Ten-year combination treatment with colchicine and ursodeoxycholic acid for primary biliary cirrhosis: a double-blind, placebo-controlled trial on symptomatic patients

BACKGROUND: Combined medical treatment may provide further benefit to primary biliary cirrhosis (PBC) patients administered ursodeoxycholic acid (UDCA). AIM: To evaluate the long-term effects of colchicine and UDCA in symptomatic PBC patients. PATIENTS/METHODS: We extended up to 10 years the double-blind treatment of 44 symptomatic PBC patients originally included in a 3-year multicentre study comparing UDCA and colchicine (U + C) versus UDCA and placebo (U + P). Outcome measures were death or liver transplantation; incidence of clinically relevant events; clinical and quantitative variables retaining prognostic information. RESULTS: Mean follow-up was 7 +/- 3 years. One patient was lost, three withdrew because of jaundice (U + P); two patients stopped colchicine but remained on UDCA. Eleven patients (two for liver-unrelated reasons, U + P) and six patients (U + C) died, three and two patients, respectively, were transplanted (incidence rate difference, five cases per 100 patient-years; 95% CI, -1 to 11). Hepatocellular carcinoma developed in one (U + P) and four (U + C) patients (difference, -2; CI, -5 to 1), portal hypertension complications in nine patients from each group (difference, 1; CI, -5 to 6). Trends of serum bilirubin, Mayo score, antipyrine clearance were similar among treatment groups. CONCLUSIONS: In cirrhotic PBC patients, colchicine does not offer additional benefits to UDCA. In this population, UDCA does not obviate disease progression.     

Long-term ursodeoxycholic acid therapy for primary biliary cirrhosis: a follow-up to 12 years

BACKGROUND: It is uncertain whether ursodeoxycholic acid therapy slows down the progression of primary biliary cirrhosis, according to two meta-analyses. However, the randomized trials evaluated had only a median of 24 months of follow-up. AIM: To evaluate long-term ursodeoxycholic acid therapy in primary biliary cirrhosis. METHODS: We evaluated 209 consecutive primary biliary cirrhosis patients, 69 compliant with ursodeoxycholic acid and 140 untreated [mean follow-up 5.79 (s.d. = 4.73) and 4.87 (s.d. = 5.21) years, respectively] with onset of all complications documented. Comparison was made following adjustment for baseline differences according to Cox modelling, Mayo and Royal Free prognostic models. RESULTS: Bilirubin and alkaline phosphatase concentrations improved with ursodeoxycholic acid (at 36 months, P = 0.007 and 0.018, respectively). Unadjusted Kaplan-Meier analysis showed benefit (P = 0.028), as 44 (31%) untreated and 15 (22%) ursodeoxycholic acid patients died or had liver transplantation. However, there was no difference when adjusted by Cox modelling (P = 0.267), Mayo (P = 0.698) and Royal Free models (P = 0.559). New pruritus or fatigue or other complications were not different, either before or after adjustment for baseline characteristics. CONCLUSIONS: Long-term ursodeoxycholic acid therapy did not alter disease progression in primary biliary cirrhosis patients despite a significant improvement in serum bilirubin and alkaline phosphatase consistent with, and similar to, those seen in ursodeoxycholic acid cohorts in randomized trials.     

Methotrexate therapy for the symptomatic treatment of primary biliary cirrhosis patients, who are biochemical incomplete responders to ursodeoxycholic acid therapy

BACKGROUND: Ursodeoxycholic acid is widely used as the standard therapy for the treatment of primary biliary cirrhosis and other cholestatic liver diseases. Although it has been shown to improve biochemical markers and delay disease progression, its effect upon fatigue and pruritus, is at best uncertain. AIM: To assess the safety and efficacy of methotrexate for treating symptomatic primary biliary cirrhosis patients who were biochemical partial responders or non-responders to ursodeoxycholic acid therapy. METHODS: We treated eight consecutive primary biliary cirrhosis patients with methotrexate who were followed in a single hepatology clinical practice, who were symptomatic, and who had had an incomplete biochemical response to ursodeoxycholic acid therapy. Pruritus and fatigue were assessed at each clinic visit and graded from 0 (asymptomatic) to 4 (incapacitating). RESULTS: The median dose of methotrexate was 13.75 mg/week (range 7.5-15) and the mean duration of methotrexate therapy was 49 months (range 11-126). At the end of follow-up pruritus in six of seven patients had improved, and fatigue in all patients had improved with the addition of methotrexate therapy (pruritus: baseline 2.9 +/- 1.1 vs. end of treatment 0.6 +/- 1.5, P < or = 0.0175, and fatigue: baseline 3.0 +/- 0.8, vs. end of treatment 1.0 +/- 0.8, P < or = 0.0023). Improvement in symptoms was associated with a significant improvement in biochemical markers of cholestasis. No significant adverse effects of methotrexate were documented. CONCLUSIONS: Methotrexate should be considered as a potential additive treatment for symptomatic primary biliary cirrhosis patients who are incomplete biochemical responders to ursodeoxycholic acid therapy.     

