Juan Sordá
University of Buenos Aires
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Juan Sordá.
Journal of Hepatology | 2002
Ruben Terg; Emma Coronel; Juan Sordá; Alberto Muñoz; Jorge Findor
BACKGROUND/AIMS To assess the efficacy and safety of naltrexone for the short and long term treatment of pruritus of cholestasis. METHODS Twenty patients with pruritus and cholestasis were included. A baseline pruritus score was obtained over 1 week. Patients were then randomized to receive 50 mg/day of naltrexone or placebo for 2 weeks. Subsequently, a 1-week washout period ensued and patients were crossed over to the other therapy for 2 additional weeks. Pruritus was assessed daily with a visual analogue scale (VAS) from 0 to 10. Patients whose pruritus decreased >50% of basal with naltrexone received naltrexone 50 mg/day for 2 additional months. RESULTS Mean basal VAS was similar in both groups. VAS showed greater and more significant changes with naltrexone than with placebo (P<0.0003). In nine out of 20 patients (45%) receiving naltrexone, pruritus decreased >50% compared to basal value, including five whose pruritus disappeared completely. No significant changes were observed in serum biochemistry. Most of the adverse events that occurred during the first 48 h of naltrexone therapy were consistent with opioid withdrawal-like phenomena and spontaneously disappeared 2 days after starting treatment. CONCLUSIONS Naltrexone can be considered as an alternative option to treat pruritus of cholestasis. In the current study, side effects were transient and did not require specific medication.
Diabetes-metabolism Research and Reviews | 2012
V. Miksztowicz; Diego Lucero; Valeria Zago; L. Cacciagiú; Graciela López; E. Gonzalez Ballerga; Juan Sordá; Eduardo Fassio; Laura Schreier; G. Berg
Hepatic lipase is a lipolytic enzyme mostly synthesized and localized at the surface of liver sinusoidal capillaries, which hydrolyses triglycerides and phospholipids of intermediate density, large low density (LDL) and high density lipoproteins. Hepatic lipase activity is increased in insulin resistant states. Non‐alcoholic fatty liver disease (NAFLD) is characterized by insulin resistance. However, at present, no data are available regarding the behaviour of hepatic lipase with regard to the degree of hepatic steatosis. Our aim was to evaluate hepatic lipase activity in NAFLD patients and its relationship to the severity of hepatic steatosis.
Clinical Science | 2015
Tomás Meroño; Fernando Brites; Carolane Dauteuille; Marie Lhomme; Martín Menafra; Alejandra Arteaga; Marcelo Castro; María Soledad Saez; Esteban Gonzalez Ballerga; Patricia Sorroche; Jorge Rey; Philippe Lesnik; Juan Sordá; M. John Chapman; Anatol Kontush; Jorge Daruich
Iron overload (IO) has been associated with glucose metabolism alterations and increased risk of cardiovascular disease (CVD). Primary IO is associated with mutations in the HFE gene. To which extent HFE gene mutations and metabolic alterations contribute to the presence of atherogenic lipoprotein modifications in primary IO remains undetermined. The present study aimed to assess small, dense low-density lipoprotein (LDL) levels, chemical composition of LDL and high-density lipoprotein (HDL) particles, and HDL functionality in IO patients. Eighteen male patients with primary IO and 16 sex- and age-matched controls were recruited. HFE mutations (C282Y, H63D and S65C), measures of insulin sensitivity and secretion (calculated from the oral glucose tolerance test), chemical composition and distribution profile of LDL and HDL subfractions (isolated by gradient density ultracentrifugation) and HDL functionality (as cholesterol efflux and antioxidative activity) were studied. IO patients compared with controls exhibited insulin resistance (HOMA-IR (homoeostasis model assessment-estimated insulin resistance): +93%, P< 0.001). Metabolic profiles differed across HFE genotypes. C282Y homozygotes (n=7) presented a reduced β-cell function and insulin secretion compared with non-C282Y patients (n=11) (-58% and -73%, respectively, P< 0.05). In addition, C282Y homozygotes featured a predominance of large, buoyant LDL particles (C282Y: 43±5; non-C282Y: 25±8; controls: 32±7%; P< 0.001), whereas non-C282Y patients presented higher amounts of small, dense LDL (C282Y: 23±5; non-C282Y: 39±10; controls: 26±4%; P< 0.01). HDL particles were altered in C282Y homozygotes. However, HDL functionality was conserved. In conclusion, metabolic alterations and HFE gene mutations are involved in the presence of atherogenic lipoprotein modifications in primary IO. To what extent such alterations could account for an increase in CVD risk remains to be determined.
