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Biomedical subjects

J Palmisano

Publications and source records attributed to J Palmisano.

18 recordsLinked to original sources
PubMed2006

The effect of simvastatin on triglyceride-rich lipoproteins in patients with type 2 diabetic dyslipidemia: a SILHOUETTE trial sub-study.

OBJECTIVE: To determine if simvastatin effectively decreases the elevated levels of triglyceride (TG), TG-rich lipoproteins, and small, dense LDL particles, which are characteristic of diabetic dyslipidemia. RESEARCH DESIGN AND METHODS: We conducted a prespecified analysis from a double-blind, placebo-controlled, randomized, 6-week crossover trial in patients with type 2 diabetes and low HDL-C (< 40 mg/dL). Each patient was randomized to 1 of 6 possible treatment arms; each patient received simvastatin 80 mg, simvastatin 40 mg, and placebo over 3 periods. We used the validated vertical auto profile (VAP) method to directly assess TG-rich lipoproteins and LDL subclasses. We assessed the efficacy of simvastatin to improve the lipoprotein profile in adult men (71%) and women (29%) (n = 151) with stable type 2 diabetes (HbA1C < 9%), LDL-C > 100 mg/dL, HDL-C < 40 mg/dL, and fasting TG level > 150 and < 700 mg/dL (median = 273 mg/dL). MAIN OUTCOME MEASURES: Percentage change from baseline in IDL and VLDL (TG-rich lipoproteins), LDL subclasses, and additional lipoproteins at the end of each 6-week treatment interval; percentage of patients who reached NCEP ATP III non-HDL goal of < 130 mg/dL by the end of each 6-week period. RESULTS: Both simvastatin 80 mg and 40 mg significantly reduced VLDL-C, VLDL3, and IDL, as well as the four LDL subclasses measured with VAP, compared with placebo. Simvastatin 80 mg, compared with simvastatin 40 mg, provided additional efficacy. With simvastatin 80 mg, 77.2% of patients not at their non-HDL-C goal of < 130 mg/dL at study baseline reached goal, compared with 65.7% following simvastatin 40 mg treatment, and 2.2% following placebo. CONCLUSIONS: Treatment with simvastatin effectively reduced the elevated levels of TG-rich lipoproteins and improved LDL composition in patients with type 2 diabetes. A large percentage of these patients attained the NCEP ATP III non-HDL-C goal of < 130 mg/dL, which demonstrates the improvement of the atherogenic profile in these patients.

Aged↗
PubMed2001

Shunt nephritis from Propionibacterium acnes in a solitary kidney.

Since its initial description in 1965, immune complex glomerulonephritis associated with ventriculoatrial shunts (VAS) has been reported widely in the literature. The most common incriminating organism is Staphylococcus epidermidis, but less often, an organism generally regarded as nonpathogenic, such as Propionibacterium acnes, has been noted as the cause. Shunt infection usually occurs within a few months after placement or manipulation of the shunt, and shunt nephritis (SN) develops gradually over months to years after. Treatment involves mandatory removal of the shunt and antibiotics; prognosis is variable. We report a case of SN with P acnes that is unusual because of its occurrence in a solitary kidney 6 years after shunt placement, persistently negative blood cultures, and normal complement levels. Percutaneous biopsy of a solitary kidney should be considered if it is expected that the result may guide therapy of progressive renal failure.

Aged↗
PubMed2000

Lactic acidosis associated with stavudine administration: a report of five cases.

Type "B" lactic acidosis has been described in patients receiving the nucleoside analogs zidovudine, didanosine, and fialuridine. Lactic acidosis has also been described in 4 patients receiving combination therapy with stavudine and lamivudine. We describe the development of chronic type "B" lactic acidosis in 3 patients receiving stavudine as a single agent and in 2 patients receiving combination therapy with stavudine and either lamivudine or delavirdine, a nonnucleoside analog. All patients presented with abdominal pain, vomiting, and hepatic steatosis. Other signs of mitochondrial toxicity included pancreatitis and myopathy (2 cases). The mean duration of stavudine therapy was 9.4 months, and the mean observed peak lactate level+/-SD was 10.3+/-5 mmol/L. After discontinuation of stavudine treatment, lactic acidosis improved in 4 patients after 4-60 weeks, and 1 patient died. Evaluations for other causes of lactic acidosis, including hypoxemia, malignancy, sepsis, and cardiogenic shock, were negative.