Current and promising therapy for primary biliary cholangitis

Introduction: Primary biliary cholangitis is a chronic, cholestatic liver disease that may progress to cirrhosis with complications of end-stage liver disease. Approved treatment options include ursodeoxycholic acid (UDCA) and obeticholic acid (OCA) but novel therapies are being investigated.

Areas covered: In this review, the authors describe the current pharmacotherapy for the treatment of primary biliary cholangitis (PBC) and for management of side effects such as pruritus and fatigue based on the currently available literature.

Expert opinion: Patients diagnosed with PBC should be offered treatment with UDCA at 13–15 mg/kg per day if liver enzymes are elevated. If they do not meet the defined criteria of response, adjunctive therapy should be considered. This may include OCA at 5 mg per day for patients without cirrhosis or investigational therapy. Management of the most common side effects, pruritus, and fatigue, is nuanced and includes lifestyle modifications as well as pharmacological approaches. Several tools such as the Mayo Risk Score and GLOBE are available for prognostic modeling. Ultimately, patients with PBC may end up requiring liver transplantation and referral to a transplant center may also be needed.     

Cholic acid and ursodeoxycholic acid therapy in primary biliary cirrhosis

Summary We treated 6 patients with Stage II primary biliary cirrhosis with cholic acid (CA) 10 mg · kg^–1 per day for 3 months and then with the same dose of ursodeoxycholic acid (UDCA). A matching group of 6 patients was observed for 3 months without any therapy. Liver function tests and serum and stool bile acids were investigated before, during and at the end of CA and UDCA therapy.The results of liver function tests deteriorated after 6–8 weeks of CA therapy and the changes were correlated (r=0.92) with an increase in -dihydroxy-bile acids (chenodeoxycholic acid and deoxycholic acid) in the serum. The 24 h excretion of DCA in 24 h faeces was markedly increased.Ursodeoxycholic acid treatment improved liver function tests; after 4 weeks glutamate dehydrogenase (GLDH) had decreased. After 8–12 weeks of therapy ursodeoxycholic acid had increased to 50–60% of the total serum bile acids whereas the more apolar bile acids were significantly decreased. No changes in liver function tests or bile acid metabolism were found in the untreated group.Since CA and UDCA are non-toxic in man, this trial indicates that the apolar bile acids chenodeoxycholic acid and deoxycholic acid may be responsible for the deterioration of liver function in primary biliary cirrhosis. However, the therapeutic effect of UDCA cannot be explained merely by the decrease in -dihydroxy-bile acids in the serum, since the laboratory results had improved prior to the decrease in the serum apolar bile acids.     

Effects of ursodeoxycholic acid (UDCA) on serum liver damage indices in patients with chronic active hepatitis

Summary The effects of ursodeoxycholic acid (UDCA, 450 mg daily) in patients with histologically proven chronic active hepatitis (CAH) have been evaluated in a randomized, double-blind, placebo-controlled study. Twenty-six patients with serum alanine aminotransferase (ALT) values at least twice the normal upper limit in two of three pre-treatment tests received UDCA or a placebo for twelve weeks.In all UDCA-treated patients, serum aspartate aminotransferase (AST), ALT, gamma-glutamyl transpeptidase (GGT) and alkaline phosphatase (AP) fell significantly after 4 weeks of treatment. There was a further decrease at the end of therapy, as well as a small but significant fall in total serum bilirubin. Conversely, 4 weeks aftersuspension of therapy, serum enzyme levels had increased, reaching values not much lower than those recorded before treatment. Total serum protein, albumin and -globulin did not change after UDCA treatment. In the placebo group no significant variation in the test results were found.The results indicate that UDCA therapy in CAH, as has been observed in primary biliary cirrhosis and primary sclerosing cholangitis, is able to improve several indices of liver damage, without producing any toxic adverse effects.     

