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Biomedical subjects

R Kohan

Publications and source records attributed to R Kohan.

31 records · Page 2Linked to original sources
PubMed1990

Intraperitoneal phosphate administration in hungry bone syndrome.

Hypophosphatemia complicating parathyroidectomy for secondary hyperparathyroidism in renal failure is usually corrected by the oral or intravenous routes. We present a case in which those methods of treatment were not possible, and the phosphate was administered intraperitoneally. Phosphate was added as one molar sodium diphosphate solution to the dialysis fluid. In our case the procedure was well tolerated, phosphate blood levels were rapidly corrected, no alterations in calcium, magnesium or other parameters were detected and the patient was discharged in good condition. In selected cases of hungry bone syndrome after parathyroidectomy, intraperitoneal phosphate can be used safely.

Adult↗
PubMed1989

[Advances in the treatment of acute myeloid leukemia in children. Experience of the Argentinian Group of Acute Leukemia Treatment and the Latin American Group of Malignant Hemopathies Treatment 1967-1987].

Three hundred and seventy-one children below 16 years, with newly diagnosed acute myeloid leukaemia, were included in six consecutive GATLA/GLATHEM protocols, from November 1967 to December 1987. The study was divided in three periods: 1967 to 1975, 1976 to 1982, and 1983 to 1987. Three induction schedules were used during the first two periods, and different maintenance schemes alternating with monthly consolidations were explored; the value of immunotherapy with C. Parvum and androgen therapy with stanozolol was also tested. Protocol 3-AML-83, representing the third period, included a four-week induction phase with vincristine, adriamycin, cytosine-arabinoside, prednisone and 6-mercaptopurine, followed by a consolidation phase with cyclophosphamide, cytosine-arabinoside and 6-mercaptopurine for four weeks. Maintenance phase included daily, oral 6-mercaptopurine, and monthly cytosine-arabinoside, both during two years, and adriamycin every eighth week, for one year. Complete remission rates for the first two periods of therapy were 40% and 55%, whereas that of the last period was 74%. The overall results of the period 1967-1982, showed actuarial duration rates of complete remission, event-free survival and survival, at 60 months, between 2% and 6%, their median duration being of 9, 8 and 10 months respectively. No significant difference was observed between the first two periods or protocols. Protocol 3-AML-83, activated in March 1983, achieved actuarial rates of continuous complete remission, event-free survival, and survival of 51%, 37% and 39% respectively, at 48 months. The difference between the first two periods and the last one was highly significant (P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Externally applied abdominal vibration as a method for improving efficiency of peritoneal dialysis.

We studied the effect of externally applied vibration onto the abdominal wall on the efficiency of peritoneal dialysis (PD). Ten patients were studied. Three consecutive PD exchanges (control sessions, CS) were compared with vibration sessions (VS). Samples of blood and dialysate were analyzed for urea nitrogen (UN), creatinine (Cr) and potassium (K). Mean clearance was calculated. We found that vibration increased significantly the mean UN, Cr and K clearances.

Abdominal Muscles↗
PubMed1985

Effect of parathyroid hormone on energy metabolism of skeletal muscle.

Clinical states with primary or secondary hyperparathyroidism are associated with muscle dysfunction, suggesting that parathyroid hormone (PTH) may affect muscle metabolism. The present study examined the effect of 1-84 PTH and its amino-terminal fragment (1-34 PTH) on energy production, transfer, and utilization by skeletal muscle. Rats weighing 150 to 200 g were injected intraperitoneally with 1-84 or 1-34 PTH, 200 U/day, for 4 days, and control animals received vehicle only. The effect of the simultaneous administration of a calcium channel blocker, verapamil, was examined also. The muscle content of inorganic phosphorus, creatine phosphate, and adenine nucleotides were significantly (P less than 0.01) lower in the PTH-treated rats than in control animals. The hormone significantly reduced mitochondrial oxygen consumption without altering ADP:0 ratio, indicating reduced phosphorylation. Both 1-84 and 1-34 PTH produced significant (P less than 0.01) reduction in the activities of mitochondrial and myofibrillar CPK, and mitochondrial MgATPase. 1-84 PTH reduced the activity of myofibrillar CaATPase as well. There was a significant (P less than 0.01) increment in muscle uptake of 45Ca in the 1-84 PTH-treated rats. Verapamil abolished all the effects of PTH. Our data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements may, at least in part, underlie the myopathy observed in conditions associated with excess PTH.

Adenosine Diphosphate↗
PubMed1985

Effect of parathyroid hormone on myocardial energy metabolism in the rat.

