[Instrumental analysis of trace elements]. / Analisi strumentale di elementi in traccia.

The study of trace elements in human medicine and toxicology requires very low concentration of these elements to be determined in biological matrices. Among the analytical methodologies of major impact there are isotopic dilution mass spectrometry, neutron activation analysis, anodic stripping voltammetry, inductively coupled plasma atomic emission spectrometry and electrothermal atomization atomic emission spectrometry. This last, in particular, provides high sensitivity and reliability for the determination of numerous elements. Instrumental and methodological improvements leading to these achievements include the adoption of the so-called stabilized temperature platform furnace, the introduction of universal matrix modifiers, oxygen charring steps and background correction systems based on the Zeeman effect.

[Lead exposure in the adult population non-occupationally exposed]. / L'esposizione al piombo nella popolazione adulta non professionalmente esposta.

Lead is added into the environment by the production, use and deposited a variety of lead-containing materials. This pollution is increasing during the last years. The major source for the human intake of lead is the food chain. The people who very hardly drinks (especially wine) have been found have very high blood lead levels. 184 hospitalized patients for alcoholic liver diseases were examined and the Pb-B levels were 36,3 +/- 10,2 micrograms/100 ml. Smoking habits are another factor that increases the blood lead levels.

Serum aluminium level in the veneto chronic haemodialysis population: cross-sectional study on 1,026 patients.

A total of 1,026 patients undergoing haemodialysis as the only chronic treatment were studied in all the dialysis units of the Veneto region, Italy. Aluminium was determined in water, dialysis fluids, and patients' serum. Aluminium mean concentration was 9.1 micrograms/l in tap water and 13.3 and 15.7 micrograms/l in bicarbonate and acetate haemodialysis fluids, respectively. Patients' serum aluminium mean level was 52.0 micrograms/l with the following frequency distribution: 59.2% below 60 micrograms/l, 25.5% between 60 and 100 micrograms, and 15.3% above 100 micrograms/l. The mean serum aluminium level was higher in patients undergoing haemodialysis with aluminium concentration in fluids over 10 micrograms/l. This was true also in patients not receiving aluminium hydroxide. Furthermore, we found higher average serum aluminium in those treated with aluminium hydroxide more than 3 g/day. No relationship was found between serum aluminium and sex, age, dialytic age, parathyroid hormone, and vitamin D treatment. Moreover, the patients with serum aluminium above 100 micrograms/l had higher serum alkaline phosphatase and lower mean cell volume values. Thus, in our haemodialysis population aluminium overloading occurred in spite of low concentration in water and fluid, and it was a result more of fluid pollution (over 10 micrograms/l) than aluminium hydroxide ingestion (over 3 g/day).

Blood-lead levels in patients with chronic liver diseases.

Blood-lead concentrations (Pb-B) were measured in 318 adult inpatients with chronic liver diseases. The Pb-B was highest (387 +/- 96 micrograms/l) in 102 patients with alcoholic liver disease without cirrhosis. The Pb-B was still high, but significantly lower in 60 patients with compensated alcoholic cirrhosis (342 +/- 100 micrograms/l) and in 72 patients with decompensated alcoholic cirrhosis (312 +/- 97 micrograms/l). This difference was in part due to a significant decrease of the hematocrit which fell from 44.4 +/- 4.9% to 42.4 +/- 27.2% and to 39.2 +/- 7.4% respectively. In patients with viral or cryptogenic liver diseases the Pb-B was 211 +/- 69 micrograms/l in 11 patients with chronic persistent hepatitis, 219 +/- 72 micrograms/l in 19 with chronic active hepatitis, 206 +/- 94 micrograms/l in 28 with compensated cirrhosis, and 226 +/- 98 micrograms/l in 26 with decompensated cirrhosis, without any significant difference. The Pb-B of the male patients showed no correlation to age, with the exception of 25 male patients with chronic persistent and active hepatitis (r = 0.626, P less than 0.001).

Dynamics of bone aluminum over one year of functioning renal graft.

The concentration of aluminum (Al) in serum, urine, and bone, as well as bone histomorphometry parameters were studied before and 1 year after kidney transplantation (Tx) in 20 dialyzed patients. One year after Tx, serum Al fell significantly from 50.3 +/- 8.8 to 23.9 +/- 2.7 micrograms/l, (53% fall). Bone Al content also decreased significantly from 62.9 +/- 9.0 to 36.5 +/- 7.0 micrograms/kg bone weight, but urine Al excretion was still above normal. The repeat bone histomorphometric examination showed a good recovery of bone resorption which correlated well with serum parathyroid hormone levels, but poorer recovery of indices of bone formation and of the extent of Al deposits in the bone as shown by aluminum staining.

Kinetics of aluminoxamine and feroxamine chelates in dialysis patients.

To achieve a rational basis for the use of deferoxamine (DFO) in aluminum (AL) -and iron (Fe)-overloaded uremic patients, important insights may be provided by the recently available micromethods to determine DFO and its metallochelates aluminoxamine (AlA) and feroxamine (FeA). With this procedure, AlA and FeA plasma kinetics were evaluated in a pilot study in 10 uremic patients during a whole week after a single DFO infusion performed during the first hour of the first standard bicarbonate hemodialysis (HD) of the week. Patients were divided into normal (n = 6) and high (n = 4) ferritin groups (1 and 2 respectively). Baseline Al concentrations were greater than 2 less than 6 in group 1 and less than 1.5 mumol/l in group 2. DFO was given at doses of 40, 20 and 10 mg/kg. AlA and FeA showed substantially different kinetics. AlA kinetics were similar in group 1 and 2: they reached their peak at the beginning of the 2nd HD, decreased during the 2nd and 3rd HD, and with the highest DFO dose still increased between the 2nd and 3rd HD. At similar pre-DFO Al values (greater than 2 less than 3.3 mumol/l), increased DFO doses produced increased AlA concentrations ranging from 95 to 40% of total plasma Al for all the week. At higher pre-DFO Al values (greater than 3.5 less than 6 mumol/l), even a DFO dose as low as 10 mg/kg was sufficient to form consistent AlA amounts (from 80 to 15% of total Al).(ABSTRACT TRUNCATED AT 250 WORDS)