SUMMARY We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: 0 (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.Controversy exists in the literature about the incidence and nature of liver lesions in obese patients. In most studies fatty liver was the only significant abnormality,1-4 but recent reports have suggested that severe liver damage, sometimes mimicking the entire histological spectrum of alcoholic liver disease, could be found in obesity.512In most of these studies, however, information on the potential hepatotoxic factors occuring in obesity was usually lacking. Thus, we undertook a crosssectional study of the liver histology in 50 nonselected obese patients with the aims: (a) to define precisely the prevalence, the nature, and the severity of the liver lesions in obesity; (b) to determine, by the multidimensional analysis, the quantitative and/or qualitative clinical variables which were related to the observed histological abnormalities. Methods PATIENTSFifty obese patients, consecutively hospitalised in a

No abstract

No abstract

27 patients on hemodialysis (dialysate aluminium < 0.7 μmol/l for 2 years, and 2 μmol/l before) whose plasma Ca and PO₄ were adequately controlled for already 6 months by high doses of CaCO₃ alone (mean ± SD: 9 ± 5 g/day), were randomly divided into 2 groups, a control group (c group) which was kept on the same treatment, and a group in which CaCO₃ was reduced to 3 g/day but in which plasma Ca was kept normal due to 1α-OH-vitamin D₃ administration (1 μg/day at the beginning, 0.3 μg/day after 6 months; 1α group) whereas plasma phosphate was kept below 6.0 mg/dl because of A1(OH)₃ (2.7–5 g/day). Initially, the 2 groups were comparable as regards the plasma concentrations of total and ionized Ca, phosphate, alkaline phosphatases, medium and C-terminal parathyroid hormone (PTH) and aluminium, but the control group had lower plasma 25-OH-vitamin D (25-OHD.) After 6 months, the same difference in plasma 25-OHD was found with comparable plasma concentrations of total and ionized calcium as well as of medium and C-terminal PTH (beta error 1%). However, plasma concentration of phosphate and the plasma Ca phosphate product, as well as the plasma aluminium were higher in the 1α group whereas their PCO₃H was lower. Although the alkaline phosphatase values were not significantly different between the 2 groups, they increased only in the control group because of 1 patient who developed a vitamin-D-deficient osteomalacia (plasma 25-OHD 3 ng/ml), which was subsequently cured by physiological doses of 25-OHD₃. The incidence of transient hypercalcemia (15 vs. 21 episodes) and worsening of soft tissue calcifications (3 in each group) was the same in the 2 groups.

No abstract

No abstract

Linear calcifications of the abdominal aorta and of the iliac and femoral arteries were measured yearly for 3 years on X rays of 24 patients on chronic hemodialysis taking variable amounts of calcium carbonate and Al(OH)₃ but no pharmacological doses of vitamin D or lα-hydroxylated vitamin D derivatives. The speed of their extension appeared exponential and covariant with the male sex, age only for men and, independently of these two factors, with diastolic blood pressure and blood triglycerides. Plasma concentrations of calcium, phosphate and glucose were covariant with the extension of calcinosis only at a borderline level. The doses of calcium carbonate and the levels of plasma alkaline phosphatase were not at all covariant. Conclusions: (1) The effect of high doses of calcium carbonate is possibly harmful only when supraphysiological levels of plasma calcium are induced, whereas plasma phosphate is not adequately decreased. The doses of calcium carbonate per se have no deleterious effect (2). Since alkaline phosphatase is not covariant with the extension of calcinosis, the degree of hyperparathyroidism per se does not seem to play a causative role in vascular calcinosis (3). The main risk factors of vascular calcinosis are: age, the male sexe, diastolic blood pressure and blood triglycerides.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while (1) on a free diet; (2) on a calcium- and oxalate-restricted diet during 4 days; (3) after an oxalate load, while on a 1.5-gram calcium diet, and (4) after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4,6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.