Acidosis, Lactic↗
PubMed1998

Carboplatin-related hematuria and acute renal failure.

Cisplatin is a potent tubular toxin with a high incidence of nephrotoxicity. Carboplatin is considered less nephrotoxic but can still cause tubular injury and interstitial nephritis in patients who have been previously treated with cisplatin. The affected individuals usually have nonoliguric renal failure with a urine output of more than a liter per day. We present a 57-year-old white woman with no history of renal disease who underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy for stage IC ovarian carcinoma. One month later, she received chemotherapy with paclitaxel (Taxol) and carboplatin. On the following day, she developed frank hematuria and flank pain associated with a diminished urine output. Intravenous pyelogram (IVP) showed bilateral hydronephrosis with a total blockage of dye flow at the level of intraureteral lucencies consistent with bilateral blood clots. Her coagulation profile and uric acid was normal. Her acute renal failure (ARF) spontaneously resolved in the following 24 hours, with a brisk diuresis presumably due to clot lysis. The follow-up IVP showed a resolution of obstructive changes. A review of the literature shows a previous case in which high doses of carboplatin were implicated as the cause of hemorrhagic cystitis, presumably by toxicity to transitional epithelium of the bladder. We believe that the current case represents carboplatin-induced damage to the transitional epithelium in the renal pelvi and ureters causing gross hematuria and blood clots, resulting in bilateral ureteral obstruction and hydronephrosis.

Acute Kidney Injury↗
PubMed1998

Successful treatment of cisplatin-induced hemolytic uremic syndrome with therapeutic plasma exchange.

Cisplatin is a known cause of hemolytic uremic syndrome (HUS). The acute, fulminant form of cisplatin-induced HUS is almost always fatal. We present a 67-year-old Hispanic woman who was treated with cisplatin for squamous cell carcinoma of the tongue. Three days after receiving the treatment, she presented with increasing fatigue, decreased urine output, and confusion. Physical examination was remarkable for tachycardia of 130 beats/min, peripheral edema, and mental obtundation. Laboratory investigations showed a white cell count of 5,500/microL, hemoglobin level of 9.6 g/dL, hematocrit of 29.6%, and platelet count of 13,000/microL. Schistocytes were present on peripheral smear. Screening for disseminated intravascular coagulation was negative. Serum chemistry values included blood urea nitrogen 111 mg/dL, creatinine 3.8 mg/dL, and lactate dehydrogenase (LDH) 927 IU. The patient underwent hemodialysis and therapeutic plasma exchange (TPE), using fresh frozen plasma (FFP). Dialysis was no longer required after the fifth day. TPE was performed daily until the platelet count normalized on the 13th day, after which intertreatment intervals were extended until normalization of LDH levels on the 50th day. We conclude that the normally fatal, fulminant form of cisplatin-induced HUS can be successfully treated with standard TPE, using FFP replacement.

Aged↗
PubMed1998

Hyperfiltration in African-American patients with type 2 diabetes. Cross-sectional and longitudinal data.

OBJECTIVE: Hyperfiltration may play a role in the development of diabetic nephropathy. African-American patients with diabetes have more than a fourfold increase in end-stage renal disease. The purpose of this study is to evaluate the impact of hyperfiltration on renal function in African-American patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Renal function of 194 African-American patients with diagnosed type 2 diabetes from 1 month to 36 years was assessed by studies of isotopic glomerular filtration rate (GFR), serum creatinine, creatinine clearance, and 24-h urinary albumin excretion rates. Thirty-four patients with a duration of diagnosed type 2 diabetes from 1 month to 10 years were found to have hyperfiltration (GFR > or = 140 ml.min-1.1.73 m-2). Fifteen of these patients received longitudinal follow-up of renal function for as long as 15 years after the initial study. RESULTS: Hyperfiltration is present in 15 (36%) of 42 patients whose duration of diagnosed type 2 diabetes is < 1 year, and it persists for up to 10 years in 14-20% of patients with diagnosed type 2 diabetes. Patients with hyperfiltration are younger than their counterparts without hyperfiltration when matched for duration of diagnosed diabetes. When followed over time, those patients with hyperfiltration were not more likely to develop impaired renal function as measured by GFR or creatinine clearance. CONCLUSIONS: Hyperfiltration does not identify patients at risk for deterioration in renal function.

