Approximately 52% of participants reported symptoms suggesting depression. Prevalence of depression was 62% using the BDI-II, 75% per the PHQ-9 and 72% per the CES-D. We observed a strong correlation between the BDI-II, CES-D and PHQ-9 in patients on and off interferon. Scores on the three questionnaires were only moderately associated with symptoms reported by the patients. There was moderate agreement between the CES-D and BDI-II and slight agreement between both these questionnaires and the PHQ-9. Scores on the PHQ-9 correlated strongly with scores on the CES-D and BDI-II and moderately with patients' symptoms.
Hepatic encephalopathy (HE) is a broad spectrum of neuropsychiatric manifestations usually affecting individuals with end-stage liver disease. The presence of HE is a poor prognostic sign, with 1-year mortality rates of almost 60%. There is much debate about the underlying mechanisms that result in this syndrome; however, elevated plasma and central nervous system ammonia levels are considered key factors in its pathogenesis. Initial evaluation of the patient presenting with overt HE should include a careful search for predisposing factors, including underlying infection, gastrointestinal (GI) bleeding, electrolyte disturbances, hepatocellular carcinoma, dehydration, hypotension, and excessive use of benzodiazepines, psychoactive drugs, or alcohol. The mainstay of treatment for many years has been nonabsorbable disaccharides, particularly lactulose. Alternative treatments, which usually are second line in patients who do not respond to lactulose, include zinc, antibiotics (neomycin, metronidazole, and rifaximin), ornithine aspartate, sodium benzoate, probiotics, and surgical intervention. Accepted treatments for HE are associated with significant unpleasant side effects, including diarrhea, renal failure, neuropathy, and other GI disturbance. Newer therapies are still in development, and most are awaiting human trials in order to confirm their benefit. These include manganese chelators, L-carnitine, N-methyl-d-aspartate receptor antagonists, blood purification dialysis system, and an intravenous combination of sodium benzoate and phenylacetate.
Background and Aims Disease recurrence following transplant occurs in 20-45% of patients with autoimmune hepatitis. Factors associated with an increased risk of recurrence include HLA DR3 and HLA DR4 positivity, inadequate immunosuppression and severity of inflammation in the native liver. Titers of several auto antibodies can be elevated in patients with autoimmune hepatitis including ANA and SMA however it is unclear whether or not the degree of elevation influences the risk of disease recurrence following transplant. Methods We conducted a retrospective study to evaluate the potential impact of pre transplant titers on post transplant outcomes for patients with autoimmune hepatitis. Sixty three patients with autoimmune hepatitis who underwent 72 liver transplants between January 1, 1989 and January 1, 2009 were included with a median follow up of 104 months. Patients were divided into group A (ANA or SMA ≥ 1:160) and group B (titers ≤ 1:160). Results There was no significant difference in recurrence rates or death between patients in group A and B respectively. Only race appeared to impact outcomes with African American patients having a higher incidence of death and recurrent disease post transplant compared to other ethnicities. Conclusions Based on our findings, pre transplant ANA and ASMA levels do not appear to impact recurrence rates or outcomes following liver transplantation for autoimmune hepatitis.
Acute sickle hepatic crisis (ASHC) has been observed in approximately 10% of patients with sickle cell disease. It occurs predominantly in patients with homozygous (Hb SS) sickle cell anemia and to a lesser degree in patients with Hb SC disease, sickle cell trait, and Hb S beta thalassemia. Patients commonly present with jaundice, right upper quadrant pain, nausea, low-grade fever, tender hepatomegaly, and mild to moderate elevations in serum AST, ALT, and bilirubin. We describe the case of a patient with a history of hemoglobin SC disease and cirrhosis caused by hepatitis C presenting approximately 1 year after liver transplantation with an ASHC. The diagnosis was confirmed by liver biopsy. Our patient was treated with RBC exchange transfusions, IV hydration, and analgesia and made a complete recovery. Only a limited number of patients with sickle cell disease have received liver transplants, and, to our knowledge, this is the first case of ASHC after transplantation in a patient with Hb SC disease.
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