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Biomedical subjects

S De Marchi

Publications and source records attributed to S De Marchi.

88 records · Page 5Linked to original sources
PubMed1983

Glycosylated hemoglobin in chronic alcoholics.

Glycosylated hemoglobin (Hb AI) is commonly accepted as a parameter of the last 2-3 months metabolism of the glucides; therefore its growth must be proportionate to the metabolic unbalance [1]. We observed that chronic alcoholics often had significantly increased levels of Hb AI when compared with normal controls, although with a normal oral glucose tolerance test (OGTT); we therefore tried to correlate other metabolic factors with glycosylated hemoglobin: uricemia, triglyceridemia, cholesterolemia and high density lipoprotein (HDL)-cholesterol.

Adult↗
PubMed1983

More on the increase of hemoglobin A1 in chronic renal failure: the role of acidosis.

In chronic renal failure both Hb A1 and Hb A1c levels have been reported to be elevated. In order to investigate the causes of such increase we measured Hb A1 (cation-exchange chromatography), blood urea nitrogen, arterial blood pH and plasma bicarbonate in 40 patients with chronic renal failure receiving conservative treatment, 45 uremic patients on intermittent hemodialysis and 60 subjects with normal renal function. In patients with chronic renal failure Hb A1 highly correlates with arterial blood pH and plasma bicarbonate, thus emphasizing the major role played by uremic acidosis in the increased Hb A1 fraction in chronic renal failure.

Acidosis, Renal Tubular↗
PubMed1983

Is renal glycosuria a benign condition?

HLA typing and a range of autoantibodies were evaluated in five families affected with type A renal glycosuria. HLA typing demonstrates that this inherited disease is controlled by an autosomal dominant gene located on chromosome six in close genetic linkage with the HLA complex. All affected family members have significant titres of autoantibodies to nuclear antigens, native DNA, smooth muscle, mitochondria, liver antigens, thyroglobulin, thyroid microsomes and renal tubule brush border with variable association. This suggests that renal glycosuria is a complex HLA-linked disease with increased susceptibility to multiple autoantibody production and this urges caution with respect to its classical definition as a benign condition.

Adolescent↗
PubMed1983

Origin of glycosylated hemoglobin A1 in chronic renal failure.

In chronic renal failure both HbA1 and HbA1c levels have been reported to be elevated. In order to investigate the causes of such increase we measured HbA1 (cation-exchange chromatography), blood urea nitrogen, arterial blood pH, plasma bicarbonate, phosphatemia, serum iron and serum ferritin before dialysis in 60 uremic patients receiving long term hemodialysis. The increased levels of HbA1 do not correlate with glucose intolerance, phosphatemia, blood urea nitrogen, time averaged concentration of urea, serum iron and serum ferritin. On the contrary the presence of a highly significant correlation between HbA1 and arterial blood pH (p less than 0.001) and between HbA1 and plasma bicarbonate (p less than 0.001) seems to emphasize a major role for acidosis in increasing the HbA1 levels in uremic patients on long term hemodialysis.

Acidosis↗
PubMedDate not supplied

Clinical and circulatory effects of Iloprost either administered for 1 week or 4 weeks in patients with peripheral obstructive arterial disease at Leriche-Fontaine stage III.

BACKGROUND: Iloprost therapy for severe peripheral obstructive arterial disease (POAD) has demonstrated to be effective in reducing the need for amputation. However the feasibility of a 28-day infusion regimen in less severe stages of the disease is poor due to the length in hospital stay. A randomized, controlled, parallel-group pilot study was carried out with the aim to evaluate clinical and circulatory effects of Iloprost, a stable prostacyclin analogue, administered with two different infusion schedules to patients with POAD at Leriche Fontaine stage III. METHODS: Twenty patients 16 males and 4 females, mean age 66 +/- 6 years) with objective signs of POAD, rest pain for at least two weeks and posterior tibial artery pressure > 50 mmHg, were randomized to either Iloprost i.v. infusion up to 2 ng/Kg/min for 6/h/day for 28 days (Group A) or to Iloprost i.v. infusion up to 1.5 ng/Kg/min for 16/h/day for 7 days (Group B). At baseline (before starting first infusion) after 7 days (for group B only, end of therapy) and after 28 days (end of therapy for Group A, end of study for Group B) the following parameters were evaluated: walking distance, rest pain and analgesic consumption, plethysmographyc parameters (first flow, peak flow and peak flow time) and laser Doppler parameters (rest flow, post ischemic flow). RESULTS: After 28 days, both Iloprost infusion schedules increased walking capacity (maximum walking distance/pain free walking distance +119/+84% +199/+85% respectively, for Group A and B respectively) reduced ischemic pain (-45% and -48% respectively for Group A and B) and analgesic consumption and improved plethysmographyc and laser Doppler parameters. Tolerability seemed to be better in Group B, suggesting that the lower dose and the shorter duration of the therapy period might result in reduced incidence of headache thus, in principle, increasing patient acceptability. CONCLUSIONS: The results of this pilot study, if confirmed by larger trials, could have important positive implications in terms of costs, patient comfort and management.

Aged↗
PubMedDate not supplied

[Neonatal hypoxic-ischemic nephropathy and urinary diagnostic indices: the utility of measuring tubular enzymes (NAG and AAP)].