Long-term results of treatment of malignant carcinoid syndrome with prolonged release Lanreotide (Somatuline Autogel)

Aliment Pharmacol Ther 2011; 33: 235–242

Summary

Background Newer therapies are needed for patients with primary biliary cirrhosis and incomplete response to ursodeoxycholic acid (UDCA). Fenofibrate is a fibric acid postulated to regulate immune response and cell proliferation. Aim To evaluate the efficacy and safety of fenofibrate in patients with primary biliary cirrhosis and incomplete response to UDCA. Methods We undertook a pilot study involving 20 patients with primary biliary cirrhosis and serum alkaline phosphatase (ALP) ≥ 2× ULN. Nonparametric statistical tests and Spearman correlation test were used as appropriate. Results Twenty patients received fenofibrate (160 mg/day) in addition to UDCA for 48 weeks. Median serum ALP decreased significantly at 48 weeks compared with baseline values [351 (214–779) U/L at baseline vs. 177 (60–384) U/L at 48 weeks, P < 0.05]. A rebound in ALP occurred upon drug discontinuation. Serum aspartate aminotransferase and Immunoglobulin M also decreased significantly, while bilirubin and albumin remained unchanged. Median IL‐1 decreased from 28.9 (2.7–10 000) to 11.3 (2.5–277.7) pg/mL (P = 0.049), and median IL‐6 from 4.6 (3.2–5205) to 3.5 (3.2–73.4) pg/mL (P = 0.027). Heartburn was the most frequent adverse event, leading to discontinuation of two study subjects. Conclusions Combination therapy of fenofibrate and UDCA induced significant biochemical improvement in patients with primary biliary cirrhosis and incomplete response to UDCA. Further studies are warranted.     

中等剂量熊去氧胆酸治疗原发性胆汁性肝硬化的临床观察

目的:观察中等剂量熊去氧胆酸治疗原发性胆汁性肝硬化的临床疗效。方法:将临床196例原发性胆汁性肝硬化患者分为2组,对照组95例,采用常规对症疗法(保肝、解毒、利尿、抗菌);治疗组101例,在对症疗法的基础上加服中等剂量的熊去氧胆酸。2组均以1个月为1个疗程,3个疗程后观察2组治疗效果和肝功能检查结果。结果:3个疗程后,治疗组的总有效率(79.2%)显著高于对照组(60.0%),差异有统计学意义(P<0.01);肝功能检测结果显示,治疗组患者的丙氨酸氨基转移酶、天冬氨酸氨基转移酶显著降低(P<0.01),接近正常水平;谷酰转肽酶、碱性磷酸酶指标虽然没有恢复到正常范围,但与治疗前比较均有所降低(P<0.01)。结论:中等剂量熊去氧胆酸对原发性胆汁性肝硬化临床疗效显著。     

Pharmacokinetics and bone effects of budesonide in primary biliary cirrhosis

BACKGROUND/AIM: To evaluate the safety of budesonide in primary biliary cirrhosis. METHODS: 77 primary biliary cirrhosis patients, with stages I-III at entry, were randomized to use either budesonide 6 mg and ursodeoxycholic acid 15 mg/kg (group A), or ursodeoxycholic acid alone (group B) daily for 3 years. In 22 patients, budesonide pharmacokinetics was determined after 3 years. Bone mass density was measured in 62 patients at baseline and 3 years; in 57 patients also liver biopsies were performed. RESULTS: At 3 years, no significant differences in the pharmacokinetics of budesonide were found between the patients with stages 0-I, II and III primary biliary cirrhosis. In group A, bone mass density in femoral neck and lumbar spine were decreased by 3.6% (P = 0.0002) and 2.8% (P = 0.003) from the baseline. In group B, the corresponding decreases were 1.9% (P = 0.029) and 0.7% (P = 0.25), but the differences between the groups were not statistically significant (P = 0.16 for femoral neck and P = 0.08 for lumbar spine). CONCLUSIONS: The plasma concentrations of budesonide do not significantly differ within stages I-III primary biliary cirrhosis patients. The combination of budesonide and ursodeoxycholic acid may decrease bone mass density in the femoral neck and lumbar spine in some primary biliary cirrhosis patients, and bone mass density is recommended to be monitored during budesonide therapy.     

