Fluoride exposure and bone status in patients with chronic intestinal failure who are receiving home parenteral nutrition.

BACKGROUND AND OBJECTIVE: Metabolic bone disease is frequent in chronic intestinal failure. Because fluoride has a major effect on bones, the status of both fluoride and bone was studied in long-term home parenteral nutrition (HPN) patients. DESIGN: We studied 31 adults aged (x +/- SD) 56.3 +/- 15.1 y, mainly patients with short-bowel syndrome, who had been receiving HPN for >1 y. Bone mineral density (BMD) was measured by absorptiometry, and serum fluoride was measured by using a fluoride-sensitive electrode. All patients ate and drank ad libitum. HPN (3.4 +/- 1.2 times/wk) complemented oral nutrition. Potential explicative factors were estimated by using a linear regression model (mixed-effects model). RESULTS: Of 120 fluoride dosages (2-6/patient), 102 were above the upper normal limit (1.58 micromol/L) at the laboratory. Mean (+/- SD) daily fluoride supply was 8.03 +/- 7.71 mg (US adequate intake: 3.1 mg/d for women and 3.8 for men; tolerable upper normal limit: 10 mg/d); intravenous fluoride varied from 0.06 to 1.45 mg, and oral fluoride varied from 0.09 to 27.8 mg. Serum fluoride concentrations were correlated with creatinine clearance and fluoride supply. BMD was significantly lower in the femoral neck than in the spinal area. After adjustment for sex and the duration of HPN, only the effect of serum fluoride on spinal BMD was significant. Two patients had symptoms of fluorosis, eg, calcaneum fissures, interosseous calcifications, or femoral neck osteoporosis. CONCLUSIONS: In chronic intestinal failure, high intakes of fluoride are frequent because of the beverages ingested to compensate for stool losses. Hyperfluoremia has an effect on bone metabolism and may increase skeletal fragility. The consumption of fluoride-rich beverages for extended periods is therefore not advisable.

Chronic dehydration may impair renal function in patients with chronic intestinal failure on long-term parenteral nutrition.

BACKGROUND & AIMS: Renal impairment is a documented complication in long-term parenteral nutrition (LTPN) patients. However, the aetiologies have remained elusive. The aim of this study was to evaluate the impact of parenteral nutrition, digestive status, and hydration level on renal function in LTPN patients. METHODS: In a prospective study of 40 LTPN patients, renal function and hydration level were assessed by measurement of inulin and creatinine clearances, plasma creatinine, urea, aldosterone and renin and urinary sodium/potassium ratio. Patients were assigned to one of two groups according to their inulin clearance (normal = Group 1, 20% decrease or more = Group 2). RESULTS: Of the patients, 52.5% (21/40) had a decrease in glomerular filtration rate (-38 +/- 15%), with age taken into consideration. Patient characteristics, parenteral nutrition composition or duration and intestinal status were not different between the two groups. Urologic or nephrologic diseases were more frequent in Group 2 patients. Moreover, in Group 2 patients, a urinary sodium/potassium excretion ratio of less than 1 in 8/21 patients and plasma renin (316 +/- 298 vs. 86 +/- 53% of normal value) and aldosterone (291 +/- 464 vs. 58 +/- 36 pmol/l) that were significantly higher than in Group 1 patients suggested a hypovolemic component. CONCLUSION: Decreased renal function is frequent (52.5%) in LTPN patients. A volemic component was associated in more than 70% of them. An elevation of serum creatinine or an inversion of the urinary Na/K ratio requires an evaluation of hydration equilibration and an oral rehydration and a modification in parenteral nutrition formulation.

Replacement of long-chain triglyceride with medium-chain triglyceride/long-chain triglyceride lipid emulsion in patients receiving long-term parenteral nutrition: effects on essential fatty acid status and plasma vitamin K1 levels.

BACKGROUND: In long-term parenteral nutrition (LTPN) patients, the use of a 50:50 mixture of medium- and long-chain triglyceride emulsion (MCT/LCT) has been suggested to prevent or correct fatty liver infiltration. However, the use of MCT/LCT lipid emulsion results in a 50% reduction of essential fatty acids and vitamin K1 supply and could induce essential fatty acid and vitamin K1 deficiencies. This study evaluated the effect of a long-term infusion of MCT/LCT lipid emulsion on plasma fatty acid (FA) and vitamin K1 levels on LTPN patients. METHODS: In a prospective nonrandomized crossover study, we measured plasma phospholipid FA composition by gas chromatography and vitamin K1 levels by high-performance liquid chromatography in 11 LTPN patients before and after a 4-month replacement of the usual 20% LCT lipid emulsion (20% Lipoven; Fresenius-Kabi France, Sèvres, France) by a 20% MCT/LCT lipid emulsion (Medialipide B; Braun Medical, Boulogne, France). RESULTS: Patient received LTPN for 46 +/- 40 months; IV lipid emulsion was 827 +/- 336 mL/week. MCT/LCT lipid substitution did not change most of the essential plasma fatty acid concentrations and did not induce essential fatty acid deficiency. With both lipid emulsions, the triene/tetraene (20:3n-9/20:4n-6) ratio remained within the normal ranges. However, with MCT/LCT lipid emulsion, 22:4n-6 (LCT: 0.50 +/- 0.12; MCT/LCT: 0.63 +/- 0.11%) and 22:5n-6 (LCT: 0.32 +/- 0.11; MCT/LCT: 0.48 +/- 0.15%) increased significantly (p = .022 and 0.011, respectively). Plasma vitamin K1 levels decreased drastically with MCT/LCT lipid emulsion. CONCLUSIONS: An amount of 2.85 +/- 1.55 g x kg(-1) week(-1) of MCT/LCT lipid emulsion neither induced essential fatty acid deficiency nor improved the fatty acid disturbances usually observed in LTPN patients but did induce a drop in plasma vitamin K1 levels.

Stimulation of cholesterol synthesis and hepatic lipogenesis in patients with severe malabsorption.

Patients with severe malabsorption have abnormal lipid metabolism with low plasma cholesterol and frequently high triglyceride (TG) levels. The mechanisms behind these abnormalities and the respective roles of malabsorption itself and of the parenteral nutrition given to these patients are unclear. We measured endogenous lipids synthesis (cholesterol synthesis and hepatic lipogenesis) and the expression (mRNA concentrations in circulating mononuclear cells) of regulatory genes of cholesterol metabolism in 10 control subjects and 22 patients with severe malabsorption receiving (n = 18) or weaned of parenteral nutrition (n = 4). Patients had low plasma cholesterol (P < 0.01) and raised TG (P < 0.05) levels. Both fractional and absolute cholesterol synthesis (P < 0.001) and hepatic lipogenesis (P < 0.01) were increased. These abnormalities are independent of parenteral nutrition since they were present in patients receiving or weaned of parenteral nutrition. No relation between hepatic lipogenesis and plasma TG levels was found, suggesting that other metabolic abnormalities participated in hypertriglyceridemia. HMG-CoA reductase and LDL receptor mRNA levels were decreased (P < 0.05) in patients on long-term parenteral nutrition. HMG-CoA reductase mRNAs were normal in weaned patients.Severe malabsorption induces large increases of cholesterol synthesis and hepatic lipogenesis independently of the presence of parenteral nutrition. These abnormalities are probably due to the malabsorption of bile acids.