FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2020159773> ?p ?o ?g. }

• W2020159773 endingPage "519" @default.
• W2020159773 startingPage "507" @default.
• W2020159773 abstract "Over the past forty years, liver transplantation (OLT) has evolved from an experimental, surgical procedure with a low likelihood of success to a universally accepted multi-disciplinary endeavor for the treatment of both acute liver failure and end-stage liver disease. In 2008, the expectation of 1-year post-transplant survival is greater than 85% for most indications, and indeed, the majority of clinical challenges have been addressed [1Seaberg E.C. Belle S.H. Berginger K.C. Schivins J.L. Detre K.M. Long-term patient and retransplantation-free survival by selected recipient and donor characteristics: an update from the Pitt-UNOS liver transplant registry.in: Cecka J.M. Teasaki P.I. Clinical transplants. UCLA Tissue Typing Laboratory, Los Angles1997: 15-28Google Scholar, 2Yoshida E.M. Marotta P.J. Greig P.D. Kneteman N.M. Marleau D. Cantarovich M. et al.Evaluation of renal function in liver transplant recipients receiving daclizumab (Zenapax), mycophenolate mofetil, and a delayed, low-dose tacrolimus regimen vs a standard-dose tacrolimus and mycophenolate mofetil regimen: a multicenter randomized clinical trial.Liver Transpl. 2005; 11: 1064-1072Crossref PubMed Scopus (116) Google Scholar, 3Laryea M. Watt K.D. Molinari M. Walsh M.J. McAlister V.C. Marotta P.J. et al.Metabolic syndrome in liver transplant recipients: prevalence and association with major vascular events.Liver Transpl. 2007; 13: 1109-1114Crossref PubMed Scopus (238) Google Scholar]. In that context, the expectation for most liver graft recipients is one of achieving long-term survival in conjunction with significantly improved quality of life [4Bravata D.M. Olkin I. Barnato A.E. Keeffe E.B. Owens D.K. Health-related quality of life after liver transplantation: a meta-analysis.Liver Transpl Surg. 1999; 5: 318-331Crossref PubMed Scopus (190) Google Scholar, 5Blanch J. Sureda B. Favia M. Marcos V. de Pablo J. de Lazzari E. et al.Psychosocial adjustment to orthotopic liver transplantation in 266 recipients.Liver Transpl. 2004; 10: 228-234Crossref PubMed Scopus (58) Google Scholar, 6Adams P.C. Ghent C.N. Grant D.R. Wall W.J. Employment after liver transplantation.Hepatology. 1995; 21: 140-144PubMed Google Scholar, 7Hunt C.M. Tart J.S. Dowdy E. Bute B.P. Williams D.M. Clavien P.A. et al.Effect of orthotopic liver transplantation on employment and health status.Liver Transpl Surg. 1996; 2: 148-153Crossref PubMed Scopus (65) Google Scholar, 8Sahota A. Zaghla H. Adkins R. Ramji A. Lewis S. Moser J. et al.Predictors of employment after liver transplantation.Clin Transplant. 2006; 20: 490-495Crossref PubMed Scopus (40) Google Scholar]. For younger patients, the expectation of contributing to society means considerably more than merely returning to the workforce or achieving specific goals. For younger patients, who have undergone successful OLT, the expectation in 2008 is one of a full and normal life, including the ability to have children, and enjoyment of normal sexual relations. In this, the 11th Forum on Liver Transplantation we examine a much neglected combination of topics reflecting the full tapestry of issues pertaining to sexual health and function, contraception and pregnancy in the OLT recipient. Additionally, we examine the rare indications for transplantation in patients who develop liver failure as a consequence of pregnancy. Alteration in aspects of liver function is normal during pregnancy. Severe liver dysfunction is rare, but when it occurs, it can do so in a catastrophic fashion for both mother and infant. Liver disease in pregnancy can be considered in three separate categories. First, liver dysfunction specific to the pregnant state, i.e. conditions occurring only in the setting of pregnancy. Second, management of the pre-existing disorders that may be provoked by the pregnant state, i.e. pre-existing liver disease that must cope with the extra physiological demands of pregnancy. Finally, liver disease coincident with pregnancy, i.e. apparent concurrent liver conditions occurring in a pregnant woman that