Choline Deficiency Is Associated With Increased Risk for Venous Catheter Thrombosis

ABSTRACT. Background: Patients with intestinal failure who require long-term parenteral nutrition (PN) make known catheter thrombosis as a complication. This patient cluster may also develop choline deficiency because of a want in the hepatic transsulfuration pathway in the setting of malabsorption. This investigation was undertaken to determine whether choline deficiency is a risk factor for disclosure of catheter thrombosis. Methods: Plasma unrestrained and phospholipid-bound choline concentrations were measured in a collection of 41 patients that required long-term PN Episodes of catheter thrombosis from charge of PN to the time of vital fluid testing were recorded. Results: Sixteen (39%) patients evolveed catheter thrombosis, and 5 of these had renewed catheter thrombosis. Plasma free choline was 77 ?± 27 nmol/mL in patients with no history of catheter thrombosis and 62 ?±17 nmol/mL in patients with previous catheter thrombosis (p = 076 through Wilcoxon rank-sum test). The partial correlation between plasma independent choline concentration and the oftenness of clots after controlling for catheter duration was r = -033 (p = 038) The relative risk for catheter thrombosis in subdues with a plasma free choline concentration

Central venous catheter thrombosis is a of frequent occurrence complication in patients who require long-term parenteral nutrition (PN)1 renewed thrombosis and loss of at least 2 major utensils is a Medicare-approved indication for small-intestinal transplant.2 Hyperhomocysteinemia is a risk factor for unravelling of venous thrombosis.3-5

Choline is a quaternary amine that functions as a methyl donor for various methylation reactions. It is also the precursor for acetylcholine and phospholipid biosynthesis.6,7 Choline deficiency has been described in a variety of animal species and manifests in development hepatic, pancreatic, lipoprotein, memory, and renal abnormalities in a certain number of species.6 Choline deficiency has previously been described in patients who require long-term PN where it manifests in hepatic8-10 and neuropsychological abnormalities.11 In gnawings choline deficiency is also associated with hyperhomocysteinemia,12-15 which is a risk factor for venous thrombosis in patients who require PN16 Therefore, the possibility exists that choline deficiency is a significant risk factor for exhibition of catheter thrombosis in patients with intestinal failure.

METHOD

This research used data obtained during a prospectively designed application of mind of plasma free choline concentrations in a random collection of long-term home PN patients17 and a retrospective inquiry of the incidence of catheter thrombosis in a clump of 527 home PN patients.1 The patients included in this application of mind represent a subset of those make submissives namely, those who had their plasma independent choline concentrations determined in 1991 Episodes of catheter thrombosis from storming of PN to the time of life-current testing were recorded. These patients were consecutively seen patients in the abode PN clinic and included children and adults. Inclusion criteria were a requirement for residence PN for at least 1 month and at least 3 times weekly. Patient diagnoses/PN indications are listed in Table I. We then retrospectively evaluated the incidence of catheter thrombosis in this subgroup

All catheters were single or double-lumen, surgically placed, subcutaneously-tunneled catheters; there were no percutaneous-inserted central catheters (PICCs). greatest in quantity but not all, were single lumen although we were unable to determine the exact number of single-lumen catheters because of inadequate documentation. Catheter tip had been verified in either the superior or inferior vena cava by the agency of fluoroscopy at the time of insertion and subsequently in greatest in quantity but not all, patients by means of chest radiograph. PN consisted of a single 1- to 3-L bag containing a mixture of dextrose ( 15%-25% final concentration), independent amino acids (3.5%-5% final concentration), electrolyte minerals, trace metals, and multivitamins. Lipid emulsion (20%) was delivered in a "piggybacked" style; no 3:1 emulsions were used. All patients do not include 1 received cyclic nighttime infusion above 8-12 hours 3-7 days for week, depending on individual nutrient and/or fluid requirements. Heparin was routinely used as a catheter flush in all patients. No patient was receiving heparin or warfarin before their catheter thrombosis. Hydrocortisone was not added to the PN solution.

Catheter thrombosis that was suspected clinically according to difficulty flushing or infusing the catheter, or extremity, neck or facial edema, was confirmed with contrast venography the two through the catheter and proximal to the catheter; patients with no evidence of thrombosis with contrast venography were not included in this inquiry Patients with thrombosis related to a malpositioned catheter were exclud as were those with symptoms solely according to localized thrombosis that resolv after instillation of urokinase 5000 through catheter lumen.

A thrombophilia evaluation was undertaken, with measurement of platelet number protein C, protein S, plasminogen, antithrombin III concentrations, and anticardiolipin and antiphospholipid antibodies using standard techniques. Thrombocytosis was defined as a platelet number of >450,000/??L.