Feto-neonatal hypoxia can cause a functional kidney impairment, which is often temporary and not clinically overt, but sometimes leading to acute renal failure. Hypoxic stress may result in a tubulo-interstitial damage, and kidney tubular enzymes determination has proved to be an easy, early, and non invasive method to define a tubular interstitial lesion. A major target of nephrotoxicity is the proximal tubular cell: alterations in brush-border membrane and cytoplasm result in increased turnover processes in the kidney cortex, following by a corresponding increased excretion of alanine-aminopeptidase (AAP) and N-acetyl-glucosaminidase (NAG) from the proximal tubular cells, long before glomerular or tubular functions are impaired. AAP and NAG excretion is directly correlated with the strength and the duration of toxic alteration of the proximal tubule. NAG and AAP have been already studied in the adults and the children; they have been chosen for this investigation with a double aim: 1) to define the amount of their urinary excretion in relation with gestational age at birth; 2) to evaluate if in the newborn, independently of the gestational age, their urinary concentration may be increased by ischaemic conditions caused by hypoxia. We studied 52 healthy newborns (7 preterm of 33-36 weeks and 45 full-term) and 16 newborns with feto-neonatal hypoxia (8 preterm of 26-36 weeks and full-term) at the forth day of life. Urinary NAG and AAP were assayed by colorimetric methods and the results expressed as mU/mg. creatininuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMedDate not supplied

[Clinical and biological significance of the correlation between glycosylated hemoglobin, blood uric acid and blood triglycerides].

An example of the correlations between sugar, fat and protein metabolisms is presented and discussed. The example is taken from a group of patients subjected to outpatient metabolic tests, among whom a sub-group was found to have a higher glycosylated haemoglobin level due to unusually high levels of uricaemia and triglyceridaemia (P less than 0.001). Alcohol abuse, common to all these patients, may explain the simultaneous increase in uricaemia and triglyceridaemia, while the increase in Hb A1, might be caused dy the hyperinsulinism provoked by the first two. Altogether these alterations may put the patients at serious risk of atherogenesis, especially considering the role of insulin in regulating the fat metabolism of the arterial wall.

Adult↗
PubMedDate not supplied

Effects of sustained-release isradipine on blood pressure and peripheral hemodynamics in hypertensive patients.

In a double-blind crossover study, 16 hypertensive patients (mean age, 41 years) were randomly assigned to receive placebo or 5 mg of an extended-release formulation of isradipine for 30 days. Blood pressure and heart rate were recorded by an automatic device and hemodynamics measured by a duplex scanner and plethysmography. After the first dose and after 30 days' treatment with isradipine, blood pressure was significantly reduced (mean arterial pressure 4 hours after the first dose, 106 +/- 3 vs 120 +/- 4 mmHg, P < 0.01; 22 hours after the last dose, 108 +/- 3 mmHg, P < 0.01) with no significant changes in heart rate. The compliance of the brachial artery was significantly increased (2.823 +/- 0.358 vs 1.204 +/- 0.156 dyn-1.cm4.10(-7), P < 0.002) and the characteristic impedence decreased (49 +/- 6 vs 91 +/- 12 dyn.s.cm-5.10(2), P < 0.05) as well as local resistances (71 +/- 5.6 vs 198 +/- 18 mmHg.ml-1.s, P < 0.001). After 30 days of isradipine treatment, 22 hours after the last dose, compliance was still increased (2.575 +/- 0.453 dyn-1.cm4.10(-7), P < 0.01) whereas impedance and forearm vascular resistances were reduced (59 +/- 8 dyn.s.cm-5.10(2), P < 0.05, and 97 +/- 14 mmHg.ml-1.s, P < 0.001, respectively). The results indicate that sustained-release isradipine ensures good blood pressure control up to the time of the following dose and restores the large artery dumping function against cyclic variations in intraluminal pressure.

Adult↗
PubMedDate not supplied

Erythropoietin and the anemia of chronic diseases.

The red-cell mass is continuously adjusted to the optimal size for its function as an oxygen carrier by messages transmitted to the bone marrow from an oxygen sensor in the kidney. These messages are mediated by the hormone erythropoietin. Erythropoietin is a glycoprotein growth factor synthesized by cells adjacent to the proximal renal tubule in response to signals from a renal oxygen-sensing device, probably a heme protein (1). In the bone marrow, erythropoietin binds to and activates specific receptors on the erythroid progenitor cells (2). In the presence of this erythropoietin-receptor complex the progenitor cells continue their predestined development into mature erythrocytes. Erythropoietin was the first hemopoietic growth factor to be molecularly cloned in 1985 (3). Our understanding of the biology and physiology of erythropoietin has been considerably improved with the advent of recombinant human erythropoietin (rHuEpo). During the past 7 years, rHuEpo has undergone extensive testing in clinical trials. It has been approved for treatment of the anemia of chronic renal failure, both in progressive renal failure and endstage renal failure (ESRD). In these instances, the administration of rHuEpo has been used in effect as a substitutive therapy, since patients' erythropoietin levels are very low despite severe anemia, due to the failure of affected kidneys to produce adequate amounts of the hormone. However, the application of rHuEpo has now moved largely from the primitive indication of renal diseases, and the hormone is currently under study in a number of anemic states of different etiologies, even with relatively high serum erythropoietin levels. Among these, some of the best documented indications are the anemia associated with malignancies, either due to neoplastic bone marrow infiltration or to chemotherapy-related myelosuppression, the anemia of myelodysplastic syndromes and AIDS, the anemia of chronic inflammatory diseases, prematurity, and bone marrow transplantation (4). The purpose of this review is to provide a summary of our present knowledge regarding rHuEpo therapy for the anemia of renal failure. We provide some clues for the correct use of rHuEpo in the treatment of the anemia of chronic inflammatory diseases. In addition, we address a series of new issues in the attempt to better understand the relationship between erythropoietin and liver disease.

Anemia↗