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1.
PLoS One ; 12(10): e0186220, 2017.
Article in English | MEDLINE | ID: mdl-29073236

ABSTRACT

AIM: To describe the prevalence of Peripheral Artery Disease (PAD) in a random population sample and to evaluate its relationship with Mediterranean diet and with other potential cardiovascular risk factors such as serum uric acid and pulse pressure in individuals ranged 45 to 74 years. METHODS: Cross-sectional analysis of 1568 subjects (mean age 6.5 years, 43% males), randomly selected from the population. A fasting blood sample was obtained to determine glucose, lipids, and HbA1C levels. An oral glucose tolerance test was performed in non-diabetic subjects. PAD was evaluated by ankle-brachial index and/or having a prior diagnosis. RESULTS: PAD prevalence was 3.81% (95% CI, 2.97-4.87) for all participants. In men, PAD prevalence was significantly higher than in women [5.17% (95% CI, 3.74-7.11) vs. 2.78% (95% CI, 1.89-4.07); p = 0.014]. Serum uric acid in the upper quartile was associated with the highest odds ratio (OR) of PAD (for uric acid > 6.1 mg/dl, OR = 4.31; 95% CI, 1.49-12.44). The remaining variables more strongly associated with PAD were: Heart rate >90 bpm (OR = 4.16; 95%CI, 1.62-10.65), pulse pressure in the upper quartile (≥ 54 mmHg) (OR = 3.82; 95%CI, 1.50-9.71), adherence to Mediterranean diet (OR = 2.73; 95% CI, 1.48-5.04), and former smoker status (OR = 2.04; 95%CI, 1.00-4.16). CONCLUSIONS: Our results show the existence of a low prevalence of peripheral artery disease in a population aged 45-74 years. Serum uric acid, pulse pressure and heart rate >90 bpm were strongly associated with peripheral artery disease. The direct association between Mediterranean diet and peripheral artery disease that we have found should be evaluated through a follow-up study under clinical practice conditions.


Subject(s)
Diabetes Mellitus, Type 2/diagnosis , Peripheral Arterial Disease/epidemiology , Prediabetic State/diagnosis , Aged , Diabetes Mellitus, Type 2/complications , Female , Humans , Male , Middle Aged , Peripheral Arterial Disease/complications , Prediabetic State/complications
2.
Rev Prat ; 39(11): 917-22, 1989 Apr 13.
Article in French | MEDLINE | ID: mdl-2717863

ABSTRACT

More than 99 p. 100 of calcium and 90 p. 100 of phosphorus are located in the bone tissue in the form of hydroxy-apatite crystals. Plasma ionized calcium is very tightly regulated, in order to stabilize the membranes of excitable cells, such as nerve and muscle. The PTH-1,25 (OH)2 D axis, triggered by very small variations in plasma ionized calcium (negative feedback) is the major control system of intestinal absorption, movements between bone cells and extracellular fluid, and tubular reabsorption of calcium by the kidney. Thus, usual variations in dietary intake induced no detectable change in plasma calcium and only small variations in 24 h-urinary calcium excretion rate. Plasma phosphate fluctuates over 24h-periods, and homeostatic mechanisms seem to control the concentration and/or content of phosphate in soft tissue cells (phosphate is necessary to ATP-synthesis and phosphorylation of intermediate metabolites). The PTH-1,25 (OH)2D axis which is not triggered by variations in plasma phosphate, does not control tightly intestinal absorption, movements between bone cells and extracellular fluid, or tubular reabsorption of phosphate by the kidney. However, the phosphate reabsorption in the proximal tubule of the kidney is rigidly adjusted to the phosphate available in the digestive lumen and the phosphate needs of soft tissue cells, probably via as yet undetermined factor(s). Thus, usual variations in dietary phosphate intake influence notably the plasma concentration and 24 h-urinary excretion rate.


