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J Mattana

Publications and source records attributed to J Mattana.

64 records · Page 4Linked to original sources

Mineralocorticoid therapy lowers serum potassium in patients with end-stage renal disease.

Hyperkalemia is a commonly encountered problem in dialysis patients with end-stage renal disease. In this study we evaluated the effect of mineralocorticoid therapy (MCT; fludrocortisone 0.1-0.3 mg per os daily) on serum potassium of hyperkalemic end-stage renal disease patients. Consecutive monthly clinical and biochemical profiles 3-6 months before and after MCT were compared. Twenty-one patients with a mean age (+/- SE) of 54 +/- 4 years (11 male and 10 female) were studied. Two patients were dropped from this study because they required a change in prescription of dialysis after starting MCT. Mean serum potassium levels significantly fell (p < 0.001) during the post-MCT period (4.9 +/- 0.1 mEq/l) compared with potassium levels during the pre-MCT (5.6 +/- 0.1 mEq/l) period. All patients except 1 showed a reduction in serum potassium levels after MCT. Pre- and post-MCT values were not different for body weight, mean blood pressure, blood urea nitrogen, serum glutamic-oxaloacetic transaminase, lactate dehydrogenase, sodium, chloride, bicarbonate, creatinine and albumin. Since the majority of the patients were anuric (n = 15), a decrease in serum potassium values in the post-MCT period was not due to loss of potassium in the urine. MCT appears to decrease serum potassium values in patients with end-stage renal disease by extrarenal mechanisms. We conclude that MCT can be used safely to lower serum potassium in patients with end-stage renal disease.

Female↗

Effects of human immunodeficiency virus sera and macrophage supernatants on mesangial cell proliferation and matrix synthesis.

Patients with human immunodeficiency virus (HIV) infection are prone to the development of focal segmental glomerulosclerosis, a lesion in which increased mesangial cell proliferation and matrix synthesis may play a role. We undertook the present study to determine whether HIV sera may affect mesangial cell proliferation and matrix synthesis either directly or indirectly via effects on macrophage supernatants. Pooled HIV sera was found to significantly enhance (P < 0.01) mesangial cell proliferation in a concentration-related manner. Mesangial cell proliferation was significantly suppressed by two medications commonly utilized in HIV-infected patients, azidothymidine and trimethoprim/sulfamethoxazole, and was not significantly altered by lipopolysaccharide, suggesting that these medications as well as recurrent infection are unlikely to account for the proliferative effect of HIV sera. Supernatants from HIV sera-treated macrophages were found to significantly enhance (P < 0.01) mesangial cell incorporation of [3H]proline, a marker for synthesis of the matrix component collagen, compared to supernatants from control sera-treated macrophages. These results suggest that HIV sera may directly enhance mesangial cell proliferation and may indirectly increase mesangial cell matrix synthesis by altering macrophage secretory products. These effects may play a role in the development of glomerulosclerosis in patients with HIV infection.

Cell Division↗

Prevalence and predictors of rhabdomyolysis in patients with hypophosphatemia.

