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Serum lipid and lipoprotein levels were evaluated in 50 insulin-treated diabetic out-patients (25 male and 25 female) and in 46 normal volunteers (22 male and 24 female). In these groups metabolic evaluation was carried out by assaying fasting plasma glucose, glucose in urine and glycosylated hemoglobin (G-HbA1). No differences were observed in the lipid and lipoprotein patterns between diabetic patients and normals. HDL values were significantly lower in male subjects, diabetic and normal, as compared to females, but there were no differences between the diabetic and the normal group. G-HbA1 was significantly correlated to fasting plasma glucose and glucose in urine, but also to WS-TG and VLDL-TG. Fasting plasma glucose too was correlated to WS-TG and VLDL-TG. Moreover, a negative correlation was found between HDL-Ch and WS-TG and VLDL-TG. These results show that sufficiently well-controlled insulin-treated diabetics do not have altered plasma lipid and lipoprotein levels. In particular, in these patients HDL-Ch values can be normal, because insulin levels are sufficient to activate lipoprotein lipase and to guarantee an adequate plasma VLDL clearance.

Gli AA. hanno eseguito uno studio sulle correlazioni tra colesterolo e trigliceridi, rispettivamente aree beta e pre-beta, in agarosio-gel (86 pazienti) e tra questi ultimi valori e quelli delle lipoproteine Sf 0-20 e Sf 20-400 determinate con il metodo nefelometrico (46 pazienti). Venticinque dei soggetti esaminati presentavano livelli lipidemici normali, i rimanenti erano affetti da forme diverse di iperlipoproteinemia (tipo Ha, IIb e IV di Fredrickson). E stata trovata una correlazione altamente significativa tra trigliceridi e area pre-beta e tra Sf 0-20 e Sf 20-400 e rispettivamente aree beta e pre-beta ottenute mediante elettroforesi su agarosio-gel, arbitrariamente espresse in unita planimetriche. Viene discusso infine, anche alla luce di recenti dati della letteratura, il possibile impiego dell’elettroforesi in agarosio-gel come metodo di determinazione quantitativa delle varie frazioni lipoproteiche del siero.

In questa rassegna viene discusso il significato fisiologico e clinico delle HDL, inquadrato nell’ampia problematica del ruolo e del metabolismo delle lipoproteine plasmatiche. Di queste vengono infatti presentate la struttura e le interrelazioni metaboliche. Le HDL, che trovano piu ampia descrizione, sono lipoproteine sintetizzate dall’intestino, dal fegato e durante il cata-bolismo delle lipoproteine ricche in trigliceridi. Esse possono essere suddivise, in base alla loro densita, in HDL2 e HDL3. Sono soprattutto le HDL2 a subire variazioni in alcune situazioni (attivita fisica, sesso, peso, diabete mellito, assunziuone di ormoni, di alcool, etc.). Il rinnovato interesse per queste frazioni lipoproteiche nel corso di questi ultimi anni e dovuto ad un attributo anti-aterogeno ad esse dato e confermato sia da esperimentiin vitro che da indagini epidemiologiche. Vengono qui discussi i possibili meccanismi di tale funzione. Attenzione hanno recentemente suscitato anche i livelli di HDL e delle sue sottofrazioni nella malattia diabetica; i dati in letteratura sono numerosi ma assai discordanti. Sembra tuttavia importante continuare tali studi mettendoli in relazione sia al tipo di diabete (I o II) che al suo grado di compensazione. I bassi livelli di HDL e quelli elevati di VLDL nel diabete in precario compenso possono essere fra le cause che danno luogo all’insorgenza della macroangiopatia aterosclerotica in tale malattia.

