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Biomedical subjects

M E Ament

Publications and source records attributed to M E Ament.

At least 37 records · Page 2Linked to original sources
PubMed1998

Red cell aplasia in children on tacrolimus after liver transplantation.

Hematological toxicity of tacrolimus has been rarely reported. We report two pediatric recipients of liver transplantation with anemia. They were treated with tacrolimus for 8 and 47 months, respectively, before developing pure red cell aplasia (PRCA) confirmed by bone marrow biopsy. The children recovered quickly on withdrawal of tacrolimus. The clinical profile of these children is compared with the only other patient reported in the literature with PRCA due to tacrolimus. All three patients had similar hematological findings. However, the mechanism of the tacrolimus-induced PRCA in these children appears to be different from that reported in the adult patient.

Adult↗
PubMed1998

Long-term quantitative results following fundoplication and antroplasty for gastroesophageal reflux and delayed gastric emptying in children.

BACKGROUND: The operative management of children with combined gastroesophageal reflux and delayed gastric emptying is controversial. This study measures the long-term follow-up of gastric emptying in children who have undergone gastroesophageal fundoplication combined with antroplasty. METHODS: Fifteen randomly selected children with gastroesophageal reflux and scintigraphically demonstrated delayed gastric emptying underwent fundoplication and antroplasty. Each patient had another gastric emptying scintigraphic study performed an average of 3.6 years postoperation. RESULTS: All patients reported improvement of their symptoms compared with before the operation, and none required further medical therapy for gastroesophageal reflux or experienced dumping syndrome. Eleven of the 15 patients had significant long-term improvement of their gastric emptying postoperatively. The mean percent of isotope meal remaining in the stomach at 90 minutes improved from 72% preoperatively to 40% postoperatively (P = 0.0005). CONCLUSIONS: Gastric emptying in children with gastroesophageal reflux and delayed gastric emptying is significantly improved for several years in three-fourths of patients after fundoplication and antroplasty. Fundoplication and concomitant antroplasty are recommended for symptomatic children with documented gastroesophageal reflux and delayed gastric emptying.

Adolescent↗
PubMed1997

Delayed encephalopathy in fulminant hepatic failure in the pediatric population and the role of liver transplantation.

BACKGROUND: Liver transplantation is the therapeutic choice for fulminant hepatic failure in children. METHODS: All 66 cases of fulminant hepatic failure in the pediatric population seen at UCLA from May, 1985 to November, 1993 were reviewed to determine changes in survival rates since the advent of liver transplantation. We evaluated the clinical course and events leading to the exclusion of surgical management of nonsurvivors, who otherwise would have benefited from a liver transplant. We also compared the latter's clinical course with the nontransplant survivors to determine parameters for screening patients for liver transplantation. RESULTS: Fifty-one patient (77%) were put on the transplant list initially but eventually, only 38 (58%) patients underwent orthotopic liver transplantation (OLT) and of these 30 (79%) patients survived. Of the remaining 29 (42%) patients who did not undergo liver transplantation, only 10 (36%) patients survived. Nine patients died while waiting for a donor liver secondary to complications of hepatic failure. The majority of nonsurvivors in the OLT and no-OLT groups succumbed because of irreversible neurologic deterioration. In the no-OLT group, comparisons between survivors and non-survivors were made. There were no significant demographic differences. It took a mean of 8 days (+/-8) versus 22 days (+/-15), (p = 0.009), from onset of illness to first hospital admission for survivors and nonsurvivors, respectively. Time to reach stage II encephalopathy was a mean of 5 days (+/-5) for survivors versus 18 days (+/-16), (p = 0.05) for nonsurvivors. Nonsurvivors were transferred to the transplant center at a mean of 12.2 days (+/-12) after being first admitted elsewhere as compared to a mean of 1.9 days (+/-18) for survivors, (p = 0.02). Mean prothrombin time decreased by a mean of 13.4 s/day (+/-16) for survivors as against 2.25 s/day (+/-6) for nonsurvivors, (p = 0.06). Mean peak total bilirubin for nonsurvivors was 460 mumol/L (27 mg/dl) versus 220 mumol/L (13 mg/dl) for survivors, (p = 0.06). Nonsurvivors died at a mean of 30 days (+/-19) from onset and survivors' liver tests started to improve at a mean of 11 days (+/-9) from onset. CONCLUSIONS: From these studies, we conclude that liver transplantation remains the therapeutic choice for fulminant hepatic failure in children. Early referral and closer follow-up is necessary for timely admission to liver transplant centers to enable screening and proper preparation of these patients for liver transplantation.

