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A prospective study of hepatic encephalopathy (HE) including neuropsychiatric and psychometric evaluation, electroencephalography, and determination of arterial ammonia levels was performed in 55 cirrhotic patients treated consecutively by transjugular intrahepatic portosystemic shunt (TIPS). The cumulative HE rate increased from 23.6% within the 3-month interval before TIPS to 50.9% within the first 3-month interval post-TIPS (P ‫؍‬ .003). Significant and independent predictors of HE post-TIPS were the presence of HE pre-TIPS and reduced liver function. The cumulative HE rate declined in the second 3-month interval post-TIPS and reached the pre-TIPS level. Chronic forms of HE exceeding grade I were not observed. In a subgroup of 22 nonencephalopathic TIPS patients, the prevalence of subclinical HE did not change after TIPS. Among individual psychometric tests, the block design test gave the highest proportion of pathological results (about 50%), whereas selective reminding gave the lowest (10%-25%). Electroencephalography (EEG) showed a temporary increase of pathological results at 1 month after TIPS, when patients with overt HE (grade I) were included (proportion of 21.1% before vs. 57.1%, P ‫؍‬ .005). Arterial ammonia concentration increased from a mean of 94 ؎ 26 g/dL to 140 ؎ 28 g/dL at 3 months after TIPS (P F .001). Elevated ammonia levels persisted. TIPS led to a temporary increase of HE incidence within 3 months. The decline of the HE rate beyond 3 months despite a sustained increase of arterial ammonia levels could not entirely be explained by reduction of shunt flow, nor by alteration of liver function. Instead, cerebral adaptation to gut-derived neurotoxins might be anticipated. (HEPATOLOGY 1998;28:1215-1225.)Hepatic encephalopathy (HE) is a well-known complication of portosystemic shunt surgery in patients with liver cirrhosis. The pathogenesis is incompletely understood. [1][2][3][4] After surgical shunts, HE (or portosystemic encephalopathy) has been observed in 4% to 80% of patients (usually in 30%-50%) including chronic forms of portosytemic encephalopathy occurring in up to 30% depending on the type and diameter of shunts used. 5-14 Lower portosystemic encephalopathy rates have been reported in patients treated by shunts that preserve prograde portal flow, i.e., the distal splenorenal shunt 7,14 and small-size (diameter between 0.8 and 1.2 cm) portocaval side-to-side shunts. 6,10,12,15 Recently, the transjugular intrahepatic portosystemic stentshunt (TIPS) has been introduced for the treatment of recurrent variceal bleeding and refractory ascites. [16][17][18][19] Because TIPS resembles a surgical side-to-side shunt, not surprisingly, an increased rate of HE was noted after TIPS. Regarding the incidence of HE after TIPS, divergent data ranging from 3% to 75% of patients affected (usually 30%-40%) have been reported. Furthermore, predicting factors for HE post-TIPS have been discussed controversially, e.g., episodes of HE before TIPS, 24,25,32,36 age, 24,25,37 nonalcoholic causes of liver cirr...

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In a prospective, randomized study we examined the influence of prophylactic short-term thyrostatic therapy on thyroid iodine metabolism in patients with euthyroid autonomy undergoing elective coronary angiography. From a total of 1177 patients, 51 fulfilled the criteria of euthyroid autonomy before coronary angiography (negative thyrotropin-releasing hormone test, 10-min uptake of at least 1.2%, 99mTc and no elevation of free thyroxine and free triiodothyronine indices) and were randomized into three groups: group 1 (N = 17) received 20mg/day of thiamazole and group 2 (N = 17) received 900 mg/day of sodium perchlorate; thyrostatic therapy was begun on the day before angiography and continued for 14 days; group 3 (N = 17) served as controls without treatment. Parameters of thyroid function-free thyroxine (FT4) index and free triiodothyronine (FT3) index, thyrotropin (TSH) and delta-TSH urine iodine excretion and 99mTc uptake were determined before and 30 days after coronary angiography. At the end of the study the mean FT4 index and FT3 index were elevated significantly in the control group compared with baseline values, but were still within the normal range. In contrast, the mean FT4 index and FT3 index remained unchanged in the treated groups. Four mild cases of hyperthyroidism were observed at the end of the study: two cases in the control group and one case in each of the treated groups. Thyrotropin suppression, urine iodine excretion and 99mTc uptake differed significantly between the treated groups and the control group. In the treated groups TSH suppression, urine iodine excretion and 99mTC uptake remained unchanged 30 days after coronary angiography compared with baseline values. In the control group the degree of TSH suppression and the level of urine iodine excretion increased (about twofold) significantly after coronary angiography, whereas 99mTc uptake decreased significantly (ca. 50%). In conclusion, short-term prophylactic thyrostatic therapy seems to have a protective effect against iodine excess in patients with euthyroid autonomy. However, mild hyperthyroidism could not be prevented in some cases. Probably a combination therapy of thiamazole and perchlorate would be more effective.

The effect of GH substitution on serum lipids and lipoproteins, and in particular lipoprotein(a) (Lp(a)), was investigated in 32 adults with postoperative (acquired) GH deficiency as part of a double-blind, placebo-controlled trial. Seventeen men and fifteen women, aged 18-59 years (mean 42 years) from two centres (Hannover and Göttingen) were randomly assigned to two groups. Group P (placebo) received placebo for the first 12 months and recombinant human GH (rhGH) for the following 12 months (open phase). Group V (verum) was treated with rhGH for two consecutive periods of 12 months each. The target dose of rhGH was 2 U/m 2 per day, given subcutaneously daily at bedtime. Serum concentrations of Lp(a), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides were determined at 0, 12 and 24 months. In group V, Lp(a) increased significantly in the first as well as in the second year of treatment (P=0.02, 12 months versus baseline; P=0.016, 24 months versus 12 months). In contrast, Lp(a) levels remained unchanged in group P during the first 12 months (P=0.826 versus baseline), but increased significantly (P=0.002) during the second year, when all patients were administered GH. The increase in Lp(a) after 12 months of rhGH replacement therapy in all 32 patients was significant for Lp(a) baseline concentrations both above and below 20 mg/dl and was independent of the apolipoprotein(a) isoforms. Total and LDL-C decreased significantly after 1 year and triglycerides after 2 years in group V. A significant reduction was also observed in the TC/HDL-C and the LDL-C/HDL-C ratios. Our study shows an unfavorable effect of rhGH replacement therapy on Lp(a) levels, which is, however, counteracted by a favorable effect of rhGH on TC, LDL-C and the TC/LDL-C and LDL-C/HDL-C ratios.

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