Twelve patients with mild and 3 with severe hypercholesterolemia were stabilized with an isocaloric diet containing less than 300 mg cholesterol daily with a P/S ratio of 1.8, and placebo period of 4 weeks. They were administered 1000 mg probucol daily for 12 weeks, followed by placebo for 6 weeks. In patients with mild disease, a significant cholesterol reduction was achieved in serum, LDL, and HDL (maximum decrease, 17%, 13%, and 31%, respectively). While HDL3 cholesterol was reduced significantly throughout the period (P less than 0.001), HDL2 cholesterol showed a significant decrease only at the 4th week of treatment (P less than 0.001), and returned to basal levels at the 8th and 12th treatment weeks. Serum apo B levels decreased only slightly, but the HDL-apo A-I fall was significant with a reduction in the HDL-CH/HDL-apo A-I ratio throughout the treatment period. In 3 patients with severe disease, cholesterol decrease in serum and in VLDL, LDL and HDL fractions varied, but on the whole was lower than in patients with mild disease. A decrease in VLDL-CH and HDL-CH was present in all 3, but LDL-CH levels were only slightly lowered in 2 patients, and unchanged in the third. Serum probucol levels fell 66% from the 4th to the 12th treatment week, and in parallel, the percentage of lipoprotein-bound drug increased about 2-fold. It is suggested that these changes in pharmacokinetics as well as the cholesterol-lowering effect of the drug may be due to a change in lipoprotein composition or structure.

Plasma lipids, apoprotein A-I and B in serum and in lipoprotein fractions (VLDL + LDL, HDL2, and HDL3) obtained by preparative ultracentrifugation, as well as postheparin lipoprotein lipase activity (H-TGL and LPL) were evaluated in 17 subjects with primary biliary cirrhosis (stage II and III) subdivided into two groups according to the presence or absence of lipoprotein X (Lp-X). A reduction in total lipoprotein lipase activity was observed in both patient groups, compared to controls (P

The presence or absence of histological signs of cholestasis (on the basis of liver specimens obtained by means of liver biopsy) was compared with total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, ornithine carbamoyltransferase, serum glutamic oxaloacetic transaminase levels and LP-X test in 157 patients suffering from different liver diseases. The LP-X test was positive in 93% of the 59 cases in whom histological evidence of cholestasis was observed and negative 95% of the 98 cases in whom histological examination was negative. LP-X concurs more frequently with the histological picture than do total bilirubin and alkaline phosphatase. These data confirm that LP-X test is more specific than the tests traditionally used to demonstrate or exclude cholestasis. An increment in gamma-GT levels was observed in 97% of the patients with a positive LP-X test. These clinical results have been discussed in the light of recent data regarding the mechanism of lipoprotein-X formation and the possible relationships between LP-X and gamma-glutamyl transpeptidase.

Fenofibrate effect on plasma lipids and lipoproteins was studied in 23 patients with primary hyperlipoproteinemias (HLP): 12 with familial hypercholesterolemia (FH), 5 with combined HLP and 6 with Type III HLP. Trial lasted from 8 to 10 months. Cholesterol and triglycerides were significantly reduced in all patients as follows: cholesterol dropped 26% in FH (p less than 0.001), 32% in combined HLP and 48% in type III HLP; triglycerides dropped 29%, 64% and 72% respectively. This drop involved LDL in FH, VLDL and LDL in combined HLP and beta-VLDL in type III HLP patients. In FH and combined HLP patients we observed a +10% (p less than 0.01) and a +9% (n.s.) increase of HDL, respectively. Two patients had a mild SGOT and SGPT increase and three had a vescicular cutaneous erythema.

In order to evaluate the relationship between triglyceride-rich lipoproteins (chylomicrons and VLDL) and HDL during alimentary lipaemia, 12 healthy volunteers, 6 male and 6 female (aged 20--40 yrs), were studied. Cholesterol, phospholipid, triglyceride and protein were evaluated in whole serum, VLDL, LDL and HDL (successively subfractionated in HDL2 and HDL3). Blood samples were collected in a fasting state, 4.5 and 9 h after a 1500 calorie meal (20% protein, 40% carbohydrate, 40% fat). A striking increase in triglyceride-rich lipoproteins after 4.5 h was observed in both sexes, but was more pronounced in males. An increase in phospholipid and triglyceride as well as a slight reduction in cholesterol was evident in HDL after 4.5 h. At the same time both lipids and proteins were decreased in HDL3 and increased in HDL2. This phenomenon is more evident in females, who showed a significantly higher basal HDL2 level. These results suggest a possible metabolic relationship in the post-prandial phase between triglyceride-rich lipoproteins and HDL, and an inverse correlation between HDL2 and HDL3.