Adult↗
PubMed1995

Interaction of hypertension and diabetes on renal function in black NIDDM subjects.

We studied renal function of 194 black subjects with duration of diagnosed NIDDM from 1 month to 36 years to determine the interaction of hypertension and diabetes on nephropathy. Renal function was assessed by isotopic GFR and RPF studies, and serum creatinine. One hundred seventeen of the 194 subjects had 24-hour urinary albumin excretion (AER). AER > 300 mg/24 h correlated with longer duration of NIDDM, decrease in GFR and RPF, and rise in serum Cr, and all subjects were hypertensive. AER 30 to 300 mg/24 h also correlated with a longer duration of NIDDM and 80% had hypertension. When 194 subjects were grouped according to duration of NIDDM and the presence or absence of hypertension, subjects who remained normotensive had normal renal function. In hypertensive subjects a decrease in GFR occurred with duration of NIDDM > 1 year and decrease in RPF with duration of NIDDM > 5 years. In hypertensive subjects with NIDDM > 10 years, 36% had impaired renal function (GFR < 80 ml/min/1.73 m2 or serum creatinine > 1.4 mg/dl) and 75% had microalbuminuria or clinical proteinuria. Within this group, those subjects who developed hypertension after their diagnosis of diabetes were likely to have evidence of nephropathy as compared to those subjects whose hypertension was diagnosed prior to or simultaneous with their diabetes: 17 of 20 (85%) versus 7 of 13 (54%), respectively (P = 0.05). These data provide insight into the relationship between hypertension and diabetes in the development of nephropathy in black NIDDM individuals.

Adolescent↗
PubMed1993

Extracorporeal life support for pediatric respiratory failure: predictors of survival from 220 patients.

OBJECTIVE: The purpose of this report was to examine the Extracorporeal Life Support Organization registry database for predictors of outcome for severe pediatric respiratory failure managed with extracorporeal life support. DESIGN: Retrospective cohort study. SETTING: Extracorporeal Life Support Organization data registry. PATIENTS: All nonneonatal pediatric patients who were treated in the United States with extracorporeal life support for severe pediatric respiratory failure reported to the Extracorporeal Life Support Organization registry as of August 1991. Patients with congenital heart disease and congenital gastrointestinal malformations were excluded from study. INTERVENTIONS: Venoarterial or venovenous extracorporeal life support for severe life-threatening pulmonary failures. MEASUREMENTS AND MAIN RESULTS: As of August 1991, 220 pediatric patients meeting study entry criteria were reported to the Registry having received extracorporeal life support for severe pulmonary failure, since 1982. Forty-six percent (102 of 220 patients) were successfully managed with this technology and survived to hospital discharge. The mean patient age was 36.8 +/- 51.6 months. Fifty-one percent of the patients were male. The mean duration of mechanical ventilation before extracorporeal life support was 6.3 +/- 5.9 days. Mean blood gas and ventilatory measurements obtained before extracorporeal life support were as follows: PaCO2 52 +/- 23 torr (6.9 +/- 3.0 kPa); PaO2 59 +/- 32 torr (7.8 +/- 4.3 kPa); estimated alveolar-arterial oxygen gradient 561 +/- 63.4 torr (74.8 +/- 8.5 kPa); peak airway pressure 49.5 +/- 13.1 cm H2O; mean airway pressure 24.3 +/- 8.2 cm H2O; positive end-expiratory pressure 11.8 +/- 6.3 cm H2O; ventilator rate 58 +/- 64.4 breaths/min; and FIO2 0.98 +/- 0.07. The mean duration of extracorporeal life support for all patients was 247 +/- 164 hrs. For the 102 survivors, the mean time for decannulation from extracorporeal life support to extubation from mechanical ventilation was 6.5 +/- 7.6 days. Stepwise multivariate logistic regression modeling found the following variables to be associated with patient survival: a) patient age, b) days of mechanical ventilation before extracorporeal life support, c) peak inspiratory pressure, d) alveolar-arterial oxygen gradient, and e) extracorporeal life support administered since December 31, 1988 (all p < .05). CONCLUSIONS: Extracorporeal life support may represent an effective rescue therapy for some selected pediatric patients with severe respiratory failure for whom conventional mechanical ventilation support has failed to improve. Predictors of survival for this life-support therapy exist that may be helpful for individual patient prognostication and future prospective study.