Primary biliary cirrhosis: safety and benefits of established and emerging therapies

Introduction: Primary biliary cirrhosis (PBC) is a chronic, cholestatic liver disease characterized histologically by lymphocytic cholangitis and intralobular bile duct destruction. It is a progressive disorder associated with increased mortality and decreased quality of life related to hepatic fibrosis, troublesome symptoms such as fatigue and pruritus, and ultimately endstage cirrhosis. PBC affects adults around the world, and therefore effective treatment of PBC and its associated symptoms constitute significant issues for patients and providers as well as on a public health level. The only approved pharmacotherapy for PBC to date is ursodeoxycholic acid (UDCA), a choleretic, hydrophilic bile acid which has been in clinical use for decades. UDCA is effective in a majority of patients with PBC, but nearly a third of patients are UDCA non-responders. Non-response to UDCA is associated with an increased risk of death or need for liver transplantation (LT). Whereas LT is an effective treatment, it engenders substantial cost and a risk of PBC recurrence, among other complications. Patients who are non-responders to UDCA or have highly symptomatic disease (e.g., intractable pruritus) are thus in critical need of novel therapeutic approaches, which are both safe and effective.

Areas covered: In this review, we provide a synopsis regarding the safety and benefits of established and emerging pharmacotherapies for PBC and present viewpoints on how they may evolve over the next several years.

Expert opinion: It is our belief that the pharmacoscope of PBC, as with other cholestatic liver diseases, is likely to see important advancements in the near future.     

Pharmacological treatment of biliary cirrhosis with ursodeoxycholic acid

Importance of the field: Primary biliary cirrhosis is a cholestatic liver disease that at one time was the leading indication for liver transplantation. Treatment with ursodeoxycholic acid has clearly improved the natural history of primary biliary cirrhosis.

Areas covered in this review: The treatment of primary biliary cirrhosis with a focus on ursodeoxycholic acid is covered. Papers related to treatment of primary biliary cirrhosis and associated conditions, using a variety of drugs but with a focus on ursodeoxycholic acid, are included. The papers reviewed date from 1984 – 2009.

What will the reader gain: The reader will gain an up-to-date understanding of current treatment strategies for primary biliary cirrhosis using ursodeoxycholic acid and an appreciation of what conditions are improved with this therapy and what associated conditions are not.

Take-home message: Ursodeoxycholic acid in a dose of 13 – 15 mg/kg/day should be considered in all patients with primary biliary cirrhosis who have abnormal liver enzymes.     

Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study

Background: Results from animal studies and preliminary data from pilot studies in patients with primary biliary cirrhosis suggest that tauro-ursodeoxycholic acid has metabolic properties that may favour its long-term use as an alternative to ursodeoxycholic acid for patients with chronic cholestatic liver diseases. No direct comparison of tauro-ursodeoxycholic and ursodeoxycholic acids have yet been carried out in primary biliary cirrhosis.
Methods: The effects of ursodeoxycholic and tauro-ursodeoxycholic acids were compared in 23 patients with primary biliary cirrhosis according to a crossover design. Both drugs were administered at the daily dose of 500 mg, in a randomly assigned sequence for two 6-month periods separated by a 3-month wash-out period.
Results: Serum liver enzymes related to cholestasis and cytolysis consistently improved, as compared to baseline values, during the administration of both ursodeoxycholic and tauro-ursodeoxycholic acids, but no significant difference between these two bile acids was found. Both treatments were well tolerated and no patient complained of side effects.
Conclusion: In the short-term, tauro-ursodeoxycholic acid appears to be safe and at least as effective as ursodeoxycholic acid for the treatment of primary biliary cirrhosis.     

Role of vitamin C transporters and biliverdin reductase in the dual pro-oxidant and anti-oxidant effect of biliary compounds on the placental-fetal unit in cholestasis during pregnancy