Serum lipid and lipoprotein levels, apolipoproteins A-I and B, and lipolytic enzyme activities were studied in 14 young male cyclists and in 21 age-matched sedentary controls. While there were no significant differences in serum cholesterol between the two groups, the cyclists showed a significant decrease in serum triglycerides (P less than 0.05) and LDL cholesterol (P less than 0.05) and had significantly higher levels of HDL cholesterol (P less than 0.01) and HDL2 cholesterol (P less than 0.001). Significantly lower serum cholesterol/HDL cholesterol (P less than 0.001) and LDL cholesterol/HDL cholesterol (P less than 0.001) ratios and a significantly higher HDL2 cholesterol/HDL3 cholesterol ratio (P less than 0.001) were observed in the athletes. Serum apolipoprotein B was lower and the Apo B/Apo A-I ratio significantly reduced in the athletes. No significant differences emerged between the two groups in plasma post-heparin lipoprotein lipase activity (LPL) and in hepatic triglyceride lipase activity (HTGL), and there were no correlations between HDL cholesterol and lipolytic enzyme activities. In conclusion, this cross-sectional study may indicate that an aerobic training program such as cycling is associated with an advantageous lipoprotein pattern; some factors other than lipolytic activity may contribute to increase the HDL cholesterol levels in physical training.

Plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic lipase (H-TGL) were studied in 7 patients with familial hyperchylomicronemia from four different families. Their first-degree relative were also studied. The patients were heterogeneous for the genetic defect; LPL activity was absent in five patients (LPL deficiency) but normal in two. However, these two did not have apo C-II, the physiological activator of LPL (C-II deficiency). There were no significant differences in the clinical picture between patients with LPL deficiency and C-II deficiency. In both mutants, marked hypertriglyceridemia was due to an accumulation of lipoproteins of density less than 1.006 g/ml. The LDL fraction was very reduced and abnormal in composition, presenting a CH/TG ratio of 0.5. The plasma apolipoprotein B (apo B) level was low (67 +/- 5.5 mg/dl) and was transported mainly in the VLDL fraction (26 +/- 3.2 mg/dl) rather than in the LDL fraction (15 +/- 1.4 mg/dl). Very low levels of cholesterol and apolipoprotein A-I in HDL subfractions HDL2 and HDL3 were also recorded. Only 3 out of the 24 first-degree relatives of patients with LPL deficiency showed even a small increase in plasma triglycerides, but 15 had low or low to normal LPL values. H-TGL levels were normal in all subjects. The 4 first-degree relatives of C-II deficiency patients showed normal levels of plasma lipids. LPL and H-TGL, and 2 children of 1 patient showed normal distribution of apo C peptides in their VLDL. A block in chylomicron catabolism, due to the absence of LPL or apo C-II, may lead to a massive accumulation of lipoproteins with a density less than 1.006 g/ml, and a drastic reduction in the LDL and HDL fractions. Low LPL values in the first-degree relatives of LPL deficiency patients might represent a biochemical marker for healthy carriers of LPL deficiency.

Applicando la tecnica della nefelometria e filtrazione su membrana, abbiamo dimostrato una stretta correlazione tra lipoproteine a densita molto bassa (Sf 20–400) e trigliceridi totali misurati con metodo chimico. Successivamente abbiamo esposto i vantaggi che la tecnica suddetta offre per l’esecuzione discreening lipidici di massa, Summary Using membrane filtration with measurement by nephelometry in the determination of serum lipoproteins, a significant correlation between plasma very low-density lipoproteins (Sf 20–400) and triglyceride levels measured by chemical method has been observed. Advantages offered by this technique in epidemiological studies are quite remarkable.

L’elettroforesi delle lipoproteine su gel di agarosio e stata eseguita in 61 pazienti affetti da iperlipemia del tipo II, IV e « misto ». I tracciati elettroforetici sono stati sottoposti a lettura densitometrica, con successivo calcolo delle percentuali densitometriche delle aree beta e pre-beta, nonche del rapporto area beta/area pre-beta. Tutti i pazienti appartenenti al tipo II e IV erano separabili sulla base delle percentuali beta e pre-beta. Infatti nel tipo II la percentuale pre-beta era sempre inferiore al 21 %, mentre nel tipo IV era sempre superiore al 35 %. L’area beta nel tipo II e sempre risultata superiore al 55 %, nel tipo IV sempre inferiore al 44 %. Nel confronto tra tipo II e « misto » e tra tipo IV e « misto » non esisteva invece altrettanto netta separazione sulla base dei valori percentuali delle bande beta e pre-beta. Il numero di sovrapposizioni si riduceva di molto se venivano invece presi in considerazione i valori dei rapporti area beta/area pre-beta. I nostri risultati dimostrano l’utilita dell’analisi densitometrica dei tracciati elettroforetici quale mezzo diagnostico per discriminare i piu comuni tipi di iperlipidemia, nel superare alcune difficolta classificative e collegate all’interpretazione solo « visiva » di alcuni «patterns » elettroforetici di tipo « misto ».