do not typically affect the pregnancy. In the context of liver transplantation, it is this first category that is most pertinent. Liver failure in its broadest sense, occurring in the context of the pregnant state is rare, and is most often caused by acute fatty liver of pregnancy (AFLP), eclampsia-related liver disease, or the haemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome. Indeed, the distinction between eclampsia-related liver disease in pregnancy, HELLP syndrome and AFLP is blurred in many cases and it is often difficult to distinguish one from another. These specific conditions typically occur in the third trimester of pregnancy but may present at any time during pregnancy or even in the early post-partum period [[9]Riely C.A. Liver disease in the pregnant patient.Am J Gastroenterol. 1999; 94: 1728-1732Crossref PubMed Scopus (63) Google Scholar]. In considering a differential diagnosis in patients who may present with liver failure, it is important to reflect on conditions outwith those that occur only in the pregnant state. These are summarized in Table 1.Table 1Liver dysfunction in pregnancy in patients without pre-existing liver diseaseLiver disease specific to pregnancyAcute fatty liver of pregnancyHypertension-associated liver disease of pregnancy Pre-eclampsia and eclampsia Hepatic infarction, hematoma and rupture HELLP syndromeLiver disease coincident with pregnancyAcute viral hepatitis Hepatitis A–E Herpes simplex hepatitisDrug toxicityAcetaminophen toxicityBudd-Chiari syndromeLiver transplant recipientsConsideration should be given in differential diagnosis to each of these conditions. For patients with liver disease specific to pregnancy, it is pertinent to consider that it is frequently clinically difficult to differentiate between HELLP syndrome AFLP and eclampsia-related liver disease. In all such instances, early delivery and intensive supportive care may abrogate the need for liver transplant. Open table in a new tab Consideration should be given in differential diagnosis to each of these conditions. For patients with liver disease specific to pregnancy, it is pertinent to consider that it is frequently clinically difficult to differentiate between HELLP syndrome AFLP and eclampsia-related liver disease. In all such instances, early delivery and intensive supportive care may abrogate the need for liver transplant. AFLP and HELLP syndromes are both infrequent with AFLP reported as occurring in 1/7000–15,000 pregnancies. First described in 1934 by Sheehan et al. as a yellow atrophy of the liver, the condition has been widely described and significant advances in the pathogenesis of the condition reported [10Sheehan H. The pathology of acute yellow atrophy and delayed chloroform poisoning.J Obstetr Gynaecol. 1940; 47: 49-62Crossref Scopus (148) Google Scholar, 11Mjahed K. Charra B. Hamoudi D. Noun M. Barrou L. Acute fatty liver of pregnancy.Arch Gynecol Obstet. 2006; 274: 349-353Crossref PubMed Scopus (42) Google Scholar, 12Castro M.A. Fassett M.J. Reynolds T.B. Shaw K.J. Goodwin T.M. Reversible peripartum liver failure: a new perspective on the diagnosis, treatment, and cause of acute fatty liver of pregnancy, based on 28 consecutive cases.Am J Obstet Gynecol. 1999; 181: 389-395Abstract Full Text Full Text PDF PubMed Scopus (208) Google Scholar, 13Ibdah J.A. Bennett M.J. Rinaldo P. Zhao Y. Gibson B. Sims H.F. et al.A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.N Engl J Med. 1999; 340: 1723-1731Crossref PubMed Scopus (398) Google Scholar]. Histological findings are those of severe microvesicular steatosis in association with minimal necrosis. Acute fatty liver of pregnancy is regarded as one of the family of diseases characterised by a mitochondrial cytopathy, which also includes conditions such as Reye’s Syndrome, drug-related liver disease and other genetic defects in mitochondrial function. Ultimately, these conditions are characterised by vomiting, hypoglycaemia, lactic acidosis, hyperammonaemia and microvesicular fat in organs. Acidosis occurs as a result in defective energy supply within the mitochondria during oxidative phosphorylation. Hypoglycaemia in these disorders may relate to failure of mitochondrial tricarboxylic acid cycle enzymes [11Mjahed K. Charra B. Hamoudi D. Noun M. Barrou L. Acute fatty liver of pregnancy.Arch Gynecol Obstet. 