Adolescent↗
PubMed1997

Combination of "patch, drain, and wait" and home total parenteral nutrition for midgut volvulus with massive ischemia/necrosis.

The successful use of a combination of "patch, drain, and wait" (PDW) and home total parenteral nutrition (TPN) in the management of a case of acute, catastrophic midgut volvulus in a 2-year-11-month-old boy with near-total ischemia/necrosis of his small intestine is reported. The PDW approach to the highly effective management of acute midgut ischemia/necrosis in infancy and childhood (necrotizing enterocolitis and midgut volvulus) involves maximum gut salvage by avoidance of resection, stoma formation, or both through the use of extensive peritoneal cavity drainage by Penrose drains, TPN, and broad-spectrum antibiotics. The extensive peritoneal drainage fosters capture of enteric fistulas with the formation of enterostomies at drain exit sites, while adhesions and ischemia/inflammation-induced hypervascular obliteration of the peritoneal cavity diminish the potential for peritonitis (no peritoneal cavity, no peritonitis) and facilitate impressive salvage of seemingly hopelessly lost ischemic/necrotic gut (a simulation of the in utero ischemic gut process leading to atresias and some varying, but generally mild, gut loss) while simultaneously contributing to the resorption of absolutely non-salvageable gut and the creation of a remarkably clean and adhesion-free peritoneal cavity resembling that of a newborn infant with midgut intestinal atresia.

Abdomen, Acute↗
PubMed1996

Malabsorption of apple juice and pear nectar in infants and children: clinical implications.

Ingestion of fruit juices in which there is an imbalance between glucose and fructose (apple, pear nectar) and the presence of sorbitol is one of the major causes of the syndrome of chronic, nonspecific diarrhea of infancy and childhood. Stools in the condition at time of symptoms are acidic with a pH < 5.5, Clinitest positive, but free of blood and white cells. Lactose and sucrose breath hydrogen tests are normal but breath hydrogen is elevated if measured between 60-120 minutes after the offending juice is taken in sufficient quantity to elicit symptoms. Elimination of the offending juices immediately stopped the diarrhea in all of the cases. Three cases are presented documenting the variability of symptoms including one adolescent who became symptomatic while on a fruit and juice diet.

Beverages↗
PubMed1996

Chronic liver disease in children on long-term parenteral nutrition.

Use of long-term total parenteral nutrition (TPN) is often presumed to be associated with serious hepatic dysfunction. In this retrospective study, we reviewed the complete charts of patients who had received TPN for more than 2.5 years, starting in infancy or childhood, for evidence of liver dysfunction. There were 16 male and 10 female patients with a total of 254.5 patient years on TPN. Seventeen patients have been on TPN since birth or early infancy. Thirteen of 26 patients derive > or = 90% of their calorie intake from TPN. Six patients had hepatomegaly; two of them also had splenomegaly. Twenty-one patients had normal transaminases, nine have had past episodes of raised enzymes ranging from 2.5 to 7.5 times normal. Seventeen patients always had normal bilirubin levels, five had past episodes of hyperbilirubinaemia, while four patients had persistently raised bilirubin levels (range 1.5-20.7 g/dl). Alkaline phosphatase was normal for age in all patients except two. Hepatic synthetic function, as measured by albumin, pre-albumin levels and prothrombin time, was within the normal range in all patients except one. Liver biopsies were performed in eight patients. Two biopsies showed cirrhosis, one showed chronic active hepatitis (CAH) with cholestasis, two patients had fibrosis, one showed cholestasis and two biopsies were normal. One patient with cirrhosis and one with CAH were positive for hepatitis C antibody. Another asymptomatic patient was positive for hepatitis B. Only the patient with CAH had hepatic decompensation. We conclude that clinical hepatic failure is uncommon in our group of patients on long-term TPN for 2.5 years or more. Cirrhosis and fibrosis, when found, could not be solely attributed to TPN.