Maternal cholestasis causes oxidative damage to the placental-fetal unit that may challenge the outcome of pregnancy. This has been associated with the accumulation of biliary compounds able to induce oxidative stress. However, other cholephilic compounds such as ursodeoxycholic acid (UDCA) and bilirubin have direct anti-oxidant properties. In the present study we investigated whether these compounds exert a protective effect on cholestasis-induced oxidative stress in placenta as compared to maternal and fetal livers, and whether this is due in part to the activation of anti-oxidant mechanisms involving vitamin C uptake and biliverdin/bilirubin recycling. In human placenta (JAr) and liver (HepG2) cells, deoxycholic acid (DCA) similar rates of free radical generation. In JAr (not HepG2), the mitochondrial membrane potential and cell viability were impaired by low DCA concentrations; this was partly prevented by bilirubin and UDCA. In HepG2, taurocholic acid (TCA) and UDCA up-regulated biliverdin-IXα reductase (BVRα) and the vitamin C transporter SVCT2 (not SVCT1), whereas bilirubin up-regulated both SVCT1 and SVCT2. In JAr, TCA and UDCA up-regulated BVRα, SVCT1 and SVCT2, whereas bilirubin up-regulated only SVCT2. A differential response to these compounds of nuclear receptor expression (SXR, CAR, FXR and SHP) was found in both cell types. When cholestasis was induced in pregnant rats, BVRα, SVCT1 and SVCT2 expression in maternal and fetal livers was stimulated, and this was further enhanced by UDCA treatment. In placenta, only BVRα was up-regulated. In conclusion, bilirubin accumulation and UDCA administration may directly and indirectly protect the placental-fetal unit from maternal cholestasis-induced oxidative stress.     

Ursodeoxycholic acid: a second look. Primary biliary cirrhosis: dashed hopes

(1) In 1996 the evidence, though limited, suggested that the hydrophilic bile acid ursodeoxycholic acid slowed the progression of primary biliary cirrhosis. Given the absence of an effective alternative, we considered that the treatment was "A real advance" in this setting. (2) The file is far bulkier now. A meta-analysis of 11 randomised placebo-controlled trials of ursodeoxycholic acid in the treatment of primary biliary cirrhosis did not show efficacy. Histologically, the data suggest that the drug lowers the risk of hepatic fibrosis, but this is based on a low level of evidence. Moreover, there was no clinical improvement in the longest randomised trial (median follow-up 3.4 years). (3) Likewise, ursodeoxycholic acid seems to have a biochemical effect but no clear clinical effect in sclerosing cholangitis or in treating the hepatic complications of cystic fibrosis. (4) The main adverse effects are gastrointestinal disorders. (5) There are still no drugs clearly capable of slowing the clinical progression of primary biliary cirrhosis. Nevertheless, given the minor adverse effects of ursodeoxycholic acid, some patients may wish to gamble on a possible benefit in the very long term. (6) When primary biliary cirrhosis becomes symptomatic (with encephalopathy, osteomalacia, etc.) pending liver transplantation, treatment is aimed at controlling symptoms and preventing the rupture of oesophageal varices.     

原发性胆汁性肝硬化的药物治疗

熊去氧胆酸是目前治疗原发性胆汁性肝硬化的唯一公认药物,可以改善早期患者的长期预后;对于熊去氧胆酸疗效不佳者迫切需要其他有效治疗药物治疗,但糖皮质激素、免疫抑制药或其他药物的疗效及安全性尚需更多的临床研究证实;终末期患者适合肝移植治疗。本文就原发性胆汁性肝硬化的药物治疗进展进行综述。     

腺苷蛋氨酸联合前列地尔治疗原发性胆汁性肝硬化的疗效观察

目的对比观察在使用传统熊去氧胆酸胶囊基础上联合腺苷蛋氨酸及前列地尔治疗原发性胆汁性肝硬化的疗效。方法将40例原发性胆汁性肝硬化患者随机分为2组,每纽20例。对照组给予熊去氧胆酸胶囊0．25g每天3次口服,共3个月。治疗组在上述基础上给予每天静滴腺苷蛋氨酸针1g联合前列地尔针20IU治疗,共10d,每月一次,共3次。结果随访3个月,按肝功能改善情况评分,治疗组优良率为82．68％,对照组优良率为65．12％,经统计分析,P〈0．05。结论腺苷蛋氨酸联合前列地尔对原发性胆汁性肝硬化的治疗可比传统单用熊去氧胆酸胶囊治疗取得更为良好的疗效。     

熊去氧胆酸治疗婴儿巨细胞病毒肝炎的疗效观察

目的观察熊去氧胆酸治疗婴儿巨细胞病毒肝炎的疗效。方法所有病例均来自本院2005年1月至2008年4月收治的患者,共计54例。将上述54例病例随机分为治疗组29例与对照组25例。两组病例均给予更昔洛韦抗病毒,三磷腺苷(三磷酸腺苷)、辅酶A、肌苷、维生素C保肝,维持水、电解质、酸碱平衡等综合治疗。治疗组加用熊去氧胆酸10mg/kg.d,分3次服用。连续应用2周。结果治疗2周后,治疗组患儿在总胆红素、直接胆红素、间接胆红素、胆汁酸、谷丙转氨酶几项指标上与对照组有显著差异(P<0.05)。结论熊去氧胆酸能保护肝细胞,刺激肝胆分泌,促进黄疸消退,明显改善患儿受损的肝脏功能。     

