PubMed Health⌕ Search

Biomedical subjects

D Berkowitz

Publications and source records attributed to D Berkowitz.

At least 19 recordsLinked to original sources
PubMed2007

Wireless video capsule in pediatric patients with functional abdominal pain.

OBJECTIVES: Upper endoscopy (esophagogastroduodenoscopy [EGD]) has a limited role, if any, in the evaluation of functional abdominal pain (FAP). Nevertheless, children with intractable FAP are occasionally referred to EGD to rule out intestinal pathology. We evaluated the role of wireless video capsule endoscopy (VCE) in children referred for EGD with a diagnosis of FAP. PATIENTS AND METHODS: Ten children older than 10 years of age were prospectively enrolled. Children were first studied with the PillCam SB (VCE; Given Imaging, Yokneam, Israel) followed by standard EGD within 2 weeks. After the completion of the study, a questionnaire of tolerance and content regarding the 2 procedures was completed by the patients. RESULTS: Physical examinations and laboratory tests were within normal limits in all of the patients. Patients swallowed the endoscopic capsules without difficulty. There were no complications. VCE identified gastritis in 4 patients (confirmed by biopsies), whereas EGD detected erosive gastritis in only 1 of the 4 children. EGD detected no duodenal abnormalities. VCE detected Crohn disease in the small intestine and cecum in 1 patient. VCE was ranked by 8 patients as convenient and as a preferable procedure compared with EGD. CONCLUSION: The results of this small cohort suggest that in children with FAP, VCE is more sensitive than EGD for detection of macroscopic gastric and small bowel pathologies.

Abdominal Pain↗
PubMed2005

Autoantibodies against bactericidal/permeability-increasing protein (BPI-ANCA) in cystic fibrosis patients treated with azithromycin.

Autoantibodies against bactericidal/permeability-increasing protein (BPI-ANCA) were found in patients with cystic fibrosis (CF). It is speculated that they represent a marker of the chronic endobronchial infection and sustained inflammatory response in CF. Our aim was to evaluate whether azithromycin (AZM), through its antiinflammatory effect, could affect the level of BPI-ANCA in CF patients. Eighteen patients with CF aged 5.5-36.3 years (median 15.1) were enrolled in a randomised, double-blind, placebo-controlled trial of AZM (250 mg twice a week to 10 patients) or placebo (8 patients) for 12 weeks. BPI-ANCA levels were recorded pre- and post-treatment and compared to a group of 18 matched healthy controls. Chi-square analysis, Kruskal-Wallis and Mann-Whitney tests were used to compare between the groups. Pre- and post-treatment values were compared using the Wilcoxon Signed-Ranked test. BPI-ANCA was found in 12 CF patients (67%) and four (22%) healthy subjects (P<0.001). The mean BPI-ANCA level was 3.94+/-6.15 U/ml (mean+/-SD) in healthy subjects and 38.11+/-42.34 U/ml in CF patients (P=0.023). The mean BPI-ANCA level was higher in patients with Pseudomonas aeruginosa compared to those without (64+/-35 U/ml and 25+/-41 U/ml respectively, P=0.032). No change in BPI-ANCA levels occurred in the AZM-treated patients [35 (0-127) U/ml (median (range) and 30 (0-120) U/ml, respectively] or in the placebo group [10 (0-66) U/ml and 13 (0-83) U/ml, respectively]. BPI-ANCA levels are significantly higher in patients with CF compared to healthy controls. BPIANCA levels are higher among patients colonised with P. aeruginosa. Twelve weeks of AZM therapy did not lower the BPI-ANCA level in patients with CF.

Adolescent↗
PubMed2005

Prevalence and significance of mutations in the familial Mediterranean fever gene in patients with Crohn's disease.

The concurrence of Crohn's disease (CD) and familial Mediterranean fever was repeatedly reported. In this study we determined the distribution and contribution of MEFV gene mutations to CD susceptibility and clinical heterogeneity. An Israeli cohort of 209 CD patients (120 men and 89 women) was investigated for mutations in the MEFV gene. A detailed chart review, interview and physical examination were used to determine sociodemographic and clinical characteristics. MEFV and NOD2/CARD15 genotypes were analyzed in all patients and a genotype-phenotype correlation analysis was undertaken. The results of this study do not implicate MEFV mutations as major modifiers in CD. However, the E148Q MEFV variant was associated with susceptibility to perianal disease. More specifically, 19% (9/47) of CD patients with perianal disease carried the E148Q mutation compared to 6.7% (11/162) of CD patients without perianal involvement (OR 3.26, 95% CI 1.2-8.8, P=0.02). Although, for all mutations taken together, the prevalence of MEFV gene mutations among CD patients and controls was similar, the hypothesis that E148Q mutation modulates the phenotypic expression of CD is corroborated by the results of this study and needs to be further evaluated.

Adolescent↗
PubMed2004

Disappearance of diffuse calcinosis following autologous stem cell transplantation in a child with autoimmune disease.

