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Biomedical subjects

J Aubia

Publications and source records attributed to J Aubia.

At least 37 records · Page 2Linked to original sources
PubMed1989

Epidemiology of fractures of the proximal femur associated with osteoporosis in Barcelona, Spain.

We studied the epidemiology of osteoporotic fractures of the proximal femur (cervical and trochanteric fractures) in residents of Barcelona, aged 45 years or over, for a 1-year period. Fractures resulting from metastases were not included. During the period of observation, a total of 1,358 patients with hip fractures were treated at acute-care hospitals in Barcelona. Of those, 1,163 were researched. For each case, age, sex, and home address were registered. The incidence of hip fractures per 100,000 inhabitants aged 45 years or over was 115.6 in men and 252.2 in women. Age was the most influencing factor in the occurrence of hip fractures. Women presented fractures of the proximal femur more frequently than men. The epidemiological curve was similar to that reported in other western countries, although the crude rate was lower than that found in northern countries. We conclude that osteoporotic fractures of the proximal femur are common processes in the Mediterranean area, and reflect the impact of osteoporosis in our environment; however, the lower incidence compared with northern geographical areas may probably reflect the influence of climatic, ethnic, or other factors.

Aged↗
PubMed1988

Osteodystrophy of diabetics in chronic dialysis: a histomorphometric study.

A decreased incidence of hyperparathyroidism in diabetic uremic patients has been reported, but comprehensive bone histomorphometric studies on uremic diabetic osteodistrophy are scarce. We present here the results of static and dynamic bone morphometry in 13 diabetic patients on dialysis (DCD) and their comparison with a pair-matched group of nondiabetic uremics with similar age, sex, and time on dialysis (NCDC), and with a group of 17 normals (N). Diabetic bone showed: (1) Low trabecular volume (Vt 9.9% in DCD and 22.8% in N), (2) Moderately increased remodeling values of intermediate intensity between N and NDCD values (Sf = 19.3% in DCD, 37.4% in NDCD, and 8.8 +/- 6% in N, Sr = 4.3% in DCD, 7.3% in NDCD and 2.04 +/- 0.9% in N), and (3) Moderate fibrosis (Sfib 1.2% in DCD, 12.9% in NDCD). Besides these confirmatory results, two suggestions emerged from the study: (1) The relative number of cells: osteoclast density (OI) and osteoblasts (Ob/OID) appears to be lower, not only than NDCD values but also lower than N values (OI = 0.04 c/mm. in DCD, 0.31 in NDCD, and 0.14 in N; Ob/OID = 5.58% in DCD, 14.6 in NDCD and 22.12 +/- 9% m N). (2) Dynamic behavior in tetracycline based studies disclosed the appearance of two populations of DCD: a subgroup of preserved calcification dynamics with values not quite different than the NDCD group and a subgroup with a significant derangement of mineralization with no measurable bone trabecular dynamics. This late subgroup also showed significantly lower number of Ob/OID values compared with the former with preserved calcification.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Relative hyperphosphaturia in diabetic chronic renal failure: a protective factor of hyperparathyroidism.

Relative low serum levels of parathormone (PTH) and low incidence of secondary hyperparathyroidism have been reported in diabetic uremic patients. The pathogenesis of this reported resistance to uremic secondary hyperparathyroidism in diabetes remains controversial. We have measured the serum C-terminal parathormone (C-PTH) renal phosphorus threshold (TmPO4) and nephrogenous cyclic AMP (N-cCAMP), in 2-hour urine collection in 22 patients with diabetic nephropathy with moderate chronic renal failure and in 27 controls with similar creatinine clearance values (18.16 +/- 9.14 and and 19.1 +/- 8.47 ml/min). In spite of the lower levels of serum C-PTH (1.07 +/- 0.43 ng/ml) diabetic patients exhibited an increased phosphaturia (TmPO4: 1.97 +/- 0.9 mg/100 ml GFR) when compared with the control group (C-PTH: 2.01 +/- 1.17 mg/ml, and TmPO4: 2.5 +/- 0.7 ml GFR). When the C-PTH values were plotted against the logarithm of creatinine clearance values, both groups showed a significant linear relationship reflecting the progressive increase in PTH when GFR fell. This progressive parathyroid stimulus was also present in diabetic patients but in a lower intensity. We believe that increased phosphaturia in diabetics with moderate chronic renal failure may be a major factor in precluding the appearance of secondary hyperparathyroidism in these patients once they reach the dialysis and transplantation programs.

Diabetic Nephropathies↗
PubMed1987

Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy.

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.

Adult↗