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Biomedical subjects

R J Shalhoub

Publications and source records attributed to R J Shalhoub.

At least 19 recordsLinked to original sources
PubMed1986

Nephrotic syndrome associated with a clonal T-cell leukemia of large granular lymphocytes with cytotoxic function.

A 51-year-old man presented with a T-cell leukemia of large granular lymphocytes and rapidly developed a nephrotic syndrome due to presumptive minimal-change glomerulopathy. The E-rosette+, Ia+ cells demonstrated cytotoxic activity similar to that of natural killer lymphocytes but lacked other T-subset markers, except that one third of them bore Fc(IgG) receptors. Cytogenetic analysis revealed loss of chromosome 10 and the translocation (1;10)(p11;q11) in all metaphases. Regression of the leukemia after chemotherapy was accompanied by a dramatic resolution of the nephrotic syndrome, suggesting that the activated granular lymphocytes induced the renal lesion. The close association of a clonal T-lymphoproliferative disorder with minimal-change nephrotic syndrome lends further support to current views implicating activated T cells or their products in the pathogenesis of this glomerulopathy.

Chromosomes, Human, 1-3↗
PubMed1985

Zinc-induced enhancement of lymphocyte function and viability in chronic uremia.

Spontaneous and phytohemagglutinin (PHA)-induced lymphocyte blastogenesis (LB) was measured by the incorporation of 3H-thymidine into lymphocytes from zinc-treated (group I) and non-zinc-treated (group II) patients on maintenance hemodialysis and from normal controls. The results were expressed as disintegrations per minute (dpm) per 200,000 cells. Spontaneous LB was comparable in the 3 groups. LB in response to PHA was impaired in group II (mean dpm 28,244 +/- 13,499 SEM) as compared to group I (163,407 +/- 14,325; p less than 0.001) or controls (193,711 +/- 9,406; p less than 0.001). In 5 group II patients the mean dpm rose from (45,630 +/- 26,334 SD to 211,795 +/- 78,231; p less than 0.025) after zinc therapy. The mean percentages of viable lymphocytes after 72 h of culture were 53.8, 85.8 and 85.5 in groups II, I, and controls, respectively. These results clearly indicate that zinc therapy improves lymphocyte function and viability in uremia and suggest that abnormal zinc metabolism may play a role in the impaired cellular immunity in this disorder.

Cell Survival↗
PubMed1982

Erythrocytosis in patients on long-term hemodialysis.

Erythrocytosis was seen in two men during maintenance hemodialysis therapy for end-stage renal disease secondary to apparent chronic glomerulonephritis. Nonrenal causes of erythrocytosis such as polycythemia vera, chronic hypoxemia, high-oxygen affinity hemoglobin, and hepatoma were excluded by appropriate clinical studies. A computed tomographic scan of the abdomen showed numerous renal cysts in each patient consistent with acquired cystic disease of end-stage kidneys. Peripheral serum erythropoietin levels were elevated as measured by sensitive radioimmunoassay. The findings suggest that the erythrocytosis is caused by an erythropoietic mechanism related to the diseased kidneys. A review of the literature failed to show previous reports of this clinical association.

Erythropoietin↗
PubMed1981

The effect of zinc on cellular immunity in chronic uremia.

Delayed hypersensitivity to mumps was examined in 25 apparently well-nourished men receiving regular hemodialysis, each of whom had a history of mumps. A positive reaction was observed in eight of nine patients already under therapy with zinc added to the dialysis bath. In contrast, 11 of 16 untreated patients were anergic. Four of the anergic patients were subsequently treated with zinc resulting in restoration of sensitivity in three patients. There were no significant differences in lymphocyte, monocyte, or T-cell counts between the two groups of patients. Consequently, zinc probably acts by improving the function of one or more of these cell types. Protracted zinc deficiency may be a major cause of impaired cellular immunity in chronic renal failure.

Adult↗
PubMed1981

Urinary zinc in relation to other cations and flow during volume expansion and intravenous chlorothiazide.

