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Andrzej Rydzewski

Publications and source records attributed to Andrzej Rydzewski.

5 recordsLinked to original sources

N-acetylcysteine does not prevent post-endoscopic retrograde cholangiopancreatography hyperamylasemia and acute pancreatitis.

AIM: Acute pancreatitis (AP) is the most common and often severe complication of endoscopic retrograde cholangiopancreatography (ERCP). The early step in the pathogenesis of acute pancreatitis is probably the capillary endothelial injury mediated by oxygen-derived free radicals. N-acetylcysteine - a free radical scavenger may be potentially effective in preventing post-ERCP acute pancreatitis and it is also known that N-acetylcysteine (ACC) can reduce the severity of disease in experimental model of AP. METHODS: One hundred and six patients were randomly allocated to two groups. Fifty-five patients were given N-acetylcysteine (two 600 mg doses orally 24 and 12 h before ERCP and 600 mg was given iv, twice a day for two days after the ERCP). The control group consisted of 51 patients who were given iv. isotonic saline twice a day for two days after the ERCP. Serum and urine amylase activities were measured before ERCP and 8 and 24 h after the procedure. The primary outcome parameter was post-ERCP acute pancreatitis and the secondary outcome parameters were differences between groups in serum and urine amylase activity. RESULTS: There were no significant differences in the rate of post-ERCP pancreatitis between two groups (10 patients overall, 4 in the ACC group and 6 in the control group). There were also no significant differences in baseline and post-ERCP serum and urine amylase activity between ACC group and control group. CONCLUSION: N-acetylcysteine fails to demonstrate any significant preventive effect on post-ERCP pancreatitis, as well as on serum and urine amylase activity.

Acetylcysteine↗

Influence of low protein diet on nonthyroidal illness syndrome in chronic renal failure.

Renal failure causes alterations in thyroid hormone metabolism known as nonthyroidal illness syndrome. In the present study we have examined the effect of a low protein diet (LPD) on circulating levels of hormones of the pituitary-thyroid axis, and tumor necrosis factor alpha (TNF-alpha) in patients with chronic renal failure. Seventeen subjects with conservatively treated chronic renal failure (estimated creatinine clearance 39.5+/-11.1 mL/min) were studied before and after 8 wk of dietary intervention (0.6 g/kg of ideal body mass protein, 30% of calories derived from fat, 62% of calories derived from carbohydrates, and 10 mg/kg of phosphorus). Body fat and fat-free mass remained unchanged. Urea and TNF-alpha serum concentrations significantly decreased, whereas T3 and total and free T4 serum concentrations increased significantly. Triiodothyronine level after treatment correlated negatively with baseline urea level. Changes in T3, T4, and fT4 serum concentrations as well as calculated peripheral deiodinase activity correlated negatively with their baseline values. Alterations in TNF-alpha correlated positively with protein intake, whereas changes in T4 and T4/TSH were inversely related to vegetal protein intake. In conclusion, low protein, low phosphorus diet, which is often prescribed to patients with moderate impairment of renal function, exerts a beneficial effect on low T3 syndrome coexisting with renal failure. The effect of low protein diet on the pituitary-thyroid axis is dependent on the degree of renal functional impairment and LPD-induced decrease in TNF-alpha may also contribute to the observed effects of dietary treatment.

Adult↗

Pancreas after kidney (PAK) transplantation--first case in Poland.

Transplantation of pancreas is a generally accepted treatment option for patients with type 1 diabetes mellitus. This procedure restores physiological insulin secretion, resulting in long-term normoglycemia and preventing complications of diabetes. One of the therapeutic possibilities is pancreas after kidney transplantation (PAK) for patients with previous successful kidney transplantation. There is evidence that patient and kidney graft survival is higher in PAK compared with diabetic recipients of kidney or pancreas alone (PTA). We report a case of pancreas after kidney transplantation in a 38 year-old male with type 1 diabetes mellitus of 21 year duration. One year before PAK he received cadaveric kidney transplant. Pancreatic graft was placed on the left side of the pelvis and enteric drainage was used. Immunosuppression consisted of antithymocyte globulin (ATG), daclizumab, tacrolimus, mycophenolate mofetil, and steroids. Ten months after surgery the patient stays normoglycemic, insulin-independent with good kidney function (Cr-1,5 mg/dl).

Adult↗

Low protein diet causes a decrease in serum concentrations of leptin and tumour necrosis factor-alpha in patients with conservatively treated chronic renal failure.

BACKGROUND: Chronic renal failure (CRF) provokes derangement in various hormonal regulations of food intake and energy expenditure. In the present study, we have examined the effect of a low protein, low phosphorus diet on circulating levels of leptin, tumour necrosis factor (TNF)-alpha, and insulin in patients with CRF. METHODS: Seventeen male, non-diabetic subjects with conservatively treated CRF (estimated creatinine clearance 39.5 +/- 11.1 mL/min), and proteinuria below 2 g/day were prospectively studied. Measurements of hormonal, metabolic and anthropometric parameters were performed before and after 16 weeks of dietary treatment (protein 0.6 g/kg of ideal body mass, 30% of calories derived from fat, 62% of calories derived from carbohydrates and 10 mg/kg of phosphorus). Actual dietary intake in patients was measured by using 3-day food records and was supervised by the dietician. RESULTS: Body mass index and body fat mass remained unchanged during the 4 months of dietary treatment. Urea, leptin, and TNF-alpha serum concentrations decreased significantly. CONCLUSIONS: A low protein, low phosphorus diet reduces TNF-alpha and leptin levels in plasma. The effect on leptin appears not to be mediated by an insulin-dependent mechanism.

Adult↗