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Gastrointestinal involvement in disseminated Langerhans cell histiocytosis (LCH) with durable complete response to 2-chlorodeoxyadenosine and high-dose cytarabine [Case Report]

Choi, Sung W; Bangaru, Babu S; Wu, C Daniel; Finlay, Jonathan L
Successful treatment of infants with gastrointestinal involvement in Langerhans cell histiocytosis (LCH) has been poor, with no specific chemotherapeutic regimen of clear benefit. An 8-month-old male, diagnosed with LCH by skin and gastrointestinal biopsies, was treated with several cycles of 2-chlorodeoxyadenosine, vinblastine and prednisone with only partial response. Ultimately, two cycles of 2-chlorodeoxyadenosine concomitant with high-dose cytarabine led to a durable complete response. Twenty-seven months since the last course of chemotherapy, the patient continues to thrive free of disease. Treatment with 2-chlorodeoxyadenosine and cytarabine should be considered for further study in patients with poor-prognosis LCH
PMID: 12794533
ISSN: 1077-4114
CID: 66509

Disseminated Langherhans cell histiocytosis(DLCH) presenting as "allergic colitis" in infancy with durable complete response to cladribine(2CDA) and high dose cytosine arabinoside(HD-AraC) [Meeting Abstract]

Bangaru, BS; Choi, SW; Wu, CD; Greco, AM; Finlay, JL
ISI:000168542800516
ISSN: 0016-5107
CID: 55077

Adenomyoma arising in a meckel diverticulum: case report and review of the literature

Yao JL; Zhou H; Roche K; Bangaru BS; Ginsburg H; Greco MA
We report a case of adenomyoma of the small intestine arising in a Meckel diverticulum. The patient was a 22-month-old boy who presented with signs and symptoms of intussusception. At surgery, a Meckel diverticulum was found and removed. On histologic examination, a tumor consisting of dilated cystic glands and smooth muscle bundles was identified. A diagnosis of adenomyoma arising in a Meckel diverticulum was made. A review of the literature showed that only six other pediatric cases of adenomyoma of the small intestine have been reported. The presence of an adenomyoma in a young patient within a Meckel diverticulum favors the view that adenomyomas are a variant of pancreatic heterotopia
PMID: 10890936
ISSN: 1093-5266
CID: 11603

Secretin in autism [Letter]

Perry R; Bangaru BS
PMID: 10214929
ISSN: 1044-5463
CID: 66510

Cholestatic hepatitis in children infected with the human immunodeficiency virus [Case Report]

Persaud D; Bangaru B; Greco MA; Nachman S; Mittal K; Chandwani S; Krasinski K; Borkowsky W; Kaul A
A distinct clinical syndrome of cholestasis and hepatitis occurred during early infancy in seven infants with perinatally acquired human immunodeficiency virus 1 infection. In five infants hepatitis was the first manifestation of human immunodeficiency virus 1 infection. The median age of onset of hepatitis was 7 months (range, 5 to 10 months). The mean total bilirubin concentration at presentation was 7.4 mg/dl (range, 3.9 to 11 mg/dl), the mean aspartate aminotransferase was 1512 IU/liter (range, 782 to 2960 IU/liter) and the mean alanine amino-transferase 512 IU/liter (range, 92 to 1247 IU/liter). The absolute CD4 count at the time of onset of hepatitis ranged from 191 to 2298 cells/mm3 (mean, 766 cells/mm3). Six of the seven children died within 12 weeks of onset of hepatitis, three as a result of complications of Pneumocystis carinii pneumonia, and two died of complications secondary to cytomegalovirus. In only one infant was the cause of death the direct consequence of liver failure. The seventh infant died 17 months after the onset of hepatitis of dilated cardiomyopathy. No specific etiologic agent has been identified as the cause of cholestatic hepatitis in these infants. In situ hybridization studies to detect human immunodeficiency virus 1 messenger RNA was negative in the liver tissue obtained at biopsy and autopsy in five of the samples tested
PMID: 8102198
ISSN: 0891-3668
CID: 6483