Urinary excretion of zinc, sodium, potassium, and calcium was studied in anesthetized dogs under conditions of volume expansion by saline infusion and volume expansion plus chlorothiazide administration. Zinc excretion was positively correlated to the fractional water excretion, as well as to th excretion of the other cations, during volume expansion. Chlorothiazide administration during volume expansion increased the zinc, sodium, and potassium excretion without changing that of calcium. The enhanced zinc excretion during chlorothiazide diuresis was equal to that expected on the basis of the increase in fractional water excretion alone. The urinary concentration of zinc appeared inversely related to the urine flow rate, reaching a minimum below that of the plasma ultrafilterable zinc concentration. The ratio of the clearance of zinc to that of sodium was 0.28, indicating a greater degree of net reabsorption for zinc than for calcium. These findings suggest that zinc and sodium reabsorption may be inhibited to a similar degree at chlorothiazide-sensitive sites in the tubule. Furthermore, the zinc reabsorptive mechanism seems capable of lowering urinary zinc concentration below that of ultrafiltrate and appears related in some way to sodium reabsorption.

Animals↗
PubMed1981

Zinc tolerance tests in chronic uremia.

The intestinal absorption of zinc was investigated in 12 control subjects and in 20 patients or maintenance hemodialysis by means of a zinc tolerance test during fasting. Ten patients (Group I) were on long-term vitamin D therapy and 10 (Group II) were not receiving vitamin D. After baseline plasma zinc measurements, a single dose of 50 mg zinc was ingested and plasma zinc levels were measured at hourly intervals for 4 hours thereafter. Peak plasma zinc levels were significantly lower in Group II patients than in controls or patients in Group I suggesting impaired absorption. No significant difference was found between controls and Group I patients. Two patients had normal zinc tolerance tests while on vitamin D therapy, but abnormal tests while off vitamin D. We conclude that the intestinal absorption of zinc may be impaired in chronic uremia, probably secondary to abnormal metabolism of vitamin D.

Adult↗
PubMed1979

Viral pericarditis in patients receiving hemodialysis.

Four patients with end-stage renal disease in whom pericarditis developed while they received intermittent hemodialysis therapy were evaluated for viral infection. We found high or rising serum antibody titers to influenza virus A (three patients) and coxsackievirus B (one patient). Cardiac tamponade occurred in three patients, requiring pericardiectomy in two; each patient eventually recovered. Viral pericarditis may be an important cause of "uremic" pericarditis in chronically dialyzed patients.

Acute Disease↗
PubMed1977

Reversal of uraemic impotence by zinc.

In eight impotent haemodialysed men with low plasma-zinc levels sexual function, including potency, frequency of intercourse, libido, and plasma testosterone, follicle-stimulating hormone, and luteinising hormone levels, was determined before and after therapy with zinc (four patients) or placebo (four patients). Dialytic administration of zinc strikingly improved potency in all patients and raised the plasma-testosterone to normal in the two with low pretreatment plasma-testosterone levels. Placebo did not improve sexual function in any patient. Zinc deficiency is a reversible cause of gonadal dysfunction in uraemia.

Adult↗
PubMed1977

Calcitonin levels in chronic renal disease.

High levels of serum calcitonin were found in patients with chronic renal failure. Serum calcitonin correlated directly with the phosphate to total calcium ratio; calcitonin levels correlated inversely with serum calcium in those patients on dialysis and directly with serum calcium in nondialysis patients. All patients had elevated serum gastrin. The high levels of serum calcitonin usually decreased following successful kidney transplantation. The pathophysiology of this hypercalcitonemia and its relationship to renal osteodystrophy and the disordered calcium metabolism of uremia remains to be elucidated.

Adult↗
PubMed1975

Effect of prostaglandin a1 on acute renal failure in the rat.

In an attempt to alter the natural course of glycerol and uranyl nitrate induced acute ranal failure in the rat, the vasodilator, prostaglandin A1 was adminstered systemically at varying times during the induction phase of renal failure. According to the method used, no significant beneficial effect could be demonstrated in either experimental model.

Acute Kidney Injury↗
PubMed1974

Pathogenesis of lipoid nephrosis: a disorder of T-cell function.

Clinical observations suggest that lipoid nephrosis is produced by a systemic abnormality of T-cell function resulting in the secretion of a circulating chemical mediator toxic to an immunologically innocent glomerular basement membrane. The lack of evidence of a humoral antibody response, remission induced by measles which modifies cell-mediated immunity, the therapeutic benefits of steroids and cyclophosphamide which also abate cell-mediated responses, and the occurrence of this syndrome in Hodgkin's disease support this hypothesis. The susceptibility of untreated patients to pneumococcal infections may be of primary or secondary pathogenetic importance. Taken together, the data suggest that this syndrome is a clinical expression of a self-limited primary immune-deficiency disease.

Basement Membrane↗