Summary High serum cholesterol is an established risk factor for cardiovascular disease and is the prime target for therapeutic intervention in large groups of patients. The development of modern treatments for this major risk factor was propelled by the early realization that forms of severe hypercholesterolemia could be caused by dominantly inherited defects in the LDL receptor or in the APOB gene. Further understanding of the mechanisms contributing to early atherosclerosis will allow for new targets for therapy. We therefore identified and investigated the genetics of families from Sardinia that have recessive inheritance of precocious hypercholesterolemia. We used five families in an analysis of linkage of the autosomal recessive hypercholesterolemia locus, termed “ARH1,” to chromosome 15q25-q26. A genomewide search mapped the disease-causing gene with a LOD score of 3.3 and excluded major contributions to the phenotype of other genes. A candidate gene present in the mapped chromosome region—the ligand-activated liver-transcription-factor gene ARP1 (apolipoprotein regulatory-protein gene)—has been excluded after DNA sequencing. The close-bred nature of the Sardinian population offers unique opportunities for isolation of this hypercholesterolemia-causing gene.

The results of plasma lipid and lipoprotein analysis in two related patients, brother (R.U.) and sister (R.R.) with analbuminemia, and three first-degree relatives (parents and sister) are reported. Both patients showed a remarkable increase in cholesterol and phospholipid levels, and there was a corresponding increase in serum apo B and apo A-I. This hyperlipidemia is due to a selective increase in LDL and HDL concentrations. R.U. showed an increase in both HDL 2 - and HDL 3 -cholesterol, R.R. only in HDL 3 -cholesterol. VLDL concentration was reduced in R.U. and normal in R.R. The plasma lipoprotein electrophoretic pattern did not correspond to any of the phenotypes in Fredrickson's classification. Composition of the different lipoprotein fractions was normal in the patients and family members. Serum FFA level in R.R. was very low. An increase in the plasma protein fractions, particularly the transport fractions, was confirmed in both patients. The possible pathophysiology of the hypercholesterolemia in these patients is discussed. Unlike other reported cases, clinical signs of atherosclerotic complications were absent.

In recent years substantial progress in the study of atherosclerosis has led to the definition of some now well known risk factors, and hence to the possibility of carrying out realistic programs of prevention and therapy. These risk factors include the hyperlipaemias, common metabolic disorders of the plasma lipoproteins which may be primary with genetic origins, or secondary to endocrine disease, organic disease, drug therapy, or dietary habits. The interest in these alterations, however, has mostly been focused on the young and middle age groups, overlooking the elder age groups (Kritchevsky).1 Moreover, the data supplied by the Lipid Research Clinic Programs of the National Heart, Lung, and Blood Institute (U.S.A.) refer to plasma lipid values for age and sex for quinguennial groups, but only up to 70 years of age. 2 Nonetheless, the increase in the population of elderly persons, which has been recorded in these years, and the consequent growth of geriatric pathology, raise, among others, the problem of defining the metabolic alterations present in this age group, and among these, the dyslipidaemias.

Gidez et al described a double precipitation method with polyanions to separate high density lipoprotein (HDL) subfractions, using sodium heparin to precipitate very low density lipoprotein (VLDL) and low density lipoprotein (LDL) first, and dextran sulphate 15000 to precipitate HDL2 from total HDL afterwards. This method has shown a very good correlation with the data from the analytical and preparative ultracentrifuge. The aim of this work is to use this method to analyse HDL2 and HDL3 levels in a population living in our district. We studied 163 subjects considered as ‘normal’ on the basis of anamnestic and clinical evaluation and routine analysis and 47 subjects with familial hyperlipoproteinemia (types IIa, IIb, and IV). The results obtained confirmed both the difference in HDL and particularly HDL2 levels between the sexes which other authors had observed with reference methods, and the significant negative correlation between plasma triglycerides and HDL2 levels. This method may be applied easily, is rather cheap and, therefore, may be used more often in future.