A 12-year-old girl presented with arthritis, myalgia, anemia and positive ANA. Subsequently, she developed recurrent episodes of pulmonary hemorrhage, thrombocytopenia, CNS abnormalities, skin ulcers and diffuse calcinosis. This was followed by secondary antiphospholipid syndrome. Despite vigorous immunosuppression, the patient became bedridden. A peripheral blood stem cell autograft was offered when she developed pulmonary hypertension and digital ischemia at the age of 16 years. The post-transplantation course was uneventful. Liquefaction of calcinosis nodules with improvement of mobility occurred gradually. She is now 24 months post-transplant with no sign of disease activity and total disappearance of calcinosis nodules.

Anemia↗
PubMed2004

Comparison of invasive and non-invasive tests diagnosis and monitoring of Helicobacter pylori infection in children.

BACKGROUND: There are few reports which the tests used for diagnosing Helicobacter pylori infection and monitoring its eradication in children. STUDY AIMS: Prospective evaluation of invasive (gastric histology, rapid urease test [RUT]) and non-invasive (stool antigen [FemtoLab H. pylori], urea breath test [UBT]) tests in the diagnosis of H. pylori infection and post-treatment eradication in children and adolescents. METHODS: Ninety-two patients (50 male, 42 female) referred for upper gastrointestinal endoscopy were prospectively enrolled. UBT was performed and stool specimens collected for monoclonal enzyme immunoassay for H. pylori antigen (FemtoLab) 1 to 4 days before endoscopy. H. pylori in gastric biopsies was evaluated by RUT and staining with hematoxylin-eosin and giemsa. Eradication therapy was given to children with abdominal pain and H. pylori gastritis. FemtoLab H. pylori and UBT were repeated 6 weeks after the end of triple therapy. RESULTS: Histology identified H. pylori in 49 of 92 (53%) subjects. Concordance between histology and RUT was found in 78 of 92 children. FemtoLab H. pylori was positive in 41 of 78 (52.6%) children with sensitivity, specificity, positive and negative predictive values of 97.5%, 94.7%, 95.1% and 97.3%, respectively. For UBT, these values were 100%, 96.9%, 97.5% and 100%, respectively. Twenty-six of 36 patients who received triple therapy returned for eradication evaluation. Tests for H. pylori antigen in stool were positive in 10 of 26 and for UBT in 11 of 26. CONCLUSION: Stool antigen (FemtoLab) and UBT were equally effective in diagnosing and confirming eradication of H. pylori infection in children.

Antigens, Bacterial↗
PubMed2001

The deoxyguanosine kinase gene is mutated in individuals with depleted hepatocerebral mitochondrial DNA.

Mitochondrial DNA (mtDNA)-depletion syndromes (MDS; OMIM 251880) are phenotypically heterogeneous, autosomal-recessive disorders characterized by tissue-specific reduction in mtDNA copy number. Affected individuals with the hepatocerebral form of MDS have early progressive liver failure and neurological abnormalities, hypoglycemia and increased lactate in body fluids. Affected tissues show both decreased activity of the mtDNA-encoded respiratory chain complexes (I, III, IV, V) and mtDNA depletion. We used homozygosity mapping in three kindreds of Druze origin to map the gene causing hepatocerebral MDS to a region of 6.1 cM on chromosome 2p13, between markers D2S291 and D2S2116. This interval encompasses the gene (DGUOK) encoding the mitochondrial deoxyguanosine kinase (dGK). We identified a single-nucleotide deletion (204delA) within the coding region of DGUOK that segregates with the disease in the three kindreds studied. Western-blot analysis did not detect dGK protein in the liver of affected individuals. The main supply of deoxyribonucleotides (dNTPs) for mtDNA synthesis comes from the salvage pathway initiated by dGK and thymidine kinase-2 (TK2). The association of mtDNA depletion with mutated DGUOK suggests that the salvage-pathway enzymes are involved in the maintenance of balanced mitochondrial dNTP pools.

Base Sequence↗
PubMed2001

The hepatic mitochondrial DNA depletion syndrome: ultrastructural changes in liver biopsies.

Mitochondrial respiratory chain disorders are an established cause of liver failure in early childhood. In some patients, the levels of mitochondrial DNA are markedly reduced, a condition referred to as mtDNA depletion syndrome (MDS). We report here on the ultrastructural changes in the livers of 10 infants with the hepatic form of this syndrome. All patients displayed progressive liver failure, neurological abnormalities, hypoglycemia, and lactic acidosis that warranted investigation of respiratory chain disorder in liver tissue, specifically expressing the disease. Decreased activity of respiratory chain complexes containing mtDNA-encoded subunits (complexes I, III, IV) was shown in 5 patients. Mitochondrial DNA depletion was confirmed by Southern blot analysis in the livers of 6 patients. We found hepatocytes filled with mitochondria having aspects of "oncocytic transformation," associated with numerous changes in shape, size, cristae, and matrix. The changes were virtually identical in all specimens. In many hepatocytes, microvesicular steatosis was the salient feature. Additional findings included cholestasis and focal cytoplasmic biliary necrosis (CBN), as well as cytosiderosis in hepatocytes and sinusoidal cells. In some hepatocytes the damage appeared extreme, but fibrosis was identified only in the few patients who died beyond 6 months of age. Although individual ultrastructural findings are not specific, when taken together, they show a diagnostic pattern highly suggestive of a respiratory chain disorder. In the appropriate clinical context, these findings can direct the clinician towards the diagnosis of hepatic MDS.

