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Biomedical subjects

J M Bergstein

Publications and source records attributed to J M Bergstein.

At least 37 records · Page 2Linked to original sources
PubMed1990

Pseudomembranous colitis: how useful is endoscopy?

Clostridium difficile colitis may be diagnosed either by endoscopy or by laboratory tests. To determine the role of endoscopy, we reviewed 59 cases of confirmed C. difficile colitis. In all patients, the etiology was confirmed by stool tests. Twenty-nine underwent lower gastrointestinal endoscopy. In 16 (55%) there was endoscopic confirmation of pseudomembranes while 4 (14%) had only nonspecific colitis. There was no apparent difference in the rate of detection of pseudomembranes between rigid sigmoidoscopy (57%), flexible sigmoidoscopy (50%), and colonoscopy (50%). Vancomycin and metronidazole were equally effective therapy but treatment with vancomycin cost more than 250 times that for metronidazole. There were no patients in whom the diagnosis was made by endoscopy alone. Endoscopy was costly and insensitive, while noninvasive stool tests were cheap and accurate. We conclude that endoscopy should be relegated to a secondary role in the workup of antibiotic-associated diarrhea.

Colonoscopy↗
PubMed1990

Glomerular fibrin deposition and removal.

Glomerular fibrin deposits may occur within vessels or in extracapillary crescents. Studies suggest that intravascular thrombosis is promoted by endothelial cell activation/injury, resulting in the release of endothelial-cell-derived tissue factor procoagulant, fibrinolytic inhibitors, platelet activating factor, and large multimers of von Willebrand factor. Fibrin in crescents may arise from coagulation of plasma in Bowman's space mediated by the release of tissue factor from infiltrating macrophages. Glomerular fibrin may be removed by fibrinolytic or phagocytic mechanisms or persist and lead to glomerular obsolescence. Suppression or elimination of factors that promote glomerular fibrin deposition and enhancement of mechanisms that remove glomerular fibrin may be important in the recovery from several forms of human kidney disease.

Animals↗
PubMed1990

Temporary abdominal closure (TAC) for planned relaparotomy (etappenlavage) in trauma.

Planned relaparotomy (temporary abdominal closure) was studied prospectively in 20 trauma patients. Four died in the first 24 hours from hypothermia, coagulopathy, shock (three), and septic shock (one). The 16 survivors had a Velcro-like prosthetic placed to facilitate abdominal closure and re-entry. Prosthetic was necessary in eight because bowel edema precluded fascial closure, and useful for removal of packing (three) and for the management of peritonitis (five). The prosthetic did not open spontaneously, nor was it associated with evisceration or bowel fistula. Temporary abdominal closure (TAC) permitted reappraisal and staged repair of intra-abdominal pathology, including bowel resection and anastomosis. TAC identified 14 problems early: bleeding (five), bile leaks (two), GI complications (six), liver necrosis (one). Five patients developed superficial wound infections, and three went on to develop fascial necrosis.

Abdominal Injuries↗
PubMed1989

Treatment of severe IgA nephropathy in children.

We treated ten children with severe IgA nephropathy (IgAN) [proteinuria greater than 1 g/day, hypertension, renal insufficiency, segmental sclerosis, crescent formation and/or glomerular basement membrane (GBM) deposition of IgA] with prednisone and azathioprine for 1 year. Following the year of therapy, seven of the ten children underwent a repeat kidney biopsy. All biopsies were scored for activity (percentage of glomeruli demonstrating crescent formation, degree of mesangial proliferation and interstitial infiltrate; maximum score = 9) and chronicity (percentage of glomeruli demonstrating fibrous crescents, segmental sclerosis, global sclerosis, and degree of tubular atrophy and interstitial fibrosis; maximum score = 12). After 1 year of therapy, the protein excretion of all the children decreased significantly (P less than 0.01) from 4,052 +/- 3,190 mg/day to 1,692 +/- 1,634 mg/day. The activity score decreased significantly (P less than 0.01) from 4.35 +/- 0.94 prior to therapy to 2.28 +/- 0.75 after therapy while the chronicity score was unchanged (5.42 +/- 1.7 vs 5.85 +/- 2.0). The percentage of glomeruli demonstrating cellular crescents decreased (P less than 0.05) from 21.2 +/- 21.7% prior to therapy to 0.94 +/- 2.4% after therapy. Mesangial deposition of IgA persisted but GBM deposition of IgA was less prominent after therapy. During the follow-up period (mean 2.6 years, range 9 months-7.5 years), one child required brief retreatment for biopsy-confirmed recurrence of active disease, two children have developed renal insufficiency due to progressive scarring in the absence of inflammation, while the remaining seven are stable. We suggest that treatment with prednisone and azathioprine may be beneficial in children with severe IgAN and that a controlled clinical trial is warranted.