Platelets from patients with familial hypercholesterolemia (type IIa hyperlipoproteinemia), a condition associated with a high prevalence of atherosclerosis and its ischemic complications, are claimed to be hyperresponsive to aggregating stimuli. We investigated the platelet responsiveness to and the binding of PGD2, a potent endogenous inhibitor of platelet aggregation via stimulation of adenylate cyclase, in a group of 7 patients affected by IIa hyperlipoproteinemia (IIa HLP) and in a control group of 10 healthy subjects. Inhibition by PGD2 of ADP-induced platelet aggregation was significantly lower in Ila HLP patients than in controls. The number of binding sites for PGD2 of platelets from IIa HLP patients was significantly reduced in comparison with that from controls (93 ± 19 and 232 ± 23 receptors/ platelet, respectively), whereas the affinity for PGD2 was comparable to that of controls (Kd = 68.8 ± 19.8 nM in patients and 66.1 ± 15.9 nM in controls). The reduced number of platelet PGD2 binding sites in IIa HLP patients may account for the impaired sensitivity to PGD2 shown in vitro by platelets and may contribute to the increased tendency to thrombotic manifestations observed in IIa HLP.

Twenty subjects with familial hypercholesterolemia (12 Type IIa and 8 Type IIb), previously treated with Colestipol for 16 months, were subjected to therapy with Colestipol (15 g/day) + clofibrate (2 g/day) for 15 months. During the second treatment period these patients continued to follow the isocaloric hypocholesterolemic diet initiated during the original trial. In Type IIa patients, the association of these drugs enhanced the decrease in plasma cholesterol levels. The total mean decrease was -40 +/- 17 mg/dl (P less than 0.05). In Type IIb patients, on the other hand, the association of clofibrate with Colestipol induced an increase in plasma cholesterol levels. The total mean increase was +24 +/- 7 mg/dl (P less than 0.05). A markedly significant decrease in plasma triglyceride levels was observed in this group (- 107 +/- 30; P less than 0.01). These results seem to indicate that, in Type IIa, clofibrate increased the resin's hypocholesterolemic effect. In Type IIb, on the other hand, the association of these drugs did not seem to be indicated since a marked hypotriglyceridemic effect was accompanied by an increase in plasma cholesterol levels. These results are briefly discussed in the light of recent data obtained on the effects of Colestipol and clofibrate on lipoprotein metabolism.

Important clinical signs are usually not present in analbuminaemia, a congenital condition inherited as an autosomal recessive trait, but several biochemical alterations in proteins, cholesterol, phospholipids and plasma beta lipoproteins have been observed. We studied two sibs, R.U. and R.R., with this disease and observed a striking increase in the variables mentioned above as well as a high LDL fraction with concomitant increase in apo B; increases in HDL3 and apo A-I and A-II levels were also observed. The lipoproteins, however, were not altered in morphology but showed a slight increase in lipid/protein ratio. Post-heparin lipolytic activity was normal in the male patient and reduced in the female while LCAT enzyme activity instead was increased in both. Fatty acids bound to phospholipids and serum cholesterol were mostly monounsaturated. Free fatty acid concentration was normal and they appeared mostly bound to the LDL and HDL3 fractions, which are increased in this disease and appear to replace albumin in one of its main carrier functions.

Results related to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolaemia, 12 with Type IIA, 8 with Type IIB and 3 homozygotes are reported. Patients were given 15 g/day active drug for a period of 12 months and a double dose (30 g/day) for a successive period of 4 months along with a low cholesterol, low saturated fat, polyunsaturated fat-rich diet. Mean cholesterol decrease was --42 +/- 18 mg/dl (P less than 0.05) after 12 months of 15 g/day Colestipol and --69 +/- 17 mg/dl (P less than 0.01) after the following 4 months of 30 g/day Colestipol. The difference between the two periods of treatment (15 g and 30 g/day was not statistically significant. A slight but not significant increase in triglyceride levels was observed. Serum uric acid showed a significant increase throughout the entire period of treatment. No malabsorption syndrome or signs of toxicity were seen. Most frequent side effects were constipation, nausea, and metheorism which, with the exception of 4 cases which were withdrawn from the study, were reported as being transitory and mild.