腺苷蛋氨酸联合熊去氧胆酸治疗早产儿肠外营养相关性胆汁淤积疗效观察

目的:探讨腺苷蛋氨酸(SAME)联合熊去氧胆酸(UDCA)治疗早产儿肠外营养相关性胆汁淤积(PNAC)的疗效.方法:32例PNAC患儿随机分为治疗组与对照组各16倒,两组病例均予保肝及基础治疗,治疗组在此基础上加用腺苷蛋氨酸30～60 mg/(ks·d)和熊去氧胆酸10 ～20 mg/( ks·d),连续应用14 d为1个疗程.检测两组患儿治疗前后血清中总胆红素(TBIL)、结合胆红素(DBIL)、谷丙转氨酶(ALT)、γ-谷氨酰转肽酶(GGT)、总胆汁酸(TBA)水平.结果:采用SAME联合UDCA治疗2周后,治疗组患儿血清中TBIL、DBIL、ALT、GGT、TBA与对照组比较均显著降低(P＜0.01),肝脏明显缩小(P＜0.01).两组均未见明显药物不良反应.结论:SAME联合联合UDCA能降低血清胆红素及内源性胆汁酸水平,可促进胆红素、TBA排泄,具有明显的利胆、退黄的疗效,是有效和安全的.     

A randomized trial in primary biliary cirrhosis comparing ursodeoxycholic acid in daily doses of either 10 mg/kg or 20 mg/kg

Background:

Ursodeoxycholic acid (UDCA) prolongs transplantation-free survival in primary biliary cirrhosis (PBC). However, the optimal therapeutic dose has not been established.

Aim:

To compare the effects of UDCA administered in daily doses of 10 vs. 20 mg/kg on symptoms, liver biochemistry and biliary UDCA enrichment.

Methods:

A 6-month multicentre randomized open controlled trial was conducted to assess the effects of an increase in the dose of UDCA to 20 mg/kg/day vs. continuation of 10 mg/kg/day for patients who had not achieved biochemical normalization during treatment for at least 6 months with the 10 mg/kg dose. Clinical and laboratory evaluations were performed at entry and at 3-month intervals. The percentage UDCA in duodenal bile was assessed at entry and at 6 months.

Results:

Sixty-one patients were enrolled. No side-effects of UDCA were observed. Within the 20 mg/kg/day group significant decreases were found for alkaline phosphatase (? 8%; P = 0.003), aspartate aminotransferase (? 11%; P = 0.01), alanine aminotransferase (? 17%; P < 0.001), γ-glutamyl transferase?(? 34%; P < 0.001), immunoglobulin M (? 11%; P = 0.002) and cholesterol (? 8.1%; P < 0.001). In the 10 mg/kg group none of these parameters differed significantly from baseline. No significant differences between dose groups for symptom scores or serum bilirubin were found. Biliary enrichment with UDCA increased from 37% to 46% in the 20 mg/kg group (P = 0.02) while remaining stable in the 10 mg/kg group.

Conclusions:

Liver biochemistry improved in PBC patients receiving UDCA 20 mg/kg/day compared to a dose of 10 mg/kg/day. Both doses were equally well tolerated. These results indicate that UDCA 10 mg/kg/day is a suboptimal dose for treating PBC.

     

熊去氧胆酸与S-腺苷蛋氨酸治疗妊娠期肝内胆汁淤积症

目的探讨熊去氧胆酸与S-腺苷蛋氨酸联合治疗妊娠期肝内胆汁淤积症(ICP)的疗效及血生化参数变化规律。方法以84例ICP患者为研究对象,给予S-腺甘蛋氨酸静滴1 500 mg/d+熊去氧胆酸250 mg4次/d口服治疗,比较治疗前后的血生化参数。结果治疗后,ICP患者总胆汁酸、甘胆酸、总胆红素、直接胆红素、天门冬氨酸氨基转移酶降低,与治疗前比较,差异有统计学意义(P<0.01)。血浆甘胆酸水平与天门冬氨酸氨基转移酶之间呈低度正相关(r=0.29,P<0.05)。结论 S-腺甘蛋氨酸、熊去氧胆酸治疗ICP疗效良好,血生化参数是对妊娠期肝内胆汁淤积症疗效评价的实用临床指标。