Fundoplication and gastrostomy in familial dysautonomia

Axelrod FB; Gouge TH; Ginsburg HB; Bangaru BS; Hazzi C
Fundoplication with gastrostomy has become a frequent treatment for patients with familial dysautonomia, so we evaluated the use of both procedures in 65 patients. Although patients differed widely in presenting signs and age, from 5 weeks to 40 years, gastroesophageal reflux was documented in 95% of patients by cineradiography or pH monitoring. Panendoscopy was a useful adjunct. Preoperative symptoms of gastroesophageal reflux included vomiting, respiratory infections, and exaggerated autonomic dysfunction. Severe oropharyngeal incoordination frequently coexisted and resulted in misdirected swallows with aspiration, dependence on gavage feedings, or poor weight gain and dehydration. Follow-up after surgical correction ranged from 3 months to 11 years; 55 patients (85%) were available for a 1-year postoperative assessment. We had no instances of surgical death. The long-term mortality rate was 14%, primarily related to severe preexisting respiratory disease. Beyond the first postoperative year, 30 patients had pneumonia attributed to continued aspiration, exacerbation of preexisting lung disease, or recurrence of gastroesophageal reflux. Of 11 patients who vomited postoperatively, six had recurrence of reflux. Recurrence of gastroesophageal reflux was documented in eight patients (12%), and we revised the fundoplication in three patients. The number of patients with cyclic crises was reduced from 18 to 7; retching replaced overt vomiting in all but two of these seven patients, neither of whom had recurrence of reflux. Because oropharyngeal incoordination was prominent, concomitant use of gastrostomy and an antireflux procedure was especially effective in the treatment of younger patients with familial dysautonomia, before the development of severe respiratory disease. Despite the development of severe morning nausea in 15 patients, the combination procedure resulted in significantly improved nutritional status, decreased vomiting, and decreased respiratory problems. Appropriate use of gastrostomy feedings also contributed to success of the operation. The generally good outcome of fundoplication with gastrostomy confirms the benefit of this procedure in familial dysautonomia
PMID: 1999777
ISSN: 0022-3476
CID: 14114

Bradycardia associated with hiatal hernia and gastroesophageal reflux relieved by surgery [Case Report]

Axelrod FB; Maayan C; Hazzi C; Bangaru BS; Shannon DC
A man known to have familial dysautonomia presented with a cardiac arrhythmia due to development of hiatal hernia and gastroesophageal reflux. Preoperative symptoms and assessment are described including use of power spectrum analysis of heart rate fluctuations which was consistent with enhanced parasympathetic stimulation. After surgical repair of hiatal hernia and fundoplication, bradycardia resolved, gastroesophageal reflux symptoms subsided, and the power spectrum analysis of heart rate confirmed decreased parasympathetic influence. Power spectrum analysis proved to be a useful adjunct in confirming preoperative autonomic imbalance and assessing the postoperative result. It is concluded that in individuals with disorders such as familial dysautonomia that are associated with autonomic dysfunction, cardiac arrhythmias may be a sign of esophageal pathology. Thus, cardiac evaluations should be accompanied by investigation of gastroesophageal structure and function and appropriate treatment may prevent a catastrophic arrhythmia
PMID: 3812423
ISSN: 0002-9270
CID: 66511

The syndrome of achalasia of the esophagus, ACTH insensitivity and alacrima [Case Report]

Ambrosino MM; Genieser NB; Bangaru BS; Sklar C; Becker MH
A 7-year-old male presented with a triple A syndrome, a tirad of ACTH insensitivity, achilasia and alacrima. His clinical course is followed and the literature reviewed
PMID: 3014426
ISSN: 0301-0449
CID: 66512

Zellweger syndrome: biochemical and morphological studies on two patients treated with clofibrate [Case Report]

Lazarow PB; Black V; Shio H; Fujiki Y; Hajra AK; Datta NS; Bangaru BS; Dancis J
Two infants with Zellweger syndrome (cerebro-hepato-renal syndrome) have been studied biochemically and morphologically. Peroxisomal enzymes involved in respiration, fatty acid beta-oxidation, and plasmalogen biosynthesis were assessed. In liver, catalase was present in normal amounts but was located in the cell cytosol. Dihydroxyacetone phosphate acyltransferase activity was less than one-tenth of normal. The amount of the bifunctional protein catalyzing two beta-oxidation reactions was found by immunoblotting to be greatly reduced. Catalase activity was normal in intestine. D-Amino acid oxidase was subnormal in kidney. The observed enzyme deficiencies may plausibly explain many of the metabolite imbalances observed clinically. Morphologically, peroxisomes were absent from liver. In intestine, normal peroxisomes were also missing, but some rare, smaller (0.04-0.13 micrometer) bodies were seen with a slight positive cytochemical reaction for catalase. These results, together with current concepts of peroxisome biogenesis, suggest but do not prove, that the primary defect in Zellweger syndrome may be in peroxisome assembly. The infants were treated with clofibrate, but it was ineffectual as assessed biochemically, morphologically, and clinically
PMID: 4080458
ISSN: 0031-3998
CID: 43294

Comparative studies of biliary atresia in the human newborn and reovirus-induced cholangitis in weanling mice

Bangaru B; Morecki R; Glaser JH; Gartner LM; Horwitz MS
The hepatobiliary histologic lesions of human newborns with biliary atresia have been compared to those induced in weanling mice by reovirus type III. Although the obliterative fibrotic lesions, the hallmark of human disease, are only transient or segmental in the mouse and therefore do not result in permanent or complete obstruction of bile flow, many of the inflammatory stages of the disease are identical in humans and in the mouse. Prompted by these similarities, antibodies to reovirus type III were sought in sera of human newborns with biliary atresia. Two of 12 babies had elevated and rising neutralizing titers to reovirus type III during the course of their illness. Using recobinant reoviruses which contain some genes from a nonpathogenic reovirus type I and other genes from the pathogenic parental reovirus type III, we have shown that hepatobiliary murine pathology is not the property of a single viral gene
PMID: 7421127
ISSN: 0023-6837
CID: 66513