Subject(s)
Calcium/metabolism , Phosphorus/metabolism , Adaptation, Physiological , Bone and Bones/metabolism , Calcitriol/metabolism , Humans , Intestinal Absorption , Kidney/metabolism , Phosphates/metabolism
3.
Rev Prat ; 39(11): 959-63, 1989 Apr 13.
Article in French | MEDLINE | ID: mdl-2717869

ABSTRACT

The first thing to do is to confirm that the number of circulating calcium ions has really decreased. This is achieved either by correction of the total blood calcium level, taking into account possible variations in albuminaemia and pH, or by direct measurement of plasma calcium ions, using a special electrode. The aetiological diagnosis may be easy in some clinical situations, but it often demands a systematic approach, which implies a specialized and brief exploration, feasible in out-patients, with simultaneous measurement, under basal conditions, not only of plasma calcium ions, but also of plasma magnesium, intact 1-84 parathyroid hormone (PTH), nephrogenic cyclic AMP and 25 (OH) D. Rationally, hypocalcaemias may be divided into two groups : (1) extraparathyroid, where hyperparathyroidism is constant and hypocalcaemia is due either to calcium intake reduction, vitamin deficiency of high bone accretion, or to a primary renal calcium leakage; (2) parathyroid, by impaired secretion of PTH or alteration of PTH receptors, which means hypoparathyroidism or pseudohypoparathyroidism. The diagnostic and therapeutic possibilities in both groups are discussed.


Subject(s)
Hypocalcemia/etiology , Hypoparathyroidism/complications , Vitamin D Deficiency/complications , Adult , Calcitriol/deficiency , Humans , Hypocalcemia/therapy , Hypoparathyroidism/diagnosis , Vitamin D Deficiency/therapy
4.
Miner Electrolyte Metab ; 15(6): 321-5, 1989.
Article in English | MEDLINE | ID: mdl-2615719

ABSTRACT

A marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica has been achieved by the intravenous administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. In a recent survey of 306 patients with primary hyperparathyroidism (PHPT), we hypothesized that the far higher degree of parathyroid hormone (PTH) hypersecretion in PHPT with osteitis fibrosa cystica than in PHPT without overt bone disease might be due to the absence of suppression of hormonal hypersecretion by the low-to-normal circulating 1,25(OH)2D reflecting a relative vitamin D deficiency. To test this hypothesis, a patient having hypercalcemic PHPT with florid osteitis fibrosa cystica and normal serum 1,25(OH)2D was given increasing daily doses of intravenous calcitriol (0.5-2 micrograms) for several days. Doubling the level of circulating 1,25(OH)2D from 48 to 100-114 pg/ml was accompanied by a marked decline (46%) in serum iPTH(1-84), without a change in the serum calcium concentration. A lowered set point of parathyroid cells for calcium, and a diminished maximum secretory rate of PTH, may contribute to the marked suppression of PHPT.


Subject(s)
Calcitriol/therapeutic use , Hyperparathyroidism/drug therapy , Osteitis Fibrosa Cystica/drug therapy , Calcium/administration & dosage , Calcium/blood , Female , Humans , Hyperparathyroidism/complications , Injections, Intravenous , Middle Aged , Osteitis Fibrosa Cystica/complications , Vitamin D Deficiency/complications , Vitamin D Deficiency/drug therapy , Vitamin D Deficiency/metabolism
5.
Miner Electrolyte Metab ; 15(6): 353-8, 1989.
Article in English | MEDLINE | ID: mdl-2615721

ABSTRACT

Thyroparathyroidectomized rats were studied during control, citrate infusion, and recovery periods to analyze the effects of citrate on urinary calcium excretion. The rats were infused with human PTH-(1-34) at a constant rate throughout the experiments that produced physiologic circulating PTH activity. Ultrafiltrable calcium was measured with a micropartition system while maintaining constant the pH and PCO2 of the sample. The plasma acid-base status, filtered load of calcium, and urinary sodium excretion rate did not vary during citrate infusion. The urinary calcium excretion rate increased from 71 +/- 9 nmol/min/g kidney during control period to 122 +/- 22 nmol/min/g kidney (p less than 0.05) during citrate infusion, and then returned below control levels during recovery period. A strong positive linear relationship was observed between the urinary excretion rates of calcium and citrate (r = 0.88; p less than 0.001). We conclude that tubular fluid citrate inhibits renal calcium reabsorption probably by forming calcium-citrate complexes.