Adolescent↗
PubMed1996

Gastroesophageal reflux in childhood.

Gastroesophageal reflux (GER) is one of the most frequent symptomatic clinical disorders affecting the gastrointestinal tract of infants and children. During the past 2 decades, GER has been recognized more frequently because of an increased awareness of the condition and also because of the more sophisticated diagnostic techniques that have been developed for both identifying and quantifying the disorder. Gastroesophageal fundoplication is currently one of the three most common major operations performed on infants and children by pediatric surgeons in the United States. Normal gastroesophageal function is a complex mechanism that depends on effective esophageal motility, timely relaxation and contractility of the lower esophageal sphincter, the mean intraluminal pressure in the stomach, the effectiveness of contractility in emptying of the stomach, and the ease of gastric outflow. More than one of these factors are often abnormal in the same child with symptomatic GER. In addition, in patients with GER disease, and particularly in those patients with neurologic disorders, there appears to be a high prevalence of autonomic neuropathy in which esophagogastric transit and gastric emptying are frequently delayed, producing a somewhat complex foregut motility disorder. GER has a different course and prognosis depending on the age of onset. The incompetent lower esophageal sphincter mechanism present in most newborn infants combined with the increased intraabdominal pressure from crying or straining commonly becomes much less frequent as a cause of vomiting after the age of 4 months. Chalasia and rumination of infancy are self-limited and should be carefully separated from symptomatic GER, which requires treatment. The most frequent complications of recurrent GER in childhood are failure to thrive as a result of caloric deprivation and recurrent bronchitis or pneumonia caused by repeated pulmonary aspiration of gastric fluid. Children with GER disease commonly have more refluxing episodes when in the supine position, particularly during sleep. The reflux of acid into the mid or upper esophagus may stimulate vagal reflexes and produce reflex laryngospasm, bronchospasm, or both, which may accentuate the symptoms of asthma. Reflux may also be a cause of obstructive apnea in infants and possibly a cause of recurrent stridor, acute hypoxia, and even the sudden infant death syndrome. Premature infants with respiratory distress syndrome have a high incidence of GER. Esophagitis and severe dental carries are common manifestations of GER in childhood. Barrett's columnar mucosal changes in the lower esophagus are not infrequent in adolescent children with chronic GER, particularly when Heliobacter pylori is present in the gastric mucosa. Associated disorders include esophageal dysmotility, which has been recognized in approximately one third of children with severe GER. Symptomatic GER is estimated to occur in 30% to 80% of infants who have undergone repair of esophageal atresia malformations. Neurologically impaired children are at high risk for having symptomatic GER, particularly if nasogastric or gastrostomy feedings are necessary. Delayed gastric emptying (DGE) has been documented with increasing frequency in infants and children who have symptoms of GER, particularly those with neurologic disorders. DGE may also be a cause of gas bloat, gagging, and breakdown or slippage of a well-constructed gastroesophageal fundoplication. The most helpful test for diagnosing and quantifying GER in childhood is the 24-hour esophageal pH monitoring study. Miniaturized probes that are small enough to use easily in the newborn infant are available. This study is 100% accurate in diagnosing reflux when the esophageal pH is less than 4.0 for more than 5% of the total monitored time.

Adult↗
PubMed1996

Orofacial lesions in Crohn's disease.

We describe a female patient with Crohn's disease who presented with longstanding gingival swelling. She went into remission after surgery, but had labial involvement while in remission. A review of the literature is presented with special reference to the clinical characteristics of orofacial Crohn's disease and Melkersson-Rosenthal syndrome, which can mimic such presentation of Crohn's disease.

Adult↗
PubMed1995

Overinterpretation of gastroduodenal motility studies: two cases involving Munchausen syndrome by proxy.

