL ratio compared with gemfibrozil. A larger, randomized trial to confirm these effects is warranted.

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