Subject(s)
Calcium/urine , Citrates/pharmacology , Kidney/metabolism , Animals , Calcium/administration & dosage , Calcium/blood , Citrates/blood , Citrates/urine , Extracellular Space/drug effects , Extracellular Space/metabolism , Humans , Kidney/drug effects , Male , Metabolic Clearance Rate , Parathyroid Hormone/pharmacology , Rats , Rats, Inbred Strains , Sodium/pharmacokinetics , Sodium/urine
6.
Miner Electrolyte Metab ; 14(4): 221-8, 1988.
Article in English | MEDLINE | ID: mdl-2850460

ABSTRACT

The characteristics of PTH secretion, which have been extensively studied in vitro with dispersed cells of normal and abnormal parathyroid glands, remain poorly studied in vivo. We performed ethylenediamine tetraacetate (EDTA) intravenous infusions in 12 normal subjects and 5 patients with hypercalcemia (serum ionized calcium between 2.72 and 2.89 mEq/l) and surgically proven primary hyperparathyroidism (PHPT) to establish the relationship between nephrogenous cyclic AMP (NcAMP) used as an index of PTH secretion and serum ionized calcium. We determined the maximal NcAMP taken as an index of maximal secretory rate for PTH, the set point and sensitivity of parathyroid cells for calcium. In normal subjects, mean values (+/- SD) were 4.04 +/- 0.47 nmol/dl glomerular filtrate (GF) for maximal NcAMP, 2.23 +/- 0.04 mEq/l for set point, and -250 +/- 58 for sensitivity when NcAMP was expressed in percent of maximal value and serum calcium in mEq/l. In patients with PHPT, the differences between maximal and basal values of NcAMP represented 50% or more of maximal NcAMP, indicating that PTH secretion was suppressible. Sensitivity values were within normal limits in all patients. Calculated set point values were abnormally elevated (between 2.64 and 2.83 mEq/l) in all patients. Maximal NcAMP values ranged from low to normal (2.77 nmol/dl GF) to abnormally high (6.64 nmol/dl GF), and a positive linear correlation was observed with parathyroid cell mass. Basal serum calcium concentrations were not correlated with either parathyroid cell mass or maximal NcAMP values, and were close to calculated set point values for each patient.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Calcium/blood , Hyperparathyroidism/physiopathology , Parathyroid Hormone/metabolism , Adult , Cyclic AMP/urine , Edetic Acid , Glomerular Filtration Rate , Humans , Hyperparathyroidism/blood , Hyperparathyroidism/urine , Male , Middle Aged , Parathyroid Hormone/blood , Phosphates/blood , Reference Values
7.
Kidney Int ; 31(5): 1174-80, 1987 May.
Article in English | MEDLINE | ID: mdl-3599657

ABSTRACT

We studied circulating 1,25(OH)2D3 and its determinants in 102 patients with primary hyperparathyroidism (PHPT), 33 of them with recurrent renal stones, 60 with non-specific symptoms, and nine with overt bone disease. Means for serum 1,25(OH)2D3 and intestinal absorption of calcium were abnormally high in the renal stone group, slightly elevated in the non-specific group, and low-normal in the bone disease group. In the whole population of patients, we found a positive correlation between circulating 1,25(OH)2D3 and creatinine clearance (taken as an index of the functional renal mass). Negative correlations were observed between 1,25(OH)2D3 and age, and between creatinine clearance and age, the latter being not different from that observed in a normal large population. In the renal stone group, means for the determinants of the renal 1 alpha hydroxylase activity, that is, PTH activity expressed as nephrogenous cyclic AMP (NcAMP), serum phosphate and calcium were identical to those of the group with non-specific symptoms. However means for age were lower and functional renal mass significantly higher in the renal stone group, which may account for the higher value of circulating 1,25(OH)2D3. In the bone disease group, means for age, renal mass and serum calcium were identical to those of the group with non-specific symptoms, and NcAMP was far higher and hypophosphatemia more marked, which may not account for the lower value of circulating 1,25(OH)2D3. However, in the bone disease group, serum 25(OH)D was abnormally low, which may limit the renal production of 1,25(OH)2D3 and explain the low-normal circulating values.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Calcitriol/blood , Hyperparathyroidism/pathology , Kidney Calculi/pathology , Kidney/pathology , Bone Diseases/complications , Creatinine/blood , Female , Humans , Kidney Calculi/blood , Male
9.
Presse Med ; 13(29): 1779-85, 1984.
Article in French | MEDLINE | ID: mdl-6235508