Cholesterol levels in high density lipoprotein subfractions (HDL2 and HDL3) were evaluated in 69 patients (55 males, average age ± sd 58.3 ± 8.8 , and 14 females, average age ± sd 63.1 ± 10.3 ) with extra-coronary arteriosclerosis (lower limbs, supraaortic trunks and both sites), and in 79 healthy age-matched control subjects. HDL cholesterol was significantly reduced in male and female patients. The HDL cholesterol decrease was due to a fall in both HDL2 and HDL3 cholesterols; nonetheless, an analysis of the HDL2-cholesterol/HDL3-cholesterol ratio disclosed that HDL2 cholesterol was the most reduced. Slightly higher plasma cholesterol and triglyceride levels were found in the patients as well as a higher plasma cholesterol/ HDL-cholesterol ratio. On the contrary, the HDL2-cholesterol/HDL3-cholesterol ratio was significantly reduced in the patients. These preliminary findings suggest that, as in ischemie heart disease, the HDL cholesterol reduction in cerebral and peripheral arteriosclerosis is also mainly due to a reduction in the HDL2 subfraction. These results also lend further support to the proposal that determination of the HDL subfractions is useful for a better assessment of the risk profile for arteriosclerosis.

Ten patients suffering from various types of hyperlipoproteinaemia, including a brother and sister with familial hyperchylomicronaemia, were treated with a tetralin derivative (Ciba Su-13′437) for a period of 11 months. The treatment involved an initial monthly period with placebo and another one of 112 months starting 4 months after the beginning of the experiment. The drug was well tolerated and signs of toxicity or side-effects were not observed. In the 2 patients with exogenous hyperchylomicronaemia the effect was very slight or absent; in the 4 patients with hyperbetalipoproteinaemia an average total decrease of cholesterol of 20% in the first stage of the treatment and of 22% in the second stage was observed. In the 4 patients with hyperprebetalipoproteinaemia the average total decrease of cholesterol was 39% during the first period of treatment and 35% during the second period. On the other hand, the decrease of triglycerides was 79% and 82% respectively. These results confirm the efficacy of the Ciba preparation Su-13′437 in the treatment of hyperlipidaemia, and in particular its remarkable action in the treatment of the hypertriglyceridaemia. No significant response was observed in the 2 patients with familial hyperchylomicronaemia.

BACKGROUND The evaluation of nutritional status is one of the primary components of multidimensional geriatric assessment. We investigated the relationship between some markers of malnutrition and the modifications in functional status in a sample of older disabled residents living in nursing homes. METHODS Ninety-eight subjects who were independent in at least two activities of daily living (ADLs) were enrolled in a 2-year longitudinal study. Anthropometric, nutritional, and metabolic parameters, as well as body composition, were measured at baseline and after 2 years. RESULTS Deteriorating functional status (> or =2 additional lost ADLs) was associated with baseline albumin levels (Tertile 3 vs Tertile 1; odds ratio [OR] 0.16, 95% confidence interval [CI] 0.04-0.67) and subscapular skinfold thickness (Tertile 3 vs. Tertile 1; OR 0.06, 95% CI 0.006-0.50). After multivariate adjustment, the OR for increasing disability was >4 in subjects with decreasing body cell mass (BCM), compared with subjects with a stable BCM. The degree of BCM reduction was strongly related to the number of additional ADLs lost at follow-up (test for trend, p = .003). CONCLUSIONS In a sample of older disabled nursing home residents, signs of malnutrition seem to predict further worsening in functional status. Furthermore, BCM declines proportionally to the loss in ADLs, suggesting the existence of a strong relationship between BCM loss and the progressive deterioration of functional status.

Background and aims: In older persons, anemia is a common medical disorder and is often associated with comorbidity and poor health outcomes. We evaluated the relationship between anemia and physical disability in a sample of older hospitalized patients, taking into account the role of comorbidity. Methods: Cross-sectional analysis of the baseline data of the Italian Group of Pharmacoepidemiology in the Elderly Study. Patients aged 65 years or older (n=10,903), admitted to participating centers in the 1993–1998 survey period, were included. Anemia was defined according to the World Health Organization (WHO) criteria; physical disability was defined as need for assistance in performing at least one Activity of Daily Living (ADL) in the week before admission. Comorbidity was ascertained using the Charlson Index. Results: Prevalence of anemia was 41.1%. In the unadjusted analysis, anemia was associated with increased likelihood of disability, in both women (Odds Ratio [OR]: 1.54; 95% Confidence Interval [CI]: 1.38–1.71) and men (OR 1.70; CI 1.52–1.90). After inclusion of demographics and life-style factors in multivariate analysis, the strength of association was only modestly attenuated, whereas nutritional factors and disease-related variables resulted in a greater reduction of the strength of association. In analyses stratified by comorbidity severity, the association between anemia and disability was statistically significant only in patients with the lowest comorbidity levels (p for anemia*Charlson Index interaction term

