Plasmapheresis in the management of acute severe hyperlipidemic pancreatitis: report of 5 cases.

BACKGROUND/AIM: Hyperlipidemic pancreatitis is an acute and potentially life-threatening complication of hypertriglyceridemia that can be provoked when triglyceride levels (TGL) exceed 11.3 mmol/l (1,000 mg/dl). Except for standard symptomatic treatment, plasmapheresis has been performed to rapidly reduce TGL and chylomicron levels in the blood. In 5 patients with hyperlipidemic pancreatitis, treatment with plasmapheresis was evaluated. METHODS: Five male patients who suffered from acute pancreatitis with severe primary hyperlipidemia were studied. In addition to the standard treatment, they were treated with plasmapheresis. RESULTS: Plasma exchange lowered the lipid level and TGLs in all cases. It also improved abdominal pain, the clinical state of the patients, and signs and symptoms of the disease. Complications of treatment were not encountered, none of the patients died and only 1 patient underwent surgery. Follow-up of the patients lasted 4-28 months, and recurrence of pancreatitis was not noted. CONCLUSION: Our study showed that plasmapheresis was successfully applied in patients with hyperlipidemic pancreatitis, especially to improve the acute phase of the disease.

Use of the low-dose desferrioxamine test to diagnose and differentiate between patients with aluminium-related bone disease, increased risk for aluminium toxicity, or aluminium overload.

BACKGROUND: Aiming at a safe method in the diagnosis of aluminium-related bone disease (ARBD)/aluminium overload the low-dose desferrioxamine (DFO) test was developed. In a multicentre study histological and histochemical data and aluminium bulk analysis of bone biopsies of 77 dialysis patients were correlated with the results of both the 5 mg/kg and 10 mg/kg DFO tests. METHODS: ARBD was considered to be present when > 15% of the bone surface was positively stained for aluminium and the bone formation rate was below 220 microns 2/mm2/day. Patients in which the Aluminon staining was positive (> 0%) were considered at an increased risk for aluminium toxicity independent of the type of renal osteodystrophy. Patients were considered aluminium overloaded when the bone aluminium content was > 15 micrograms/g wet weight and/or the Aluminon staining was positive (> 0%). RESULTS: Using the proposed criteria 15 patients were found to have ARBD; 13 of them presenting with a serum iPTH below 150 ng/l. In conjunction with an iPTH measurement the DFO test had a more than acceptable sensitivity and specificity in the diagnosis of ARBD. The test was considered positive when a post-DFO serum aluminium increment (delta sA1) above 50 micrograms/l (5 mg/kg) or 70 micrograms/l (10 mg/kg) together with a serum iPTH below 150 ng/l was found. Using these cut-off levels the 5 and 10 mg/kg tests in the diagnosis of ARBD had a sensitivity of 87% and a specificity of 95% and 92% respectively whereas the predictive value for a positive test for the population under study was 80% (5 mg/kg). Not a single patient with a serum iPTH > 650 ng/l had a positive staining (> 0%) even when the bone aluminium level was elevated (> 15 micrograms/g wet weight). In the detection of patients at risk for aluminium toxicity delta sA1 thresholds of 50 micrograms/l (5 mg/kg) and 70 micrograms/l (10 mg/kg) in combination with a serum iPTH < 650 ng/l had a sensitivity of 92% and specificity of 86% and 84% respectively. In the clinical setting of aluminium overload, threshold delta sA1 levels of 50 micrograms/l (5 mg/kg) and 70 micrograms/l (10 mg/kg) had a sensitivity of 91% and a specificity of 95% and 90% respectively. CONCLUSIONS: The low-dose DFO test is a reliable test for the detection of aluminium overload; however, it is not specific enough to differentiate between ARBD, increased risk of aluminium toxicity, and aluminium overload unless it is used in combination with a serum iPTH measurement. In conjunction with a serum iPTH measurement it is an important tool in the differential diagnosis and may avoid the necessity of a bone biopsy in the majority of patients. Data obtained in the present study have allowed us to update the strategies for monitoring, diagnosis and patient follow-up proposed at the Consensus Conference on Diagnosis and Treatment of Aluminium Overload in End-Stage Renal Failure; Paris, 1992.

Urinary and biliary excretion of aluminoxamine and ferrioxamine in dogs with various renal function.

We assessed the pharmacokinetics of aluminoxamine and ferrioxamine in dogs with sustained intermittent bile duct ligation and either normal renal function or stable chronic renal failure. A first group of male beagle dogs were given aluminoxamine and ferrioxamine, while a second group received desferrioxamine after loading them with iron and aluminum. Only minute amounts of ferrioxamine and aluminoxamine were found in the bile after administration of these compounds. The distribution volume of aluminoxamine and ferrioxamine appeared to be confined to the extracellular space and their renal excretion correlated with renal function. Administration of desferrioxamine to iron and aluminum-loaded dogs resulted in an increased biliary ferrioxamine but negligible aluminoxamine excretion. Renal clearance of the in vivo formed ferrioxamine and aluminoxamine in this group strongly correlated with renal function. Our observations indicate that biliary excretion of intravenously administered ferrioxamine and aluminoxamine is negligible even in renal failure. The data presented in this study provide indirect evidence that desferrioxamine administration to iron- and aluminum-loaded dogs results in the intra-hepatic formation of ferrioxamine which is partly excreted in the bile. Biliary excretion of aluminoxamine after desferrioxamine administration remained negligible.

Removal of aluminoxamine and ferrioxamine by charcoal hemoperfusion and hemodialysis.

We studied the removal of aluminoxamine (AlO) and ferrioxamine (FO) by (i) hemoperfusion/hemodialysis using an AluKart in combination with either a Cuprophan F-120 or a Hemophan FH-160 membrane, or (ii) hemodialysis with a high-flux F-60 polysulfone membrane. The same six dialysis patients underwent in a random order dialysis by the three set-ups after i.v. infusion of 30 mg/kg of desferrioxamine (DFO) during the last half an hour of the preceding dialysis session. The mean +/- SD plasma AlO and FO clearances of the AluKart combined with either a F-120 or FH-160 membrane were 194.3 +/- 25.8 ml/min (AlO) and 164.2 +/- 41.3 ml (FO) at the start of dialysis declining to respectively 76.6 +/- 27.3 and 68.5 +/- 42.6 ml/min at the end of dialysis. With a high-flux dialysis membrane the intra-dialytic plasma clearance remained constant at 81.5 +/- 6.8 ml/min for AlO and 60.0 +/- 2.8 ml/min for FO. In the presence of an AluKart combined with a FH-160 up to 84 +/- 27% and 84 +/- 19% of the available AlO and FO could be removed during a four-hour hemoperfusion/hemodialysis session. During the first hour of dialysis, respectively 59 and 58% of the total amount of AlO and FO extracted by the AluKart was removed compared to only 9 and 16% during the last hour.(ABSTRACT TRUNCATED AT 250 WORDS)