Leuprorelin acetate is an agonist of gonadotropinreleasinghormone, used as a first choice treatment in patientswith prostate carcinoma. The impact of leuprorelin therapy inliver function and metabolism is largely unknown. We reportabout a patient who had been treated for 32 months withleuprorelin acetate, who developed a nonalcoholic fatty liverdisease (NAFLD), associated with a focal lesion at the IVhepatic segment where histologic features appeared to be moresevere. The patient, in addition to NAFLD, presented a markediatrogenic hypotestosteronemia and full-criteria meeting thediagnosis of metabolic syndrome, including insulin resistance.The radiologic and clinical findings, the histopathologicfeatures, and the absence of any hepatic abnormalities beforetreatment, support a causal role of leuprorelin in inducingmetabolic derangement that, most likely secondary to androgendeprivation, were, in turn, responsible for the development of NAFLD. This is the first case report of NAFLDwith focal fatty liver associated with leuprorelin therapy.Patients in leuprorelin should be carefully monitored for thedevelopment of liver disease.

Nonalcoholic fatty liver disease induced by leuprorelin acetate / Gabbi, C.; Carubbi, Francesca; Losi, L.; Loria, Paola; Costantini, M.; Bertolotti, Marco; Carulli, N.. - In: JOURNAL OF CLINICAL GASTROENTEROLOGY. - ISSN 0192-0790. - STAMPA. - 42:1(2008), pp. 107-110. [10.1097/01.mcg.0000225583.32588.5e]

Nonalcoholic fatty liver disease induced by leuprorelin acetate

CARUBBI, Francesca;LORIA, Paola;BERTOLOTTI, Marco;
2008

Abstract

Leuprorelin acetate is an agonist of gonadotropinreleasinghormone, used as a first choice treatment in patientswith prostate carcinoma. The impact of leuprorelin therapy inliver function and metabolism is largely unknown. We reportabout a patient who had been treated for 32 months withleuprorelin acetate, who developed a nonalcoholic fatty liverdisease (NAFLD), associated with a focal lesion at the IVhepatic segment where histologic features appeared to be moresevere. The patient, in addition to NAFLD, presented a markediatrogenic hypotestosteronemia and full-criteria meeting thediagnosis of metabolic syndrome, including insulin resistance.The radiologic and clinical findings, the histopathologicfeatures, and the absence of any hepatic abnormalities beforetreatment, support a causal role of leuprorelin in inducingmetabolic derangement that, most likely secondary to androgendeprivation, were, in turn, responsible for the development of NAFLD. This is the first case report of NAFLDwith focal fatty liver associated with leuprorelin therapy.Patients in leuprorelin should be carefully monitored for thedevelopment of liver disease.
2008
42
1
107
110
Nonalcoholic fatty liver disease induced by leuprorelin acetate / Gabbi, C.; Carubbi, Francesca; Losi, L.; Loria, Paola; Costantini, M.; Bertolotti, Marco; Carulli, N.. - In: JOURNAL OF CLINICAL GASTROENTEROLOGY. - ISSN 0192-0790. - STAMPA. - 42:1(2008), pp. 107-110. [10.1097/01.mcg.0000225583.32588.5e]
Gabbi, C.; Carubbi, Francesca; Losi, L.; Loria, Paola; Costantini, M.; Bertolotti, Marco; Carulli, N.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/721854
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