Adolescent↗
PubMed1992

Extracorporeal life support for pediatric respiratory failure.

OBJECTIVES: The purposes of this report are to a) describe the University of Michigan experience with venoarterial or venovenous extracorporeal life support for severe pediatric pulmonary rescue therapy, and b) examine survivors and nonsurvivors for differences that might be useful for examination in future, prospective studies. DESIGN: Case series report. Phase I study of safety and effectiveness of extracorporeal life support for pediatric respiratory failure. SETTING: University of Michigan Medical Center. PATIENTS: Non-neonatal pediatric patients treated with extracorporeal life support for severe respiratory failure at the University of Michigan. INTERVENTIONS: Extracorporeal life support for pulmonary failure. MEASUREMENTS AND MAIN RESULTS: From November 1982 until May 1991, 25 pediatric patients underwent extracorporeal life support for severe pulmonary failure. Twenty patients were treated in the last 36 months. Sixty percent (15/25 patients) survived their life-threatening respiratory illness, were weaned from mechanical ventilation, and were discharged home. The mean patient age was 4.1 yrs, and mechanical ventilation duration before extracorporeal life support was 5.9 days. Mean blood gas data and mechanical ventilation pressures before extracorporeal life support were: peak inspiratory pressure of 48.6 cm H2O, mean airway pressure of 21.9 cm H2O, positive end-expiratory pressure of 9.7 cm H2O, PaCO2 of 43 torr (5.7 kPa), PaO2 of 69 torr (9.1 kPa), estimated alveolar-arterial oxygen gradient of 563 torr (75 kPa), and FIO2 of 0.98. Variables associated with survival included: age of survivors vs. nonsurvivors, 2.1 vs. 7.1 yrs (p less than .02); peak inspiratory pressure of survivors vs. nonsurvivors, 43.1 vs. 57.9 cm H2O (p less than .03); mean airway pressure of survivors vs. nonsurvivors, 18.4 vs. 27.2 cm H2O (p less than .03); and positive end-expiratory pressure of survivors vs. nonsurvivors, 8.1 vs. 12.1 cm H2O (p less than .01). There were no differences detectable in the blood gas values (PaO2, PaCO2, P[A-a]O2) in survivors and nonsurvivors before extracorporeal life support. The number of days mechanical ventilation was used before extracorporeal life support in survivors and in nonsurvivors was similar. CONCLUSION: Extracorporeal life support is an effective rescue therapy for pediatric patients with severe respiratory failure (University of Michigan survival rate of 60%).

Age Factors↗
PubMed1992

Respiratory syncytial virus morbidity and mortality estimates in congenital heart disease patients: a recent experience.