Adolescent↗
PubMed1989

Tissue plasminogen activator therapy of glomerular thrombi in the Shwartzman reaction.

To study the effect of tissue plasminogen activator (TPA) therapy on glomerular fibrin deposition in the generalized Shwartzman reaction, rabbits were given an intravenous injection of TPA immediately following or three, four, or five hours after the second injection of endotoxin. Animals were sacrificed six hours after the second dose of endotoxin. Glomerular fibrin deposition was reduced in animals receiving TPA four hours after the second injection of endotoxin and was absent in animals receiving TPA five hours after the second dose of endotoxin. Glomerular fibrinolytic activity was reduced following development of the generalized Shwartzman reaction but was normal in animals that received TPA five hours after the second injection of endotoxin. TPA did not produce a systemic fibrinolytic state and did not prevent the decline in hematologic and coagulation factors typical of the Shwartzman reaction, despite the elimination of glomerular fibrin. These results suggest that TPA effectively removes glomerular thrombi in the generalized Shwartzman reaction and infers that TPA may be of value in the treatment of human diseases with similar pathology, such as the hemolytic uremic syndrome.

Animals↗
PubMed1988

Analysis of the plasminogen activator activity of the human glomerulus.

An assay was developed to measure plasminogen activator activity from isolated human glomeruli. Activator was extracted from individual glomeruli with 0.2 M phosphate-buffered saline, pH 7.4 (PBS), containing 0.01% Triton X-100 and quantitated in 125I-fibrin films. Quenching studies using antibodies to tissue plasminogen activator and urokinase revealed that the extracted glomerular plasminogen activator activity contained both tissue plasminogen activator of urokinase. Monoclonal and polyclonal antibodies raised to tissue plasminogen activator demonstrated low-level inhibition of urokinase activity and monoclonal and polyclonal antibodies to urokinase demonstrated low-level inhibition of tissue plasminogen activator activity. The assay should be applicable to the study of glomerular plasminogen activator activity in experimental and human kidney diseases. The detection of antibody cross-reactivity to tissue plasminogen activator and urokinase may be related to the sensitivity of the 125I-fibrin assay and to the structural similarities of these activators.

Humans↗
PubMed1987

Calcium carbonate is an effective phosphorus binder in children with chronic renal failure.

We evaluated the effectiveness of calcium carbonate as a phosphate binder in 19 children with chronic renal failure; ten children were undergoing dialysis therapy (eight maintained by CAPD and two by hemodialysis). Twelve children had previously received aluminum hydroxide, while calcium carbonate was the primary phosphate binder used in seven children. Among all the children, the serum phosphorus level on no phosphate binder was 7.4 +/- 0.9 mg/dL, which decreased significantly (P less than .001) to 5.9 +/- 0.8 mg/dL during calcium carbonate therapy, while the serum calcium, bicarbonate, and creatinine were unchanged. The reduction in the serum phosphorus level occurred while dietary intake of calcium and phosphorus were unchanged, as demonstrated by three-day dietary records. The dose of calcium carbonate required to maintain the serum phosphorus in the normal range varied from 600 mg to 15 g/d (mean 7.4 g/d). Among the 12 children and four others who had received aluminum hydroxide, serum aluminum levels fell from 108.8 +/- 121.8 ng/mL to 36.1 +/- 29.1 ng/mL after aluminum hydroxide was stopped (P less than .05). Serum alkaline phosphatase and parathyroid hormone (PTH) levels during aluminum hydroxide therapy were similar to levels obtained during calcium carbonate therapy, while PTH levels fell in children treated initially with calcium carbonate. All the children have been observed for a mean of 12.0 months (range 4 months to 3 1/2 years). Hypercalcemia occurred in seven children, usually when vitamin D therapy was initiated or the dose changed. Hypercalcemia resolved with adjustment of the vitamin D or calcium carbonate dose in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Purine excretion during tumor lysis in children with acute lymphocytic leukemia receiving allopurinol: relationship to acute renal failure.

