039 × age(years) + 2.38 × loge(prothrombin time [s]) + 0.859 edema (0 = no edema, no diuretic therapy; 0.5 = edema, no diuretic therapy or no edema, diuretic therapy; 1 = edema and diuretic therapy); MELD score is calculated using the following equation: = 3.8 × loge[bilirubin(mg/dL)] + 11.2 × loge(INR) + 9.6 × loge[CRE(mg/dL)] + 6.4 × (biliary
Ensartinib or alcoholic = 0; others = 1). Statistical analyses were performed using SPSS statistical software (version 13.0; SPSS Inc., Chicago, IL). The two-tailed Wilcoxon matched pairs test was used to evaluate paired biochemical values. Values with P < 0.05 were considered statistically significant. The demographic and clinical characteristics of patients at the time of enrollment are summarized in Table 1; this table also indicates when patients
begun UDCA therapy. These patients included one male and six females, Selleck CT99021 ranging from 33 to 58 years of age. All of the patients had been on UDCA therapy for at least one year and had shown an incomplete response to this treatment. All of the patients had reported fatigue, and five of them had pruritus at the beginning of UC-MSC therapy. Patient medication was not changed during the study period. The timeline of UC-MSC treatment in this group of patients is shown in Figure 1; note that clinical parameters were tested at the 0-, 24-, and 48-week time points during the study period. Because safety is a major concern regarding UC-MSC therapy for PBC patients, we examined the short-term side-effects and long-term adverse events during the 48 weeks of follow-up. All the seven patients tolerated the UC-MSC treatment well; only one patient developed a self-limiting fever (body temperature: 37–38°C) within 5 h of UC-MSC transfusion, which recovered within 12 h without any additional treatments. No short-term clinical adverse effects, such as right upper quadrant pain, skin rash, infection, coma, or shock, were reported. There were no occurrences of long-term complications,
such as hepatocellular carcinoma, upper gastrointestinal hemorrhage, hepatic encephalopathy, or primary PDK4 peritonitis within one year of follow-up. Additionally, in all the seven patients, no significant alterations were observed in renal function parameters such as urea, CRE, and UA levels during the one-year follow-up period. Routine blood tests (peripheral white blood counts, hemoglobin, platelet, etc.), serum electrolyte levels (serum Na, serum K and serum Cl, etc.), and serum AFP levels also remained stable (Table 2). The combined treatment of UC-MSC and UDCA led to a significant decrease in serum ALP levels at the endpoint of the follow-up period (474.29 ± 223.26 vs 369.86 ± 168.35 IU/L, P = 0.044). Interestingly, GGT, another biochemical marker of cholestasis, also indicated a reduction from baseline (194 ± 140.65 IU/L) compared with the endpoint of the treatment (132.71 ± 129.4 IU/L, P = 0.049).