PURPOSE: We undertook this study to determine the prevalence and predictors of rhabdomyolysis in the hypophosphatemic state. PATIENTS AND METHODS: To identify patients with hypophosphatemia, we reviewed medical admissions for the period of January through December 1989. The hypophosphatemic state was considered whenever the serum phosphate was less than or equal to 2.0 mg/dL. Rhabdomyolysis secondary to hypophosphatemia was defined when serum creatine kinase levels were greater than or equal to 224 IU/L; it occurred within 72 hours of the hypophosphatemic episode; and it subsequently normalized. Patients who had any other independent etiology for rhabdomyolysis were excluded. Clinical and biochemical characteristics of patients with rhabdomyolysis (Group I) and patients without rhabdomyolysis (Group II) were compared. Variables that predicted rhabdomyolysis in hypophosphatemia were identified by stepwise logistic regression using a backward elimination procedure. RESULTS: One hundred twenty-nine patients were found to have hypophosphatemia. Forty-six (Group I) of 129 patients (36%) showed biochemical evidence of rhabdomyolysis. There was no difference in serum phosphate and potassium concentrations between Group I and Group II patients. Patients in Group I showed higher values for serum osmolality (p less than 0.05), serum glutamic oxaloacetic transaminase (p less than 0.001), chloride (p less than 0.01), and blood urea nitrogen (less than 0.05) when compared with Group II patients. When biochemical profiles of patients with rhabdomyolysis were evaluated on the day of their peak creatine kinase level, only 16 patients were hypophosphatemic, and the majority of patients showed a transient increase in serum phosphate levels because of ongoing muscle cell injury. Of 17 potential predictors, six variables emerged including sodium, chloride, glucose, blood urea nitrogen, uric acid, and osmolality. These variables provided high sensitivity (0.88) as well as moderate specificity (0.79) for predicting the occurrence of rhabdomyolysis in hypophosphatemia. CONCLUSION: We conclude that rhabdomyolysis commonly occurs in the hypophosphatemic state and that at times severe hypophosphatemia as an etiology may be masked because of ongoing rhabdomyolysis. Serum sodium, chloride, glucose, blood urea nitrogen, uric acid, and osmolality have a predictive role for the occurrence of rhabdomyolysis in the hypophosphatemic state that shows a high specificity and a moderate sensitivity.

Adult↗

Determinants of elevated creatine kinase activity and creatine kinase MB-fraction following cardiopulmonary resuscitation.

OBJECTIVE: We undertook this study to determine the occurrence and the determinants of elevation of serum creatine kinase (CK) levels and CK MB-fraction following cardiopulmonary resuscitation (CPR). DESIGN: Four hundred twenty consecutive adult admissions to the Long Island Jewish Medical Center from January 1989 through December 1990 with a diagnosis of cardiac arrest were reviewed. SETTING: The Long Island Jewish Medical Center, New Hyde Park, NY, the Long Island Campus for the Albert Einstein College of Medicine, Bronx, NY. PATIENTS: Sixty-three patients survived for at least 12 h following cardiac arrest for evaluation of post-CPR CK levels and were included into the study. MEASUREMENTS: Clinical features, biochemical profiles, and administered drug profiles were studied in these patients. The clinical and biochemical features of the patients with (CK greater than 224 IU/L [3.7 mu kat/L]) and without rhabdomyolysis were also compared. MAIN RESULTS: Two major determinants responsible for elevated CK levels emerged, including physical injury (number of chest compressions during CPR) and electrical injury (cumulative number of joules administered during defibrillation). Post-CPR CK levels showed positive correlations with both the number of chest compressions given (p less than 0.001) and the number of joules administered during defibrillation (p less than 0.001). Post-CPR CK-MB levels also showed a positive correlation with the number of joules administered (p less than 0.005) and the number of chest compressions (p less than 0.02). Forty-three (68.3 percent) of the 63 patients developed rhabdomyolysis. Serum CK levels were higher (p less than 0.005) in the patients who received electrical countershock therapy as well as chest compressions when compared with patients who received chest compressions alone. There were no significant differences in electrolyte levels between patients with and without rhabdomyolysis. Thirty patients had a history of coronary artery disease (CAD) and 18 (60.0 percent) of these had a positive MB-fraction post-CPR while only ten of the 33 patients without known CAD had a positive MB-fraction post-CPR (30.3 percent, p less than 0.05). Patients with no known CAD but positive CK-MB fraction had significantly higher total CK levels, physical injury, and electrical injury compared with patients with negative CK-MB fraction. Twenty patients survived CPR and were discharged from the hospital without significant neurologic sequelae. The remaining 43 either died or suffered severe neurologic injury. The patients who survived CPR had a significantly shorter duration of CPR (p less than 0.01) compared with those who did not. Patients who did not have long-term survival following CPR were more likely to have elevated serum potassium, phosphate, and creatinine values. CONCLUSIONS: CK elevation is a common finding following successful CPR after cardiac arrest and this elevation of post-CPR CK levels is related to both physical as well as electrical injury sustained during CPR. Elevation of post-CPR CK-MB fraction seems to be only a crude indicator of preexisting CAD; however, a positive CK-MB fraction in patients without CAD is related to severity of physical injury and electrical injury during CPR. Patients who survive CPR without neurologic impairment appear to be those with a shorter duration of CPR. Elevated serum potassium, phosphate, and creatinine values may be related to an adverse effect on long-term survival.