We measured serial urine levels of hypoxanthine, xanthine, and uric acid in 19 children with acute lymphocytic leukemia (ALL) receiving allopurinol therapy during tumor lysis; four of these children developed acute renal failure. The urinary excretion of uric acid rose moderately from 447 +/- 251 micrograms/dl glomerular filtrate before chemotherapy to 778 +/- 463 micrograms/dl glomerular filtrate during tumor lysis (P less than 0.05) whereas the urinary excretion of hypoxanthine (17.9 +/- 15 to 292 +/- 213 micrograms/dl glomerular filtrate) and xanthine (74 +/- 62 to 1091 +/- 1085 micrograms/dl glomerular filtrate) rose dramatically (P less than 0.001). The urinary excretion of uric acid, hypoxanthine, and xanthine per deciliter of filtrate was significantly higher (P less than 0.001) in those who developed acute renal failure than in those who did not, but the highest urine concentration of these purine metabolites did not differ in the two groups. In all 19 children, the highest urine concentration of uric acid and hypoxanthine during tumor lysis did not exceed the solubility limit of each in an alkaline urine specimen. In contrast, the peak urine concentration of xanthine exceeded its solubility limit in an alkaline urine specimen in 16 of 19 children. The urine sediment during the period of tumor lysis was examined by diffuse reflectance infrared spectroscopy; precipitated xanthine was found in sediment from eight of the 19 children, was significantly (P less than 0.001) associated with a urine xanthine level greater than 350 mg/dL, and occurred with equal frequency in those who did or did not develop acute renal failure. We conclude that urinary excretion of hypoxanthine and xanthine increases dramatically whereas uric acid excretion rises moderately in children undergoing tumor lysis while receiving allopurinol, that acute renal failure occurs in children with a higher purine load per deciliter of glomerular filtrate, but that factors other than tubular precipitation of purine metabolites are likely to be involved in the pathogenesis of renal failure during tumor lysis.

Acute Kidney Injury↗
PubMed1986

IgA nephropathy in children: significance of glomerular basement membrane deposition of IgA.

Seventeen children with IgA nephropathy were grouped according to the absence (group I, n = 10) or presence (group II, n = 7) of glomerular basement membrane (GBM) deposition of IgA to determine whether GBM deposition of IgA correlated with laboratory or pathologic data at diagnosis or clinical status at follow-up. Children in group II had significantly (p less than 0.01) more proteinuria at diagnosis than children in group I. The percentage of glomeruli demonstrating crescent formation was significantly (p less than 0.05) higher in group II biopsies. Chronic changes of fibrous crescents, segmental sclerosis, global obsolescence, tubular atrophy, and interstitial fibrosis were also significantly (p less than 0.001) more common in group II biopsies. After a mean follow-up period of 2 years, all children in group II have persistent proteinuria of more than 1 g/24 h, and 3 of 5 have renal insufficiency (2 require dialysis). In contrast, 2 of 9 group I children have proteinuria exceeding 1 g/24 h, and only 1 has renal insufficiency. We conclude that, as compared to children with IgA localized to the mesangium, children with IgA nephropathy and GBM deposition of IgA have a higher urinary protein excretion at the time of diagnosis, more severe histologic alterations including a greater percentage of glomeruli demonstrating crescent formation, more chronic changes of segmental or global sclerosis, tubular atrophy, and interstitial fibrosis. Such children usually have persistent proteinuria and are more likely to develop progressive renal disease.

Adolescent↗
PubMed1986

Role of glutathione in protecting endothelial cells against hydrogen peroxide oxidant injury.