Serum lipid, lipoprotein and apoprotein parameters were evaluated in 15 patients (7 males and 8 females) with Friedreich’s ataxia. Serum lipid levels in patients showed no significant differences compared to controls. Small reduction in serum phospholipid and in total HDL and HDL3 cholesterol levels were observed, and the female patients presented a slight reduced total cholesterol level; among the serum apoproteins, apo B was reduced only in the males. The most interesting findings concerned the lipoproteins, since both lipid and protein masses of the VLDL, LDL and HDL2 fractions were reduced. In reference to lipoprotein composition, however, HDL2 was the most modified fraction, showing an important protein reduction. From this point of view, this lipoprotein seems the most responsible for the changes observed in our patients. The meaning of this modified lipoprotein pattern in the pathophysiology of Friedreich’s ataxia is not clear.

Plasma glucose has been regarded as a risk factor for macrovascular complications in diabetes, but less is known about its role in the development of cardiac impairment other than coronary heart disease (CHD). The aim of our study was to determine the relationship between basal and post-OGTT (Oral Glucose Tolerance Test) plasma glucose levels and some ECG parameters in a group of elderly women with normal or impaired glucose tolerance (IGT). One-hundred and one women with normal fasting glucose (

Several pieces of evidence support a role of inflammatory processes in the pathogenesis of atherosclerosis; it is also known that endothelial dysfunction is the initial lesion of the atherosclerotic process. Among other markers of endothelial dysfunction, some adhesion molecules seem to play an interesting role. The aim of the present study was to evaluate the effect of atorvastatin vs placebo on some indexes of leukocytes adhesion in a group of Type 2 diabetic patients. Twenty-five Type 2 diabetic patients free from microangiopathic complications and with LDL-cholesterol lower than 180 mg/dl were randomized to receive either atorvastatin (T2DA) or placebo (T2Dp) for twelve months. BMI, fasting plasma glucose, glycated hemoglobin (HbA1c), albumin excretion rate (AER), lipid profile, and serum concentrations of vascular cell adhesion molecule-1 (VCAM1), E-selectin and cadherin-5 were measured at baseline and at the end of the follow-up. At T0 E-selectin was 16 +/- 6 ng/ml in T2DA and 17 +/- 13 in T2Dp; VCAM1 was 413 +/- 112 ng/ml in T2DA and 411 +/- 112 in T2Dp. At T12 VCAM1 and E-selectin did not vary in T2Dp, while a significant reduction was observed in T2DA (VCAM1 275 +/- 104 ng/ml and E-selectin 8 +/- 3 ng/ml; p0.001 and p0.01, respectively). T2DA also showed a reduction of total and LDL cholesterol and an improved glycemic control respect to T2Dp. Hypolipidemic therapy was the strongest independent predictor of the cytokines variations along the time. These results confirm the role of statins in modulating endothelial function also in Type 2 diabetes, outlining a therapeutic role of these molecules probably independent from the hypolipidemic effect.

Hyperammonemia, with confusion and lethargy, developed in a 83-year-old woman during a urinary tract infection by Morganella morganii, a urea-splitting Gram-negative bacillus. In this patient, it is thought to have resulted from the production of excessive amounts of ammonia due to bacterial urease and its subsequent reabsorption into systemic circulation. The patient was treated with specific antibiotic therapy, with resolution of the urinary tract infection, progressive reduction in ammonia blood levels, and a parallel improvement in her consciousness and cognitive status.