Microcirculation | 2018
Esteban Gonzalez Ballerga; Mario Omar Pozo; Paolo N. Rubatto Birri; Vanina Siham Kanoore Edul; Juan Sordá; Jorge Daruich; Arnaldo Dubin
To assess sublingual microcirculation in cirrhotic patients and its relationship to spider angiomas, complications, and outcome.
Frontiers in Microbiology | 2017
Olga Quintero; Carolina Berini; Carlos Waldbaum; Alejandra Avagnina; María Juarez; Silvia Repetto; Juan Sordá; Mirna M. Biglione
Strongyloides (S.) stercoralis and Human T-Lymphotropic Virus 1 (HTLV-1) share some endemic regions such as Japan, Jamaica, and South America and are mostly diagnosed elsewhere in immigrants from endemic areas. This co-infection has not been documented in Argentina although both pathogens are endemic in the Northwest. We present a case of S. stercoralis and HTLV-1 co-infection with an initial presentation due to gastrointestinal symptoms which presented neither eosinophilia nor the presence of larvae in stool samples in a non-endemic area for these infections. A young Peruvian woman living in Buenos Aires attended several emergency rooms and finally ended up admitted in a gastroenterology ward due to incoercible vomiting, diarrhea, abdominal pain, fever, and weight loss. Gastrointestinal symptoms started 3 months before she returned to Argentina from a trip to Peru. She presented malnutrition and abdominal distension parameters. HIV-1 and other immunodeficiencies were discarded. The serial coproparasitological test was negative. Computed tomography showed diffuse thickening of duodenal and jejunal walls. At the beginning, vasculitis was suspected and corticosteroid therapy was initiated. The patient worsened rapidly. Skin, new enteral biopsies, and a new set of coproparasitological samples revealed S. stercoralis. Then, HTLV-1 was suspected and infection was confirmed. Ivermectin and albendazole were administrated, until the stool sample remained negative for 2 weeks. Larvae were not observed in fresh stool, Ritchie method, and agar culture 1 week post-treatment. Although she required initial support with parenteral nutrition due to oral intolerance she slowly progressed favorably. It has been highly recommended to include a rapid and sensitive PCR strategy in the algorithm to confirm Strongyloides infection, which has demonstrated to improve early diagnosis in patients at-risk of disseminated strongyloidiasis.
Gastroenterología y Hepatología | 2015
Andrés Wonaga; Carolina Ozollo-Landa; María Marta Piskorz; Carlos Waldbaum; Juan Sordá
4. Sarlon G, Bartoli MA, Muller C, Acid S, Bartoli JM, Cohen S, et a Congenital anomalies of inferior vena cava in young patients wi iliac deep venous thrombosis. Ann Vasc Surg. 2011;25:265. 5. Tsuji Y, Inoue T, Murakami H, Hino Y, Matsuda H, Okita Deep vein thrombosis caused by congenial interruption the inferior vena cava ----a case report. Angiology. 2001;5 721--5. 6. D’Aloia A, Faggiano P, Fiorina C, Vizzardi E, Bontempi L, Grazio L, et al. Absence of inferior vena cava as a rare cause of dee venous thrombosis complicated by liver and lung embolism. Int Cardiol. 2003;88:327--9. 7. Cho BC, Choi HJ, Kang SM, Chang J, Lee SM, Yang DG, et al. Co genital absence of inferior vena cava as a rare cause of pulmona thromboembolism. Yonsei Med J. 2004;31:947--51. 8. Tanabalan C, Papatsoris AG, Masood J. Absent inferior vena cav with resulting bladder varices: A rare cause of frank hematuri
Medicina-buenos Aires | 1999
Jorge Findor; Juan Sordá; Daruich J; Bruch Igartua E; Manero E; Avagnina A; Benbassat D; Rey J; Nakatsuno M
Medicina-buenos Aires | 1998
Jorge Findor; Juan Sordá; Estela Bruch Igartua; Alejandra Avagnina
Medicina-buenos Aires | 2002
Jorge Findor; Juan Sordá; Jorge Daruich; Estela Manero
Acta gastroenterologica Latinoamericana | 2005
Luis Colombato; Silva M; Juan Sordá