2006; 274: 349-353Crossref PubMed Scopus (42) Google Scholar, 12Castro M.A. Fassett M.J. Reynolds T.B. Shaw K.J. Goodwin T.M. Reversible peripartum liver failure: a new perspective on the diagnosis, treatment, and cause of acute fatty liver of pregnancy, based on 28 consecutive cases.Am J Obstet Gynecol. 1999; 181: 389-395Abstract Full Text Full Text PDF PubMed Scopus (208) Google Scholar, 13Ibdah J.A. Bennett M.J. Rinaldo P. Zhao Y. Gibson B. Sims H.F. et al.A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.N Engl J Med. 1999; 340: 1723-1731Crossref PubMed Scopus (398) Google Scholar]. The understanding of the pathogenesis of the condition has been greatly enhanced by the description of full term infants born to mothers with AFLP in whom hypoglycaemia, hepatic encephalopathy and steatosis developed. The infants were found to have a defect in fatty acid oxidation, and specifically were deficient in long-chain 3-hydroxyacyl coenzyme A dehydrogenase (LCHAD)[[13]Ibdah J.A. Bennett M.J. Rinaldo P. Zhao Y. Gibson B. Sims H.F. et al.A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.N Engl J Med. 1999; 340: 1723-1731Crossref PubMed Scopus (398) Google Scholar]. In a seminal investigation, this pattern was noted in 11 women whose pregnancies were complicated by acute fatty liver with features of HELLP syndrome. Six babies from this series were found to have LCHAD deficiency[[13]Ibdah J.A. Bennett M.J. Rinaldo P. Zhao Y. Gibson B. Sims H.F. et al.A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.N Engl J Med. 1999; 340: 1723-1731Crossref PubMed Scopus (398) Google Scholar]. Heterozygosity for LCHAD in the mother appears to be responsible at least in part for the development of disease in the infant. The molecular basis has been identified as the substitution of guanosine to cytosine in the alpha-subunit that catalyses the last three steps of beta oxidation. Consistent with these findings is the fact that in murine models, pregnancy decreases fatty oxidation with the effect mediated by estrogens and progesterones. Patients with AFLP present in the third trimester at a mean gestational age 34 weeks with non-specific symptoms, such as vomiting, malaise, fever, and abdominal pain [[13]Ibdah J.A. Bennett M.J. Rinaldo P. Zhao Y. Gibson B. Sims H.F. et al.A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.N Engl J Med. 1999; 340: 1723-1731Crossref PubMed Scopus (398) Google Scholar]. In later stages, patients develop jaundice, coagulopathy, hypoglycaemia, and encephalopathy. Serum transaminases rarely exceed 1000 IU/L, and usually ranges from 300 to 500 IU/L [[14]Hamid S.S. Jafri S.M. Khan H. Shah H. Abbas Z. Fields H. et al.Fulminant hepatic failure in pregnant women: acute fatty liver or acute viral hepatitis?.J Hepatol. 1996; 25: 20-27Abstract Full Text PDF PubMed Scopus (115) Google Scholar]. Disseminated intravascular coagulation (DIC) may occur in up to 70% of cases. In severe cases, the clinical course may be complicated by hepatic necrosis and liver rupture. The differential diagnosis includes acute viral hepatitis and HELLP syndrome. Ultrasound imaging and viral serological assessment are required in all cases. Liver biopsy is not mandatory but may be necessary if the diagnosis is clinically unclear, the liver function tests do not normalise after delivery or, the diagnosis of ALFP is required as an indication for delivery [[15]Vigil-De Gracia P. Lavergne J.A. Acute fatty liver of pregnancy.Int J Gynaecol Obstet. 2001; 72: 193-195Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar]. The therapy of choice is rapid delivery, usually by caesarian section. In the past, AFLP was considered to be universally fatal, but aggressive optimization in the peri-delivery period, has improved the prognosis with both maternal and foetal mortality rates ranging from 0% to 20% reported in the literature [[16]Fesenmeier M.F. Coppage K.H. Lambers D.S. Barton J.R. Sibai B.M. Acute fatty liver of pregnancy in 3 tertiary care centers.Am J Obstet Gynecol. 