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Biomedical subjects

J J Altman

Publications and source records attributed to J J Altman.

At least 37 records · Page 2Linked to original sources
PubMed1992

Lipoprotein(a) in diabetic patients with and without chronic renal failure.

OBJECTIVE: To examine the distribution of Lp(a) plasma levels in patients with IDDM and NIDDM, and in nondiabetic and IDDM patients with chronic renal failure. RESEARCH DESIGN AND METHODS: Cross-sectional study of Lp(a) plasma levels in a population of diabetic patients with stable metabolic control, with simultaneous determination of plasma lipids, fasting plasma glucose, and HbA1. Thirty-six patients with IDDM, 90 with NIDDM, and 41 with chronic renal failure (20 IDDM, 21 nondiabetic) were compared with 78 control subjects. RESULTS: Lp(a) plasma levels were significantly higher in IDDM and NIDDM patients, as well as in nondiabetic and IDDM patients with chronic renal failure compared with control subjects. No correlation was observed between Lp(a) and lipid plasma levels, fasting plasma glucose, and HbA1. CONCLUSIONS: Lp(a) may contribute to the increased prevalence of atherosclerotic disease in diabetic patients and patients with chronic renal failure, especially in IDDM patients whose lipoprotein pattern was not different from that of the control group.

Adult↗
PubMed1990

Transjugular renal biopsy.

A novel technique to obtain renal biopsy specimens from patients in whom percutaneous renal biopsy is contraindicated is described. After adaptation of equipment used for transjugular liver biopsy, 50 such patients underwent transjugular renal biopsy: specimens of renal tissue were obtained from 44 patients, and glomeruli were found in 38 specimens. No major complications were observed and histological examination of the biopsy specimens led to changed diagnosis or management in 13 patients. Transvenous renal biopsy should be considered when percutaneous biopsy is contraindicated or has failed.

Aged↗
PubMed1990

[Implantation of pancreatic islets in arteriolar epiploic flap. Preliminary note on 3 cases].

Presently, no long-term insulin withdrawal after islet graft in a diabetic patient has been reported. From October 1988 to December 1989 we have performed 3 pancreatic islet grafts in 3 type I diabetic patients. Islets were isolated from pancreatic glands collected during multiple organs harvesting. Implantation was conducted in an original site, by an arteriolar embolization of an epiploic flap pedicled from the right gastroepiploic vessels. Those grafts were combined twice with a kidney and in one occasion with a liver transplant. After 15 months, this last case is an unique metabolic success with complete insulino-independence. Endogenous insulin-secretion determined by C-peptide measurement was not detectable before surgery but was normalized and stimulable 6 months after the graft. Insulin injections were stopped one month later. Blood glucose is fully normal since 8 months without insulin. For the two other cases with kidney transplants after two months, endogenous insulin is already detectable. Compared with 3 segmental pancreatic grafts performed during the same period, islet graft in diabetic patients appears as a promising approach.

Adult↗
PubMed1989

[Hyperphosphoremia and hypophosphoremia].

Disorders of phosphate metabolism are caused by a disrupted balance between intestinal absorption and renal excretion or by an altered distribution between intra- and extracellular pools. Hyperphosphatemia per se does not have any clinical effects except for ectopic calfifications. The most frequent cause is chronic renal disease. Other causes - increased tubular reabsorption as seen for instance un hypoparathyroïdism; increased intertinal absorption as seen with vitamin D excess; redistribution to the extracellular pool, as seen with the tumor lysis syndrome, are uncommon; and no one cause is outstanding in frequency. Hypophosphatemia is frequent caused by a redistribution of phosphate to the cellular pool, associated for instance with respiratory alkalosis or infusion of glucose and fructose. Hyperphosphaturia as a cause of hypophosphatemia is seen in primary and secondary hyperparathyroïdism as well as in familial hypophosphatemic rickets. Decreased intake of phosphate may be secondary to intravenous hyperalimentation, chronic ingestion of phosphate-binding antacids or vitamin D deficiency. Hypophosphatemia does not appear to produce any harmful effects. However acute hypophosphatemia, if it occurs in the presence of preexisting cellular injury and phosphate depletion, as in chronic alcoholic patients for instance, has been implicated as a cause of severe clinical syndromes. Chronic hypophosphatemia in children may induce rickets, and osteomalacia in adults.

Humans↗