To determine the mechanism responsible for the enhanced susceptibility of endothelial cells to oxidant injury in the absence of glucose, we induced endothelial cell injury with oxygen radicals in the presence of various oxygen radical scavengers and measured endothelial cell levels of glutathione after oxidant injury in the presence and absence of glucose. Endothelial cells were damaged with toxic oxygen radicals generated by phorbol myristate acetate (PMA)-activated polymorphonuclear leukocytes (PMNs) or xanthine-xanthine oxidase in the presence and absence of glucose and catalase (scavenger of hydrogen peroxide), superoxide dismutase (scavenger of superoxide radical), isoleucine, valine, and serine (scavengers of hypochlorous acid), or mannitol, ethanol, benzoic acid, dimethyl sulfoxide, and dimethyl thiourea (scavengers of hydroxyl radical). Endothelial cell injury was quantitated by 2-deoxy-[1-3H] glucose or chromium 51 release assays or both. In each oxidant-generating system, in the presence and absence of glucose, only catalase significantly protected endothelial cells from oxidant injury (P less than 0.001). When endothelial cells were damaged by hydrogen peroxide generated with xanthine-xanthine oxidase in the presence of glucose, endothelial cell levels of glutathione remained unchanged. In contrast, when endothelial cells were damaged with xanthine-xanthine oxidase in the absence of glucose, endothelial cell levels of glutathione fell to less than 50% of baseline (P less than 0.05). Xanthine-xanthine oxidase-mediated endothelial cell damage and depletion of glutathione in the absence of glucose were similar to results obtained in the presence of glucose when glutathione was depleted with buthionine sulfoximine, diethyl maleate, or 1-chloro-2,4-dinitrobenzene.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzoates↗
PubMed1985

Decreased plasma fibronectin levels in children with hemolytic-uremic syndrome.

Fibronectin is a normal plasma glycoprotein thought to have an important role in platelet aggregation and clot formation. Because of the participation of the coagulation system in hemolytic-uremic syndrome, the present study sought to determine if fibronectin plays a role in the pathogenesis of this disease. With this purpose in mind, plasma fibronectin levels were measured in 17 children with the clinical diagnosis of hemolytic-uremic syndrome and in 22 age-matched control subjects. Fibronectin levels were significantly depressed in 13 of 17 (76 percent) patients with hemolytic-uremic syndrome during the acute phase of their illness. The levels did not correlate with age, sex, serum creatinine level, platelet count, or hemoglobin concentration. Serial plasma samples were available in eight of these patients: fibronectin remained depressed from two to 10 days and then returned toward the normal range concomitant with increasing platelet counts and improvement in renal function. During remission, fibronectin levels were normal in all nine patients tested. To try to determine if fibronectin is deposited in the kidney during hemolytic-uremic syndrome, kidney biopsy specimens from six patients with hemolytic-uremic syndrome were examined by immunofluorescence for the presence of fibronectin, fibrinogen, and platelet antigens. Extensive deposition of all three antigens was demonstrated along the glomerular capillary wall in all biopsy specimens. In conclusion, plasma fibronectin levels are decreased during the acute phases of hemolytic-uremic syndrome in the majority of patients. Kidney biopsy findings suggest that fibronectin is intimately involved in the activation of the coagulation system in this disease and that decreased plasma fibronectin levels in hemolytic-uremic syndrome may be due, at least in part, to accelerated consumption of the protein at the sites of injury.

Adolescent↗
PubMed1985

Nephrolithiasis in childhood inflammatory bowel disease.

Six children with inflammatory bowel disease and nephrolithiasis are reported. Their mean age at the passage of the first stone was 12.5 years and the mean duration of active inflammatory bowel disease was 34.5 months. Four had ulcerative colitis and two had Crohn's disease. In three patients, the onset of stone disease was associated with a flare in the bowel disease. Stone passage in four patients was accompanied by an increase in abdominal pain; three experienced gross hematuria. Stones from four of the patients were composed primarily of calcium phosphate; stones from the remaining patients contained uric acid and/or calcium oxalate. The pathogenesis of nephrolithiasis as it relates to inflammatory bowel disease is considered and an approach to therapy offered.

Adolescent↗
PubMed1985

Aluminum bone disease in children: radiographic features from diagnosis to resolution.

Two children with chronic renal failure developed aluminum intoxication as a result of long-term ingestion of aluminum hydroxide for the control of hyperphosphatemia. In each child, bone biopsy confirmed severe osteomalacia, the absence of features of hyperparathyroid bone disease, and massive aluminum deposition at the bone-osteoid junction. Radiographs during the period of aluminum intoxication demonstrated osteopenia, pathologic fractures, fraying of the metaphyses of the long bones, and widening of the physis. When aluminum hydroxide therapy was discontinued (each patient) and aluminum was removed with chelation therapy (one patient), radiographs demonstrated a distinctly unusual pattern of healing. Calcification of the long bones began at the most recently formed osteoid and then proceeded toward the diaphysis. This unusual healing pattern created lucent defects and a transient "bone within a bone" appearance, which resolved with further healing.