2005; 192: 1416-1419Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar]. Although AFLP may progress to acute liver failure (ALF), liver transplantation is rarely indicated/required since the condition is typically reversible following delivery. Liver transplantation should be considered in cases with severe disseminated intravascular coagulation (DIC), rupture of the liver, or severe encephalopathy. Where present, the cardinal management paradigm is emergency delivery by caesarian section, with aggressive supportive care. OLT is performed only in the context of failure to recover liver function. In the European Liver Transplantation Registry (ELTR) database (www.eltr.org) 75,530 liver transplantations have been recorded since 1968. OLT has been performed in only six instances for AFLP during this time, (René Adam, personal communication) demonstrating that transplantation is rarely required, and is only indicated in exceptional cases of advanced disease. The second clinical scenario associated with liver failure during pregnancy is the HELLP syndrome, which was first described by Weinstein et al. in 1982 and usually occurs towards the end of pregnancy in young primagravidae [[17]Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy.Am J Obstet Gynecol. 1982; 142: 159-167Abstract Full Text PDF PubMed Scopus (1098) Google Scholar]. The pathogenesis of HELLP syndrome is unclear but an imbalance of prostacyclin and thromboxane has been suggested [18Fitzgerald D.J. Mayo G. Catella F. Entman S.S. FitzGerald G.A. Increased thromboxane biosynthesis in normal pregnancy is mainly derived from platelets.Am J Obstet Gynecol. 1987; 157: 325-330Abstract Full Text PDF PubMed Scopus (98) Google Scholar, 19Fitzgerald D.J. Rocki W. Murray R. Mayo G. FitzGerald G.A. Thromboxane A2 synthesis in pregnancy-induced hypertension.Lancet. 1990; 335: 751-754Abstract PubMed Scopus (186) Google Scholar]. Patients with HELLP syndrome typically have evidence of pre-eclampsia as well as thrombocytopenia. The HELLP syndrome affects about 6/1000 pregnancies and manifests most frequently in the 34th gestational week. However, 10–30% of cases occur within the first six days post-partum [[9]Riely C.A. Liver disease in the pregnant patient.Am J Gastroenterol. 1999; 94: 1728-1732Crossref PubMed Scopus (63) Google Scholar]. The most common presenting symptom is abdominal pain but as many as 40% of all cases may be asymptomatic. The clinical course can be complicated by renal failure, pulmonary edema, cerebral hemorrhage, and seizures. Serum aspartate aminotransferase (AST) is usually elevated to a mean level of 250 IU/L, but levels in excess of 7000 IU/L have been reported. The condition may not meet criteria for ALF since the prothrombin time is typically normal, except in its most extreme form when DIC may exist. The severity of the histological changes are not usually reflected by the laboratory abnormalities, and biopsy of the liver is not mandatory for diagnosis. The most important differential diagnoses are acute viral hepatitis, idiopathic thrombocytopaenia purpura, and AFLP. The treatment of choice is early delivery. Once delivered, the infants have no liver involvement and an appropriate outcome for the gestational age may be anticipated. In most instances there are no long-term sequelae for the mother although the condition may recur in subsequent pregnancies. In 2–3% of the cases, HELLP syndrome can lead to a variety of hepatic complications such as subcapsular liver hemorrhage and subsequent hepatic rupture, resulting in the death of either mother and/or foetus [[20]Audibert F. Friedman S.A. Frangieh A.Y. Sibai B.M. Clinical utility of strict diagnostic criteria for the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome.Am J Obstet Gynecol. 1996; 175: 460-464Abstract Full Text Full Text PDF PubMed Scopus (245) Google Scholar]. Such patients present in shock, with abdominal hemorrhage and require rapid laparotomy and surgical management with packing of the liver. In addition, HELLP syndrome can also lead to hepatic infarction with significant aminotransferase elevation. This is typically identified on axial imaging such as computed tomography and frequently is accompanied by coagulopathy and progressive encephalopathy, i.e. ALF. While the overall mortality of the HELLP syndrome is 2–3%, the presence of hepatic complications increases the maternal mortality to 50%, and in such cases, transplant should be considered [[21]Sibai B.M. Ramadan M.K. Usta I. Salama M. Mercer B.M. Friedman S.A. et al.Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome).Am J Obstet Gynecol. 1993; 169: 1000-1006Abstract Full Text PDF PubMed Scopus (889) Google Scholar]. Only case reports and one small series about liver transplantation for HELLP syndrome have been reported. Zarrinpar et al. reported the largest series of liver transplantation for HELLP syndrome [[22]Zarrinpar A. Farmer D.G. Ghobrial R.M. Lipshutz G.S. Gu Y. Hyatt J.R. et al.Liver transplantation for HELLP syndrome.Am Surg. 2007; 73: 1013-1016PubMed Google Scholar]. A review of 3090 adult liver transplant operations performed at a single center revealed that eight patients were transplanted for this indication [[22]Zarrinpar A. Farmer D.G. Ghobrial R.M. Lipshutz G.S. Gu Y. Hyatt J.R. et al.Liver transplantation for HELLP syndrome.Am Surg. 2007; 73: 1013-1016PubMed Google Scholar]. The most frequent clinical manifestations in this group were encephalopathy, renal failure, DIC, and respiratory failure. A mean model for end-stage liver disease (MELD) score of 40 at the time of OLT typifies the severity of liver disease. In the report, four patients developed primary non-function after transplantation resulting in one death. After three successful re-transplantations in the remaining patients, a 5-year patient survival of 88% was reported. In the European Liver Transplant Registry (www.eltr.org) only four of 75,530 liver transplantations were performed for liver involvement of HELLP syndrome (René Adam personal communication), suggesting that only selected cases with severe liver involvement require transplantation. Despite the great wealth of accumulated post-transplant medical knowledge, sexuality or “sexual health” remains largely unexplored post-liver transplantation out-with questions and variables on generic quality of life instruments. There are many possible reasons why sexual health has been poorly studied following OLT, despite its importance to recipients and their partners. In the highly specialized arena of the post-transplant clinic, physicians, surgeons and allied health care professionals may not feel comfortable dealing with questions regarding sexual health. Many healthcare providers feel that it is outside of their area of expertise and that they have too little to offer patients. Similarly, primary care physicians who are less familiar with liver transplantation often assume that post-transplant patients have more life-threatening transplant-related issues to contend with, and that a return to “normal” life after transplantation is unlikely. From an academic perspective, the topic itself is, admittedly, a difficult one to study. Sexual attitudes and practices amongst patient populations are heterogeneous and vary from community to community and temporally from generational cohort to generational cohort. Even within individual patients, sexuality changes with time. The subject matter itself is also controversial, just as it is in the greater society. Similar to contemporary society, some patients may perceive any enquiry or investigation of post-transplant sexuality to be “offensive” and a factor that will negatively affect participation rates in clinical studies. This in turn leads to questions regarding the internal validity of studies, since participation and non-participation may reflect systemic bias that skews the results. Lastly, the generalisability of study findings from one country to another and from one time-point to another becomes problematic. End-stage liver disease is well recognised as altering the normal physiology of the hypothalamic–pituitary–gonadal axis, which in turn can affect sexual function in these patients. In male patients, cirrhosis is associated with decreased levels of serum testosterone [23Van Thiel D.H. Gavaler J.S. Spero J.A. Egler K.M. Wright C. Sanghvi A.T. et al.Patterns of hypothalamic–pituitary–gonadal dysfunction in men with liver disease due to differing etiologies.Hepatology. 