Two children were thought to have an atypical gastroduodenal motility disorder because of the history and clinical course; both had received parenteral alimentation because of claims of inability to tolerate enteral feedings, and both continued to have unusual medical problems during parenteral alimentation. Both children had motility studies that were interpreted by a pediatric gastroenterologist to be "abnormal" and "diagnostic" of a motility disorder, but each was eventually shown to have a behavioral abnormality related to Munchausen syndrome by proxy.

Child, Preschool↗
PubMed1995

Excessive urinary oxalate excretion occurs in long-term TPN patients both with and without ileostomies.

OBJECTIVE: To determine if excessive oxalate and deficient citrate excretion were associated with TPN-associated nephropathy. DESIGN: Crossectional cohort. SETTING: Outpatient clinic. SUBJECTS: Twenty-five patients (15 males, 10 females) aged 51 +/- 17 (mean +/- SD) years who had received home total parenteral nutrition (TPN) for 10 +/- 4 years. Fifteen subjects had ileostomies (Group A) and 10 had functional colons (Group B). OUTCOME MEASURES: Glomerular filtration rate (GFR), tubular reabsorption of phosphate (TRP), urinary oxalate and citrate excretion. RESULTS: The mean GFR was 68.1 +/- 34.5 ml/minute/1.73 m2 and did not differ between Groups A and B. The mean TRP was 65.0 +/- 32.2% for Group A and 80.5 +/- 16.0% for Group B. The difference was not statistically significant. Urinary oxalate and citrate excretion were 40.2 +/- 30.2 and 324.4 +/- 239.0 mg/day respectively for Group A, and 63.2 +/- 34.2 and 474.8 +/- 936.3 respectively for Group B. The differences were not statistically significant. Thirty-eight percent (38%) of patients with ileostomies and 78% of patients without ileostomies had excessive urinary oxalate excretion (> 40 mg/day). Fifteen percent (15%) of patients with ileostomies and 50% of patients without ileostomies had decreased urinary citrate excretion (< 140 mg/day). CONCLUSIONS: Increased endogenous oxalate production may occur in patients receiving long-term TPN.

Absorption↗
PubMed1995

Metabolic alterations of zinc and prostaglandins in both human and animal colonic tumor cells.

OBJECTIVE: To understand the relationship between zinc and prostaglandin (PG) metabolisms in inducing colon cancer incidence in human and animals. METHODS: Human colonic tumor and normal cells were obtained from Departments of Surgery and Pathology at the Kaiser Permanente Medical Center, Los Angeles, CA and US VA Medical Center, North Hills, CA. Rat colonic tumor and normal cells were isolated from the rats that received two injections of 50 mg/kg of Azoxymethan (AOM) in 2 weeks and then kept 30 weeks in the animal facility. Then, the effects of zinc on the PGE2 synthesis and PGE2 on zinc metabolism in tumor and normal cells were determined. RESULTS: PGE2 concentrations in both human and AOM-induced rat colonic tumor cells increased compared to those in adjacent normal colonocytes, whereas PGF2 alpha concentrations did not change. Gene expression of inducible form of prostaglandin synthase (PGS-2) is stimulated in rat colonocytes by epidermal growth factor and by tetradecanoyl 13-phorbol acetate (a tumor promoter and mitogen) only in the presence of zinc. PGE2 binding activity of rat enterocytes was maximum at 15 microM of zinc (normal plasma zinc concentration), but PGE2 synthesis activity increased for the first 15 minutes when extracellular zinc concentrations were either higher or lower than the normal extracellular zinc concentration. However, variations in extracellular zinc concentrations did not change the rate of PGF2 alpha synthesis in the normal rat enterocytes. PGE2 significantly increased zinc uptake rates of colonic tumor cells but PGF2 alpha showed only moderate effect. CONCLUSIONS: These results suggest that zinc is required for PGS-2 gene expression, that maintaining an optimal zinc nutriture is important for normal PG synthesis of intestinal cells, and that only PGE2 synthesis mechanisms rather than PGS-2 gene expression are altered in colonic tumor cells resulting in the abnormal zinc nutriture of these cells.

Animals↗
PubMed1995

Intestinal immune function is unaffected by parenteral nutrition in man.