Aluminum Hydroxide↗
PubMed1985

In vitro detection of endothelial cell damage using 2-deoxy-D-3H-glucose: comparison with chromium 51, 3H-leucine, 3H-adenine, and lactate dehydrogenase.

To develop a sensitive in vitro assay for detecting endothelial cell damage, we radiolabeled endothelial cell monolayers with tracer amounts of 2-deoxy-D-[1-3H]-glucose (3HDOG). We damaged identical cohorts of endothelial cells radiolabeled with 3HDOG or chromium 51 by exposing monolayers to toxic oxygen radicals generated by xanthine-xanthine oxidase or phorbol myristate acetate (PMA)-activated polymorphonuclear leukocytes (PMNs), a surface active agent (Triton X-100), and anti-HLA antibodies and complement. With each mechanism of injury, the 3HDOG assay detected significant (P less than 0.01) endothelial cell damage at lower concentrations of the injurious agent than the 51Cr assay. When endothelial monolayers were damaged by xanthine-xanthine oxidase or PMA-activated PMNs, efflux of 3HDOG was reduced (range 71% to 94% reduction) by superoxide dismutase and catalase, indicating that efflux of 3HDOG was mediated by toxic oxygen radicals. When monolayers were damaged with xanthine oxidase in the absence of glucose, a much lower concentration of xanthine oxidase was required to initiate efflux of 3HDOG as compared with xanthine oxidase injury in the presence of glucose. Additional studies compared the 3HDOG assay with 3H-adenine, 3H-leucine, and lactate dehydrogenase (LDH) release when endothelial cells were exposed to toxic oxygen radicals generated by PMA-activated PMNs and xanthine-xanthine oxidase. Again, the 3HDOG assay was more sensitive in detecting in vitro endothelial cell damage. We conclude that the 3HDOG assay is more sensitive than the 51Cr, 3H-adenine, 3H-leucine, or LDH release assays in detecting endothelial cell damage in vitro.

Adenine↗
PubMed1984

Aluminum intoxication from aluminum-containing phosphate binders in children with azotemia not undergoing dialysis.

Aluminum intoxication developed in three infants with azotemia who were not undergoing dialysis and who had been treated with aluminum hydroxide from the first month of life. Biopsies of the iliac crest demonstrated the presence of severe osteomalacia and massive deposition of aluminum in the bone. Serum aluminum levels were significantly (P less than 0.001) higher in these 3 infants and in 1 other, all of whom received more than 100 mg of elemental aluminum per kilogram of body weight per day (mean +/- S.D., 371.0 +/- 178.9 ng per milliliter [13.75 +/- 6.6 mumol per liter] ) than they were in 8 older children with azotemia who were not undergoing dialysis and who received less than 100 mg of elemental aluminum per kilogram per day (27.0 +/- 18.6 ng per milliliter [1.0 +/- 0.68 mumol per liter] ), 7 such children who did not receive aluminum hydroxide (20.28 +/- 9.2 ng per milliliter [0.75 +/- 0.34 mumol per liter] ), and 16 children with normal renal function (21.04 +/- 4.9 ng per milliliter [0.78 +/- 0.18 mumol per liter] ). In all the children with azotemia who were treated with aluminum hydroxide, there was a positive correlation (r = 0.90; P less than 0.01) between the serum aluminum level and the daily dose of elemental aluminum. These studies indicate that gastrointestinal absorption of aluminum can lead to aluminum intoxication in children with azotemia, and that infants may be particularly susceptible to this complication of therapy.

Adolescent↗
PubMed1983

Long-term outpatient amphotericin B therapy via a silicone central alimentation catheter.

A 6-yr-old boy with systemic histoplasmosis received intravenous amphotericin B for two months as an outpatient utilizing techniques developed for home parenteral nutrition. The therapy was administered on alternate days in the emergency room by nurses trained to use aseptic technique. No complications occurred. The merits of this technique include avoidance of prolonged hospitalization with its high cost and risk of nosocomial infection and better patient acceptance with the patient living at home and continuing many of his usual activities.

Ambulatory Care↗