1981; 1: 39-46Crossref PubMed Scopus (50) Google Scholar, 24Guechot J. Vaubourdolle M. Ballet F. Giboudeau J. Darnis F. Poupon R. et al.Hepatic uptake of sex steroids in men with alcoholic cirrhosis.Gastroenterology. 1987; 92: 203-207PubMed Google Scholar, 25Van Thiel D.H. Kumar S. Gavaler J.S. Tarter R.E. Effect of liver transplantation on the hypothalamic–pituitary–gonadal axis of chronic alcoholic men with advanced liver disease.Alcohol Clin Exp Res. 1990; 14: 478-481Crossref PubMed Scopus (30) Google Scholar, 26Guechot J. Chazouilleres O. Loria A. Hannoun L. Balladur R. Parc R. et al.Effect of liver transplantation on sex-hormone disorders in male patients with alcohol-induced or post-viral hepatitis advanced liver disease.J Hepatol. 1994; 20: 426-430Abstract Full Text PDF PubMed Scopus (38) Google Scholar, 27Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar], inappropriately low levels of the pituitary gonadal stimulating hormones, lutenizing hormone (LH) [23Van Thiel D.H. Gavaler J.S. Spero J.A. Egler K.M. Wright C. Sanghvi A.T. et al.Patterns of hypothalamic–pituitary–gonadal dysfunction in men with liver disease due to differing etiologies.Hepatology. 1981; 1: 39-46Crossref PubMed Scopus (50) Google Scholar, 24Guechot J. Vaubourdolle M. Ballet F. Giboudeau J. Darnis F. Poupon R. et al.Hepatic uptake of sex steroids in men with alcoholic cirrhosis.Gastroenterology. 1987; 92: 203-207PubMed Google Scholar, 25Van Thiel D.H. Kumar S. Gavaler J.S. Tarter R.E. Effect of liver transplantation on the hypothalamic–pituitary–gonadal axis of chronic alcoholic men with advanced liver disease.Alcohol Clin Exp Res. 1990; 14: 478-481Crossref PubMed Scopus (30) Google Scholar, 27Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar] and follicular stimulating hormone (FSH) [23Van Thiel D.H. Gavaler J.S. Spero J.A. Egler K.M. Wright C. Sanghvi A.T. et al.Patterns of hypothalamic–pituitary–gonadal dysfunction in men with liver disease due to differing etiologies.Hepatology. 1981; 1: 39-46Crossref PubMed Scopus (50) Google Scholar, 25Van Thiel D.H. Kumar S. Gavaler J.S. Tarter R.E. Effect of liver transplantation on the hypothalamic–pituitary–gonadal axis of chronic alcoholic men with advanced liver disease.Alcohol Clin Exp Res. 1990; 14: 478-481Crossref PubMed Scopus (30) Google Scholar, 26Guechot J. Chazouilleres O. Loria A. Hannoun L. Balladur R. Parc R. et al.Effect of liver transplantation on sex-hormone disorders in male patients with alcohol-induced or post-viral hepatitis advanced liver disease.J Hepatol. 1994; 20: 426-430Abstract Full Text PDF PubMed Scopus (38) Google Scholar, 28Mooradian A.D. Shamma’a M. Salti I. Cortas N. Hypophyseal-gonodal dysfunction in men with non-alcoholic cirrhosis.Andrologia. 1985; 17: 72-79Crossref PubMed Scopus (18) Google Scholar] and possibly blunting of pituitary responses to gonadotrophic-releasing hormones [[29]Sorrell J. Brown J.R. Sexual functioning in patients with end-stage liver disease before and after transplantation.Liver Transpl. 2006; 12: 1473-1477Crossref PubMed Scopus (58) Google Scholar] resulting in a hypogonadal state. In addition, serum levels of oestrogens [24Guechot J. Vaubourdolle M. Ballet F. Giboudeau J. Darnis F. Poupon R. et al.Hepatic uptake of sex steroids in men with alcoholic cirrhosis.Gastroenterology. 1987; 92: 203-207PubMed Google Scholar, 28Mooradian A.D. Shamma’a M. Salti I. Cortas N. Hypophyseal-gonodal dysfunction in men with non-alcoholic cirrhosis.Andrologia. 1985; 17: 72-79Crossref PubMed Scopus (18) Google Scholar] and prolactin [26Guechot J. Chazouilleres O. Loria A. Hannoun L. Balladur R. Parc R. et al.Effect of liver transplantation on sex-hormone disorders in male patients with alcohol-induced or post-viral hepatitis advanced liver disease.J Hepatol. 