OBJECTIVE: To determine recent morbidity and mortality rates from respiratory syncytial virus infection in a pediatric congenital heart disease population. DESIGN: Retrospective cohort study design. SETTING: The C. S. Mott Children's Hospital, University of Michigan Medical Center. PATIENTS: A total of 740 pediatric patients hospitalized at the University of Michigan Medical Center for symptomatic respiratory syncytial virus infection, of whom, 79 patients had clinically important congenital heart disease. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We retrospectively examined the charts of 740 patients hospitalized at our children's hospital from July 1, 1983 to June 30, 1990 with symptomatic respiratory syncytial virus infection to assess morbidity and mortality outcomes. Seventy-nine patients had congenital heart disease and 40 of these patients had pulmonary hypertension. For the entire cohort and a subset of patients with community-acquired infection, those patients with congenital heart disease had longer durations of hospitalization and greater need for, and days of, both intensive care and mechanical ventilation than patients without congenital heart disease. Mortality risk for respiratory syncytial virus community-acquired infection was not different for congenital heart disease vs. noncongenital heart disease patients (0.0% vs. 0.2%; p = 1.00). When examining only patients with congenital heart disease, those patients with pulmonary hypertension had increased hospital days and greater intensive care and mechanical ventilation durations compared with patients without this diagnosis. The overall mortality rate was low and was equally low for congenital heart disease groups with or without pulmonary hypertension (2.5 vs. 2.6). For community-acquired illness, no mortality was found in either congenital heart disease group. When the cohort of congenital heart disease patients was divided into pre- and postribavirin administration eras, no differences in mean hospital duration, ICU days, and mechanical ventilation days were noted. Of the 79 congenital heart disease patients, only two died during their hospitalization in which respiratory syncytial virus infection occurred. Both patients had nosocomial-acquired respiratory syncytial virus and both were from the postribavirin administration cohort. One of these two patients had received antiviral therapy. Neither death was secondary to respiratory syncytial virus respiratory failure (based on pathologic examination). CONCLUSIONS: We conclude that respiratory syncytial virus mortality risk in pediatric patients with congenital heart disease is less than the risk reported a decade ago. Respiratory syncytial virus infection in congenital heart disease patients with pulmonary hypertension is associated with increased morbidity but not increased mortality rates. The markedly decreased respiratory syncytial virus mortality risk in patients with congenital heart disease currently experienced is likely secondary to improvements in intensive care management and advances in the surgical correction in this population rather than antiviral therapy.

Academic Medical Centers↗
PubMed1990

Cross-sectional analysis of renal function in black Americans with NIDDM.

Our objective was to define glomerular filtration rate (GFR) and renal plasma flow (RPF) in Black Americans with non-insulin-dependent diabetes mellitus (NIDDM). This was a cross-sectional study of 71 Black NIDDM patients with diagnosed diabetes duration from 1 mo to 21 yr. Hyperglycemia was regulated and stabilized before patients were entered into the study. GFR and RPF were determined by the clearance of [125I]iothalamate and 131I-labeled hippuran, respectively, with a constant-infusion technique and four urine collection periods. Hyperfiltration, as defined by a GFR of greater than 140 ml.min-1.1.73 m-2, was found in 7 of 20 patients (35%) with newly diagnosed (less than 2 yr duration) NIDDM. The percentage of patients with hyperfiltration decreased with increasing duration of diagnosed diabetes. Decreasing GFR and RPF occurred with increasing duration of diagnosed diabetes. In conclusion, renal hemodynamic changes in Black Americans with NIDDM are similar to those known to occur in White populations with IDDM.

Adult↗
PubMed1989

NBD-taurine uptake by alpha-type carbonic anhydrase cells of turtle bladder.

The uptake of the fluorescent anion, N-(7-nitrobenz-2-oxa-1,3 diazol-4-yl)aminoethanosulfonic acid-taurine (NBD-T) was examined in sheets of turtle bladder epithelial cells after either serosal or mucosal exposure to the fluorescent anion. Serosal uptake of NBD-T into a population of epithelial cells was demonstrated in thin epithelial sheets scraped from bladder sacs exposed to low (0.5 mM) concentrations of NBD-T sufficient to cause fluorescence in turtle erythrocytes. In nine sheets NBD-T fluorescence was observed in 14.4 +/- 1.3% of epithelial cells; by phase-contrast microscopy of the same fields, these cells were nongranular or carbonic anhydrase (CA) cells. An additional 8.1 +/- 1.0% of cells was nongranular, but failed to exhibit fluorescence after serosal NBD-T exposure, consistent with a beta-CA cell population. Apical uptake of NBD-T into epithelial cells was demonstrable only at high (5 mM) mucosal concentrations in both thin sheets and superfused bladder segments. In thin sheets, NBD-T fluorescence was observed in 15.8 +/- 0.7% of cells and appeared to have a punctate subapical distribution; phase-contrast of the same fields (n = 46) revealed a nongranular cell population of 21.9 +/- 0.9%. Nongranular cells corresponded closely to CA cells as identified with carboxyfluorescein fluorescence. Hence, apical NBD-T was taken up primarily by alpha-CA cells. In conclusion, NBD-T is transported by alpha-CA cells either across the basolateral membrane with high affinity comparable to that of turtle red cell band 3 protein or across the apical membrane with low affinity via a less-specific mechanism such as endocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Absence of anion gap metabolic acidosis in severe methanol poisoning: a case report and review of the literature.