Biopsy↗
PubMed2001

Differential gene expression in a murine model of cancer cachexia.

Murine adenocarcinoma 16 (MAC16) tumors and cell lines induce cachexia in NMRI nude mice, whereas histologically similar MAC13 tumors do not. After confirming these findings in BALB/c nude mice, we demonstrated that this tissue wasting was not related to decreased food intake or increased total body oxidative metabolism. Previous studies have suggested that MAC16's cachexigenic properties may involve the production of tumor-specific factors. We therefore screened for genes having increased expression in the MAC16 compared with the MAC13 cell line by performing hybridization to a murine cDNA expression array, by generation and comparison of cDNA libraries from each cell line, and by PCR-based subtractive hybridization. Northern blot hybridization was performed to confirm differences in transcript expression. Transcripts encoding insulin-like growth factor binding protein-4, cathepsin B, ferritin light and heavy chain, endogenous long-terminal repeat sequences, and a viral envelope glycoprotein demonstrated increased expression in the MAC16 cell line. The roles of a number of these genes in known metabolic pathways identify them as potential participants in the induction of cachexia.

Adenocarcinoma↗
PubMed2000

Efficacy of bismuth-based triple therapy in children with abdominal pain and Helicobacter pylori gastritis.

BACKGROUND: To evaluate the effect of a therapeutic regimen of 7 days versus 14 days on the clinical manifestations of Helicobacter pylori gastritis in children. METHODS: Ninety children (age 2-19 years) who had abdominal pain and/or recurrent vomiting were determined to have H. pylori gastritis by endoscopy, histology, and a Giemsa stain positive for H. pylori. The patients were randomized to receive amoxicillin, metronidazole, and bismuth subcitrate for 7 days (group A; 45 children) or 14 days (group B; 45 children) and were observed clinically for 19 +/- 11.5 months. Resolution of all abdominal and gastrointestinal symptoms was considered a good response. RESULTS: A good response was obtained in 36 (80%) children from group A, and in 37 (82%) from group B. A recurrence of symptoms occurred in four (11%) of the responders from group A, and in six (15.2%) from group B. CONCLUSIONS: A 7-day course of bismuth-based triple therapy for H. pylori gastritis in children appears to be clinically as effective as a 14-day regimen. The feasibility of a shorter therapeutic regimen may enhance patient compliance and provide a better chance of clinical benefit.

Abdominal Pain↗
PubMed1999

Pulmonary vascular endothelial responses are differentially modulated after cardiopulmonary bypass.

The aim of this study was to characterize the mechanisms underlying pulmonary vascular dysfunction after cardiopulmonary bypass (CPB) by examining responses of isolated pulmonary arteries to selective endothelium-dependent and -independent activators in control and post-CPB dogs. Adult male mongrel dogs were placed on closed-chest, hypothermic CPB for 2.5 h, and then allowed to recover. Anatomically matched pulmonary arterial rings were isolated and suspended for isometric tension recording. Contractile responses to the alpha1-adrenergic agonist phenylephrine were similar in endothelium-containing arteries from control and CPB animals. Endothelium denudation increased contractions to phenylephrine to a similar extent in both groups. Endothelium-dependent relaxation to acetylcholine was decreased 4 days after CPB compared with controls. In contrast to acetylcholine, endothelium-dependent relaxation to bradykinin or to A23187 were not impaired 4 days after CPB. Inhibition of nitric oxide synthase (NOS) with L-NAME depressed the response to acetylcholine in control vessels, confirming that a component of the response to acetylcholine was nitric oxide (NO) dependent. At lower concentrations of acetylcholine, this component of the response was abolished after CPB. The residual relaxation evoked by acetylcholine in the presence of L-NAME also was impaired in CPB compared with control arteries. This suggests that the CPB-induced impairment of acetylcholine-evoked relaxation may not involve both an NO-mediated and an NO-independent component. L-NAME depressed the response to bradykinin to a similar degree in control and CPB arteries. Vascular smooth-muscle dilatation to the NO donor, SIN-1, or to the K+ATP-channel opener, cromakalim, were similar in endothelium-denuded arteries from CPB and control animals. These results suggest that CPB causes a selective impairment in endothelial dilator function without changing the vascular smooth-muscle response to vasodilator or vasoconstrictor stimuli.

Acetylcholine↗