1994; 20: 426-430Abstract Full Text PDF PubMed Scopus (38) Google Scholar, 27Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar] are elevated in cirrhotic men that may further contribute to sexual dysfunction. Although these endocrinologic effects affect patients with cirrhosis of any aetiology, it has also been suggested that ongoing alcohol consumption associated with end-stage alcoholic liver disease may have additional detrimental effects on the hypothalamic–pituitary–gonadal axis in men and women [[25]Van Thiel D.H. Kumar S. Gavaler J.S. Tarter R.E. Effect of liver transplantation on the hypothalamic–pituitary–gonadal axis of chronic alcoholic men with advanced liver disease.Alcohol Clin Exp Res. 1990; 14: 478-481Crossref PubMed Scopus (30) Google Scholar]. From a functional perspective, cirrhosis in men has been reported to be associated with decreased volume of ejaculatory fluid [[27]Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar], and reduced libido/interest in sex [27Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar, 29Sorrell J. Brown J.R. Sexual functioning in patients with end-stage liver disease before and after transplantation.Liver Transpl. 2006; 12: 1473-1477Crossref PubMed Scopus (58) Google Scholar]. Erectile dysfunction including frank impotence, has been reported to some degree in anywhere from 60% to 90% of patients with cirrhosis [27Madersbacher S. Ludvik G. Stulnig T. Grunberger T. Maier U. The impact of liver transplantation on endocrine status in men.Clin Endocrinol. 1996; 44: 461-466Crossref PubMed Scopus (49) Google Scholar, 29Sorrell J. Brown J.R. Sexual functioning in patients with end-stage liver disease before and after transplantation.Liver Transpl. 2006; 12: 1473-1477Crossref PubMed Scopus (58) Google Scholar]. In women, one survey documented close to 60% of patients with chronic liver disease pre-transplant suffering menstrual irregularities: half of this group had amenorrhea compared to less than 20% of women classified as ALF pre-transplant experiencing menstrual problems [[30]Mass K. Quint E.H. Puch M.R. Merion R.M. Gynecological and reproductive function after liver transplantation.Transplantation. 1996; 62: 476-479Crossref PubMed Scopus (91) Google Scholar]. Of some interest is a recent report that found 60% of women on a transplant waiting list suffered amenorrhea compared to 19% with cholestatic liver disease (p = 0.0009) [[31]Gomez-Lobo V. Burgansky A. Kim-Schluger L. Berkowitz R. Gynecologic symptoms and sexual function before and after liver transplantation.J Reprod Med. 2006; 51: 457-462PubMed Google Scholar]. One of the difficulties in interpreting studies that report sexual function in patients with cirrhosis is that the severity of the end-stage disease may be either unclear or simply not stated. Although it would appear intuitive that patients with more severe cirrhotic decompensation would suffer worse sexual dysfunction, until recently, this has not been definitively correlated with any index of liver function. In an important paper, using MELD scores as an indicator of liver disease severity, Sorrell and Brown, from the University of Nebraska, correlated sexual activity pre-transplant with MELD scores [[29]Sorrell J. Brown J.R. Sexual functioning in patients with end-stage liver disease before and after transplantation.Liver Transpl. 2006; 12: 1473-1477Crossref PubMed Scopus (58) Google Scholar] They found that patients with no reported sexual activity had the highest mean MELD scores of 15.18, whereas those patients that reported no change in sexual activity had the lowest MELD scores of 10.74. Those who were in-between the highest and lowest MELD scores (=13.88) also reported decreased sexual activity. These investigators also found a similar correlation between MELD score and erectile dysfunction [[32]Wiesner R.H. McDiarmid S.V. Kamath P.S. Edwards E.B. Malinchoc M. Kremers W.K. et al.MELD and PELD: application of survival models to liver allocation.Liver Transpl. 2001; 7: 567-580Crossref PubMed Scopus (726) Google Scholar], thereby scientifically and definitiv" @default.
• W2020159773 created "2016-06-24" @default.
• W2020159773 creator A5013018249 @default.
• W2020159773 creator A5040857444 @default.
• W2020159773 creator A5067141465 @default.
• W2020159773 creator A5074491754 @default.
• W2020159773 date "2008-10-01" @default.
• W2020159773 modified "2023-10-11" @default.
• W2020159773 title "Pregnancy and sexual function in liver transplantation" @default.
• W2020159773 cites W1821098129 @default.
• W2020159773 cites W1855786064 @default.
• W2020159773 cites W1919907783 @default.
• W2020159773 cites W1964595588 @default.
• W2020159773 cites W1968267110 @default.