Methanol poisoning in humans is characterized by a latent period with subsequent development of anion gap metabolic acidosis and blindness. We describe a patient with potentially lethal methanol ingestion as evidenced by an admission serum methanol level of 403 mg/dL and sustained serum methanol levels greater than 50 mg/dL for more than 18 hours after ingestion, despite hemodialysis therapy. That anion gap metabolic acidosis or visual impairment did not develop in this patient was attributed to documented prior ethanol ingestion (admission serum ethanol level of 158 mg/dL) and continued ethanol administration during hospitalization (sustained serum ethanol levels greater than 100 mg/dL). This case demonstrates the ability of ethanol to inhibit the metabolism of methanol to formic acid in humans. This inhibition was achieved without induction of lactic acidosis. Thus this case documents the efficacy of ethanol therapy in patients with methanol poisoning.

Acid-Base Equilibrium↗
PubMed1986

Exercise-induced hypertension after repair of coarctation of the aorta: arm versus leg exercise.

The etiology of exercise-induced upper limb hypertension after repair of coarctation of the aorta is unknown. We hypothesized that blood flow across the coarctation repair site is a major determinant of such exercise-induced hypertension. Because arm ergometry should produce a smaller increase in descending aortic blood flow than treadmill exercise, we compared the changes in upper limb pressure and the coarctation gradient produced by each type of exercise at equivalent levels of heart rate and peak oxygen consumption in 28 children with repaired coarctation of the aorta. The children were classified into three groups: Group I, resting gradient less than 15 mm Hg and treadmill gradient less than 20 mm Hg; Group II, resting gradient less than 15 mm Hg and treadmill gradient greater than 20 mm Hg; and Group III, resting gradient greater than or equal to 15 mm Hg. Twelve children with no heart disease served as control subjects. All children were exercised to exhaustion with 45 minutes' rest between the two exercise protocols. There were no differences in maximal heart rate and oxygen consumption between the two types of exercise. In all groups, treadmill exercise produced a larger increase in arm systolic blood pressure and arm-leg gradient than did arm exercise. With treadmill exercise coarctation Groups II and III developed a greater rise in both arm-leg gradient and arm systolic pressure than was observed in the control subjects (p less than 0.05). However, with arm exercise, Group III developed a significantly greater rise in both arm pressure and arm-leg gradient (p less than 0.05) than was observed in the control subjects.

Adolescent↗
PubMed1985

A double-membrane model for urinary bicarbonate secretion.

To define the transport pathway for HCO-3 secretion (JHCO3) across the apical and basolateral membranes of turtle bladder, we examined the effects of cAMP, isobutylmethylxanthine (IBMX), the Cl- channel blocker 9-anthroic acid (9-AA), and the disulfonic stilbene DIDS (4,4'-diisothiocyanostilbene-2,2'-sulfonic acid) on the electroneutral and electrogenic components of JHCO3. Total JHCO3 was measured by pH stat titration of the mucosal compartment after Na+ absorption and H+ secretion were abolished by ouabain and a delta pH, respectively. Addition of cAMP or IBMX increased total JHCO3 and induced a short-circuit current (ISC), accounting for a large part of JHCO3; net Cl- absorption was reduced. Mucosal 9-AA inhibited the IBMX-induced electrogenic component of JHCO3, whereas mucosal DIDS inhibited the electroneutral component and acetazolamide reduced both. We suggest that HCO-3 is generated within the cell by a Na-independent primary active acid-base transport at the basolateral membrane (H+ extrusion into the serosal compartment). Cellular HCO-3 accumulation drives JHCO3 via a Cl-HCO3 exchanger at the luminal membrane. IBMX and cAMP activate a 9-AA-sensitive anion conductance parallel to the exchanger. The apparent reversal of the transport elements between the two cell membranes (compared with H+-secreting cells) led to an ultrastructural examination of the carbonic anhydrase-rich cells.

1-Methyl-3-isobutylxanthine↗