This study examined the effect of parathyroid hormone (PTH) on myocardial energy production, transfer, and utilization. Rats (150 to 200 g) were injected with 1-84 PTH, 200 U/day i.p., or 1-34 PTH, 200 or 300 U/day i.p., for 4 days. Control animals received the vehicle only. The effect of the simultaneous administration of calcium channel blocker, verapamil, was also examined. Myocardial contents of Pi, ATP, and CP were significantly (P less than 0.01) lower in the 1-84 PTH-treated rats than in control animals. Both 1-84 PTH and 1-34 significantly (P less than 0.01) reduced mitochondrial oxygen consumption without altering ADP:O ratio indicating reduced phosphorylation. 1-84 and 1-34 PTH significantly (P less than 0.01) reduced the activities of mitochondrial and myofibrillar creatine phosphokinase and 1-84 PTH inhibited (P less than 0.01) the activities of mitochondrial Mg ATPase and those of myofibrillar Ca ATPase. There were significant (P less than 0.01) increments in myocardial 45Ca and in total calcium content in 1-84 PTH-treated rats. Verapamil abolished all the effects of 1-84 PTH. Similarly, inactivation of 1-84 PTH abolished its effects. Treatment with 1-84 PTH for 10 days was associated with a significant decrease in cardiac index and mean arterial pressure. Our data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements, if maintained, produce a decrease in cardiac index. It appears that the enhanced entry and the accumulation of calcium in the myocardium, either directly and/or indirectly, are responsible for the action of PTH on energy metabolism of the heart.

Adenine Nucleotides↗
PubMed1985

Acquired factor X and antithrombin III deficiency in a patient with primary amyloidosis and nephrotic syndrome.

A 45-year-old man with primary amyloidosis was initially seen with nephrotic syndrome. Factor X was found to be 5% and antithrombin III (AT III) 45% of normal plasma values. During an 11-month period, despite severe factor X deficiency, the patient did not have any bleeding complications. He developed progressive renal failure and AT III levels increased to normal, at which time he developed severe bleeding complications. These findings suggest a protective role of AT III deficiency against bleeding in a patient with severe factor X deficiency.

Amyloidosis↗
PubMed1983

Impaired energy metabolism in skeletal muscle during phosphate depletion.

The effects of phosphate depletion (PD) of 4, 8, and 12 weeks on skeletal muscle energy metabolism were studied in rats fed a phosphate deficiency diet and compared with rats pairfed with a normal phosphate diet. Skeletal muscle biopsy specimens were examined for energy production, transport, and utilization. The results show that already by 4 weeks of PD, the concentration of inorganic phosphorus of the skeletal muscle was significantly reduced and remained low thereafter. There was significant (P less than 0.01) and direct correlation between the cellular inorganic phosphorus and that of serum phosphorus. Adenine nucleotides, ATP, ADP, AMP, and creatine phosphate levels did not change. Mitochondrial respiration and oxidative phosphorylation were impaired by PD. Total cellular mitochondrial and myofibrillar creatine phosphokinase activities were significantly reduced at 4 weeks of PD and fell further at 8 and 12 weeks. There was a significant (P less than 0.01) and direct correlation between the activity of total extractable creatine phosphokinase and both serum and cellular levels of inorganic phosphorus. These data show that chronic PD is associated with a decrease in energy production, transfer, and utilization by skeletal muscle and provides information on the molecular events responsible for the myopathy of PD.

Animals↗
PubMed1982

Non oliguric acute renal failure after treatment with sulfinpyrazone.

Two cases with acute reversible renal failure while receiving sulfinpyrazone after acute myocardial infarction are presented. Sulfinpyrazone 200 mg q.i.d. was started a few days after the myocardial infarction. In both patients BUN and creatinine rose significantly, and returned to previous values when the drug was discontinued. No other known causes of renal failure were present in either of the patients.

Acute Kidney Injury↗
PubMed1975

Delayed excretion of conjugated sulphamethoxazole in uraemia.

Persistence in the serum of free and conjugated sulphamethoxazole was estimated in five normal controls and in nine uraemic patients with creatinine clearances under 20 ml/min, after a single one-gram dose of the drug. In the uraemic group delayed disappearance of the free drug was found. Conjugated sulphamethoxazole retention was 62.44% at 24 hr after the oral load, and 13.7% 19 days later. Risk of accumulation of sulphamethoxazole in uraemia is emphasised. Re-evaluation of the use of this drug in patients with impaired renal function is recommended.

Humans↗