ABSTRACT

The availability of accurate and inexpensive methods for measuring serum calcium levels has resulted in a rapid increase in the number of diagnoses of primary hyperparathyroidism, notably in its asymptomatic hypercalcemic forms. In addition, the development of a radioimmunoassay of the parathyroid hormone and, more recently, measurements of nephrogenous cyclic AMP during fasting and after calcium loading have led to the recognition of clinical variants of the disease, such as intermittent or borderline hypercalcemia and pure hypercalciuria with normal calcemia. The degree of hypercalcemia in stable primary hyperparathyroidism depends on renal tubular reabsorption of calcium rather than on bone resorption. The poor correlation observed between calcium tubular reabsorption rate and magnitude of parathyroid hormone hypersecretion suggests that as yet undetermined factors interfere with the effects of parathyroid hormone on renal tubules and probably account for the fluctuations in calcemia reported during serial determinations in patients. The sigmoid relationship between parathyroid hormone release and extracellular calcium concentrations has been analyzed from recent in vitro studies with dispersed parathyroid cells. In primary hyperplasia of the parathyroid glands hypersecretion of parathyroid hormone seems to depend principally upon the increase in tissue mass with normal sensitivity to calcium at cellular levels, whereas in adenoma the primary abnormality responsible for hypersecretion of parathyroid hormone would be an alteration in cell sensitivity to calcium, as indicated by an elevated "set point". Finally, while complicated primary hyperthyroidism requires surgery, our limited knowledge of the natural history of asymptomatic forms makes it impossible to decide which of these patients will ultimately need to be operated upon.


Subject(s)
Hyperparathyroidism/physiopathology , Calcium/blood , Humans , Hypercalcemia/etiology , Hyperparathyroidism/diagnosis , Hyperparathyroidism/therapy , Parathyroid Hormone/metabolism , Retrospective Studies
10.
Lima; Perú. Ministerio de Salud. Escuela Nacional de Salud Pública; 1 ed; Feb. 1974. 45 p. ilus, tab.
Monography in Spanish | MINSAPERÚ | ID: pru-4873

ABSTRACT

La presente publicación señala , a grandes rasgos, las características de la escuela de salud pública, que pueden relacionarse más con el tema que tratan, así como hacer una referencia a aquellas instituciones que constituyen las entidades de los servicios de los egresados(AU)


Subject(s)
Public Health , Schools, Public Health , Schools, Public Health/organization & administration , Scientific and Educational Events , Peru
11.
Lima; Perú. Ministerio de Salud. Escuela Nacional de Salud Pública; 1 ed; Feb. 1974. 45 p. ilus, tab.
Monography in Spanish | MINSAPERÚ | ID: biblio-1181989

ABSTRACT

La presente publicación señala , a grandes rasgos, las características de la escuela de salud pública, que pueden relacionarse más con el tema que tratan, así como hacer una referencia a aquellas instituciones que constituyen las entidades de los servicios de los egresados


Subject(s)
Scientific and Educational Events , Schools, Public Health , Schools, Public Health/organization & administration , Public Health , Peru
12.
Lima; Perú. Ministerio de Salud. Escuela Nacional de Salud Pública; 1 ed; 1970. 41 p. ilus.(Serie Trabajos Científicos, 8).
Non-conventional in Spanish | MINSAPERÚ | ID: pru-4498

ABSTRACT

En el presente documento se estudia el nivel de salud del lactante y pre-escolar peruano a través de los indicadores negativos (morbimortalidad) y de los factores que están condicionando este nivel de salud(AU)


Subject(s)
Child Health , Infant Welfare , Peru
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