Dementia is one of the most pressing public health problems with social and economic implication. The form called cognitive impairment non-dementia (CIND)represents a subclinical phase of dementia. Different studies have shown a possible effect of micro- and macro-nutrients on cognitive function. Trace elements, being involved in metabolic processes and redox reactions in the central nervous system (CNS), could influence the cognitive functions. This study evaluated the presence of an eventual correlation between serum trace element concentrations and cognitive function in a group of subjects with CIND and manifest dementia (Alzheimer dementia = AD, and vascular dementia = VaD), and compared them with a control group. Thirty -five patients were enrolled in this study. Each patient underwent a clinical and biochemical examination. We also performed a neuropsychological and functional assessment (the Milan overall dementia assessment = MODA, activities of daily living = ADL, and instrumental activities of daily living = IADL), and a computerized tomographic (CT) cerebral scan. Patients were than divided in 4 groups according to the obtained diagnosis (Controls, CIND, AD, VaD). The presence of any acute or chronic conditions, affecting cognitive functions, was considered as exclusion criteria. A blood sample was collected to determine iron (Fe), zinc (Zn), manganese (Mn), selenium (Se), cobalt (Co), chromium (Cr), copper (Cu),molybdenum (Mo) and aluminium (Al) serum concentrations (chromatographic,spectrophotometric methods). In our cohort we found a positive correlation between cognitive function, expressed as the MODA score, and Se, Cr, Co and Fe serum levels,while a negative correlation was observed between MODA score, Cu and Al serum levels.Moreover, some statistically significant differences in Se, Cr, Co, Cu and Al concentrations were found among the groups. According to these results, we may suppose that Se, Cr and Co protect cognitive function, Cu influences the evolution of cognitive impairment, while Al contributes to the pathogenesis of AD.

Hormone replacement therapy (HRT) seems to have a favorable influence on the plasma lipid profile. Only a few investigations have examined the effects of HRT versus hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors. We compared the relative effects of different hypolipidemic strategies on lipoproteins and coagulative parameters in women with recent-onset spontaneous menopause. In this 24-week, placebo-controlled trial, 60 consecutive healthy women aged [ge ] 45 years, with amenorrhea from 6 to 60 months (mean, 1.9 [plusmn] 1.4 years), serum follicle stimulating hormone (FSH) greater than 40 U/L, and slight to moderate hypercholesterolemia (low-density lipoprotein-cholesterol [LDL-C] 160 to 250 mg/dL, high-density lipoprotein-cholesterol [HDL-C] [lt ] 75 mg/dL, and triglycerides [lt ] 200 mg/dL) were enrolled and randomized to dietetic advice (placebo group), simvastatin 10 mg, 0.625 mg of conjugated equine estrogen (CEE), or 50 [mu ]g estrogen transdermal patch (ETP). In the latter 2 cases, the progestative nomegestrol was added to estrogens (days 17 to 28 of the cicle). Lipoprotein parameters were evaluated after separating very[ndash ]low-density lipoproteins (VLDLs) by ultracentrifugation, while fasting glucose and insulin, homocysteine, and hemocoagulative parameters were determined in plasma. Fifty-four patients completed the trial. Total cholesterol (TC) and LDL-C significantly decrased in the simvastatin ([minus ]62 mg/dL [[minus ]20%] and [minus ]72 mg/dL [[minus ]30%], respectively), CEE ([minus ]42 mg/dL [[minus ]13%] and [minus ]45 mg/dL [[minus ]18%]), and ETP ([minus ]30 mg/dL [[minus ]10%] and [minus ]26 mg/dL [[minus ]11%]) groups compared to baseline, but only simvastatin showed an effect significantly superior to diet alone. Apolipoprotein (Apo) B was decreased by simvastatin ([minus ]25%, P [lt ] .001) and by CEE ([minus ]10%, P [lt ] .05); again, simvastatin was more effective than either diet or ETP. Triglyceride concentration and VLDL-C were unmodified by treatments. HDL-C and Apo A-I significantly increased in the simvastatin group (+18% and +8%, respectively), while HDL-C was unmodified by both HRT regimens and Apo A-I was reduced by ETP treatment ([minus ]17%); lipoprotein[a] (Lp[a]) was decreased by both HRTs ([minus ]38%, P [lt ] .05, and [minus ]22%, P = .07, for CEE and ETP, respectively). Among coagulative parameters, plasminogen activator inhibitor-1 (PAI-1) was significantly reduced by CEE ([minus ]29%, P [lt ] .05) but not ETP treatment (+16%, P = not significant), while fibrinogen, antithrombin, and homocysteine were unaffected by therapy. Thus, HRT, particularly CEE, seems well tolerated and moderately effective in improving the lipid pattern and, perhaps, the coagulative/fibrinolytic balance in postmenopausal hypercholesterolemic women; it may represent a therapeutic option in slightly dyslipidemic subjects. Statins are preferred in case of more severe disease.