Histological improvement of PSC on the treatment with UDCA has been demonstrated too [29]. In PSC patients who had dominant structure with severe biochemical deterioration, or recurrent septic cholangitis,
percutaneous or endoscopic cholangiographic approaches can be used to relieve the obstruction [4, 26]. The autoimmune overlap syndromes (AOS) are supposed to arise as distinctive cholestatic liver diseases or an outcome of two coexisting AILDs [4]. AOS account for 13.9-18% of all patients with AILDs [30, 31]. The pathogenesis of the AOS is not clear [32]. AIH-PBC overlap is the most common form [32]. They are thought to arise from AIH and PBC developing simultaneously or one preceding the other [33]. Diagnostic scoring criteria for AIH-PBC have been developed [34] and recently a simplified diagnostic RO4929097 nmr score have been suggested [35]. AIH-PSC overlap is
a disorder with ill-defined immune mediated backgrounds [3]. It is more common in children and adolescent [3, 32]. Although no specific diagnostic criteria have been established for AIH-PSC overlap, in the largest reported number of patients with this syndrome — they had clinical, biochemical and immunological features of AIH coexisting with radiological evidence of PSC [36]. The treatments of AOS are empiric and involve the use of this website both immune suppressive therapy and UDCA [3, 30, 32, 37]. Patients with AIH-PBC overlap have treatment
response and prognostic outcome that is poorer compared with those with isolated AIH and BPC; but patients with AIH-PSC overlap have treatment response and prognosis that have worse prognosis when compared to patients only with AIH and otherwise find more better when compared pheromone to patients only with PSC [37, 38]. Case presentations First patient A 27-year-old Chadian lady, mother for 2 children, had a history of progressive jaundice and itching for 2 years. She denied the ingestion of medication and herbal medicines, previous similar attacks, jaundice during pregnancy, contact with jaundice patient and blood transfusion. She also denied a family history of liver disease or similar presentations. On physical examination, she was slim (weight: 36 kg) with stable vital signs. Examination was only positive for deep jaundice and scratch marks all over the body; the rest of the examination was unremarkable. The lab tests showed normal CBC apart from mild anemia; hemoglobin of 11.3 g/dl, white blood cells (WBC) 5.9 k/μl and platelets (Plat) of 190 k/μl. The prothrombin time (PT) of 15 seconds was normal (11-14). The liver function tests showed ALT 40 U/L (normal 30-65), AST 74 U/L (normal 15-37), ALP 231 U/L (normal 50-136), GGT 321 U/L (normal 5-85), total protein 60 g/L (normal 64-82), albumin 25 g/L (normal 35-50), and total and direct bilirubin 325 μmol/L (normal 0-17) and 274 μmol/L (0-5), respectively.