• W2020159773 cites W1968774836 @default.
• W2020159773 cites W1970055976 @default.
• W2020159773 cites W1970860796 @default.
• W2020159773 cites W1975691075 @default.
• W2020159773 cites W1978802909 @default.
• W2020159773 cites W1987244955 @default.
• W2020159773 cites W1988805633 @default.
• W2020159773 cites W1999240313 @default.
• W2020159773 cites W2000110498 @default.
• W2020159773 cites W2003507288 @default.
• W2020159773 cites W2009388851 @default.
• W2020159773 cites W2009410288 @default.
• W2020159773 cites W2012246981 @default.
• W2020159773 cites W2013196611 @default.
• W2020159773 cites W2020148339 @default.
• W2020159773 cites W2020785491 @default.
• W2020159773 cites W2021334445 @default.
• W2020159773 cites W2021496262 @default.
• W2020159773 cites W2023665902 @default.
• W2020159773 cites W2025088670 @default.
• W2020159773 cites W2027769144 @default.
• W2020159773 cites W2028790185 @default.
• W2020159773 cites W2029068104 @default.
• W2020159773 cites W2034365124 @default.
• W2020159773 cites W2034859527 @default.
• W2020159773 cites W2035285899 @default.
• W2020159773 cites W2035803709 @default.
• W2020159773 cites W2036230402 @default.
• W2020159773 cites W2036816866 @default.
• W2020159773 cites W2046422668 @default.
• W2020159773 cites W2046433849 @default.
• W2020159773 cites W2053767063 @default.
• W2020159773 cites W2054417747 @default.
• W2020159773 cites W2054871495 @default.
• W2020159773 cites W2063291526 @default.
• W2020159773 cites W2065342543 @default.
• W2020159773 cites W2065381864 @default.
• W2020159773 cites W2077975666 @default.
• W2020159773 cites W2083598737 @default.
• W2020159773 cites W2083936564 @default.
• W2020159773 cites W2083970148 @default.
• W2020159773 cites W2084023071 @default.
• W2020159773 cites W2085064791 @default.
• W2020159773 cites W2086695142 @default.
• W2020159773 cites W2087460598 @default.
• W2020159773 cites W2088987111 @default.
• W2020159773 cites W2089786934 @default.
• W2020159773 cites W2090816965 @default.
• W2020159773 cites W2100965532 @default.
• W2020159773 cites W2101381163 @default.
• W2020159773 cites W2105408030 @default.
• W2020159773 cites W2109665285 @default.
• W2020159773 cites W2114167307 @default.
• W2020159773 cites W2119329086 @default.
• W2020159773 cites W2132364301 @default.
• W2020159773 cites W2135677964 @default.
• W2020159773 cites W2143751630 @default.
• W2020159773 cites W2156507091 @default.
• W2020159773 cites W2164229583 @default.
• W2020159773 cites W2335787889 @default.
• W2020159773 cites W2438612023 @default.
• W2020159773 cites W2615003835 @default.
• W2020159773 cites W3023519786 @default.
• W2020159773 cites W4237279145 @default.
• W2020159773 cites W4246704121 @default.
• W2020159773 doi "https://doi.org/10.1016/j.jhep.2008.07.011" @default.
• W2020159773 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18715668" @default.
• W2020159773 hasPublicationYear "2008" @default.
• W2020159773 type Work @default.
• W2020159773 sameAs 2020159773 @default.
• W2020159773 citedByCount "53" @default.
• W2020159773 countsByYear W20201597732012 @default.
• W2020159773 countsByYear W20201597732013 @default.
• W2020159773 countsByYear W20201597732014 @default.
• W2020159773 countsByYear W20201597732015 @default.
• W2020159773 countsByYear W20201597732016 @default.
• W2020159773 countsByYear W20201597732017 @default.
• W2020159773 countsByYear W20201597732018 @default.
• W2020159773 countsByYear W20201597732019 @default.
• W2020159773 countsByYear W20201597732020 @default.
• W2020159773 countsByYear W20201597732021 @default.
• W2020159773 countsByYear W20201597732022 @default.
• W2020159773 countsByYear W20201597732023 @default.
• W2020159773 crossrefType "journal-article" @default.

• next