BACKGROUND: Animal studies have demonstrated intestinal immunoglobulin production is decreased when luminal nutrition is withheld and nutrition is provided solely on the basis of total parenteral nutrition (TPN). METHODS: Eight normal volunteers were hospitalized in the Clinical Research Center for three weeks. The subjects received TPN as an exclusive means of nutritional support for 14 days followed by 5 days of enteral feeding with either standard or a glutamine- and arginine-supplemented formula in which the protein source was primarily free amino acids and peptides. Endoscopic jejunal biopsies obtained before and after TPN and following enteral refeeding were evaluated by immunofluorescence for the number of IgA, IgM and IgG-producing cells; T and B cells as well as intraepithelial and lamina propria lymphocytes were also counted. Serum immunoglobulins and the molecular forms of serum IgA were determined at the same intervals. RESULTS: The number of intestinal IgA-, IgM- and IgG-producing cells was unaffected by TPN (676 +/- 58 vs. 643 +/- 38, 101 +/- 14 vs. 98 +/- 18, 10 +/- 1 vs. 11 +/- 2 per low power field). The total number of intestinal lymphocytes, and CD3+ lymphocytes in the intraepithelial area was unaffected by TPN (10.4 +/- 0.4 vs. 10.2 +/- 1.3, 7.3 +/- 0.8 vs. 8.6 +/- 1.6 per 100 epithelial cells). Similarly, the total number of lymphocytes and CD3+ lymphocytes in the intestinal lamina propria was unaffected by TPN (4.4 +/- 0.2 vs. 6.2 +/- 0.8, 3.3 +/- 0.7 vs. 4.5 +/- 0.8). A small, but statistically significant increase in serum IgA and IgM was seen with TPN 314 +/- 11 vs. 342 +/- 16 mg/dL and 154 +/- 25 vs. 226 +/- 47 mg/dL, although IgG remained unchanged (1262 +/- 69 vs. 1207 +/- 57 mg/dL). The proportion of polymeric and monomeric serum IgA remained unchanged after TPN (19.2 vs. 22.1% polymeric). CONCLUSIONS: The use of TPN is not associated with intestinal immune dysfunction in man. A small, but statistically significant increase in serum IgM, and a borderline statistically significant increase in serum IgM were associated with TPN. The etiology and clinical significance of these observations is unclear.

Adult↗
PubMed1995

The treatment of intractable rejection with tacrolimus (FK506) in pediatric liver transplant recipients.

We report our experience in 17 pediatric orthotopic liver transplant (OLT) patients converted from cyclosporine (CsA) to FK506 for intractable acute and chronic rejection. FK506 was initiated orally at a dose of 0.3 mg/kg/day in most patients; the dose was then adjusted to achieve serum levels of 0.5-1.5 ng/ml. Azathioprine was discontinued and low-dose prednisone maintained. The median time between liver transplantation and FK506 conversion was 41 months. Patients have been treated for an average of 14.8 +/- 9.6 months. Six patients were converted for acute rejection and 11 for chronic rejection, i.e., vanishing bile duct syndrome (VBDS). After FK506 conversion, the actual patient and graft survival was 88% and 82%, respectively, in the group as a whole. Two patients died, one of chronic active hepatitis C and the other of lymphoma. Three patients, all with VBDS, did not respond to FK506 and therefore required retransplantation. The serum bilirubin is currently normal in 14 patients and the serum transaminases < 100 IU/ml in 12. The mean bilirubin pre-FK506 of patients successfully converted to FK506 was 4.2 mg/dl compared to 11.8 mg/dl in patients who failed conversion. Major complications included nephrotoxicity, neurotoxicity, and lymphoma. The mean glomerular filtration rate (GFR) of 97 +/- 29 mls/min/1.73m2 prior to FK506 conversion dropped to 51 +/- 20 mls/min/1.73m2 (p = 0.0001) after a mean of 13.6 months of FK506 therapy. Three patients have developed B-cell lymphomas; two of them responded to decreased immunosuppression and one died. We conclude that intractable liver graft rejection in children is most successfully reversed if FK506 is instituted before cholestasis becomes pronounced.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