Adult↗

Effects of prostaglandin E2 and cyclic AMP on uptake of immunoglobulin G complexes by cultured macrophages.

The uptake of immune complexes by macrophages (MP) may be important in disease states in which circulating immune complexes are increased. We undertook the present study to determine the effects of prostaglandin E2 (PGE2) and adenosine 3',5'-cyclic monophosphate (cAMP) on the uptake of immunoglobulin G complexes (IgG complexes) by MP. The uptake of 125I-IgG-gold particles (IgG-gold) was measured in the established MP cell line J774.16 following pretreatment with PGE2, the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), PGE2 plus IBMX, the cyclooxygenase inhibitor indomethacin (IM), and dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP). Preincubation with PGE2 at concentrations from (10(-12)) to (10(-5) M) revealed significantly diminished uptake of IgG-gold at (10(-6)) and (10(-5) M) (in counts per min per well, PGE2 [10(-6) M], 5,401 +/- 140; control, 17,150 +/- 493, p less than 0.001); (PGE2 [10(-5) M], 3,835 +/- 172; control, 17,150 +/- 493, p less than 0.001). IBMX (10(-3) M) alone did not significantly alter IgG-gold uptake (IBMX, 14,450 +/- 1938; control, 14,840 +/- 995, p less than 1.0). PGE2 (10(-6) M) plus IBMX (10(-3) M) significantly suppressed IgG-gold uptake (in counts per min per well, PGE2 plus IBMX, 3,659 +/- 129; control 18,296 +/- 486, p less than 0.001). PGE2 (10(-6) M) alone also suppressed IgG-gold uptake versus control (PGE2, 4,578 +/- 105; control, 18,296 +/- 486, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗

Hypokalemia and rhabdomyolysis.

Since the occurrence of rhabdomyolysis may elevate the serum concentration of potassium, hypokalemia as a cause of rhabdomyolysis often goes unrecognized in many instances. We undertook this study to evaluate the occurrence and determinants of rhabdomyolysis in the hypokalemic state. To identify patients with a hypokalemic state, we reviewed medical admissions for the period January 1988 through December 1989. A total of 120 patients (42 men and 78 women) were included in the present study. Thirty-eight hypokalemic patients showed biochemical evidence of rhabdomyolysis (serum creatine phosphokinase greater than 244 IU/l). The clinical and biochemical characteristics of the patients with rhabdomyolysis (group I) and the hypokalemic patients without rhabdomyolysis (82 patients, group II) were compared. There was no difference in age, sex and race of the patients of group I vs. group II. The mean serum values for potassium, bicarbonate, chloride, blood urea nitrogen, glucose, lactate dehydrogenase and uric acid were also not different between the two groups. The mean serum osmolality was higher (p less than 0.001) in patients with rhabdomyolysis (297.6 +/- 4.3 mosm/kg) than in those without rhabdomyolysis (283.5 +/- 5.0 mosm/kg). The levels of serum glutamic-oxaloacetic transaminase were elevated (p less than 0.001) in group-I patients (69.6 +/- 8.4 IU/l) but not in group-II patients (36.7 +/- 3.5 IU/l). The concentrations of serum creatinine were also higher (p less than 0.05) in patients with rhabdomyolysis (1.4 +/- 0.2 mg/dl) than in those without rhabdomyolysis (1.0 +/- 0.1 mg/dl). The mean values for serum sodium were higher (p less than 0.02) in group-I patients when compared to group-II patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