Pramila Ramani
Bristol Royal Hospital for Children
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Featured researches published by Pramila Ramani.
European Journal of Pediatrics | 2007
Madhur Ravikumara; Pramila Ramani; Christine Spray
In this article, we report a case of collagenous gastritis in a child and review the paediatric cases reported to date. Collagenous gastritis is a rare entity, with only less than 30 cases reported so far, including 12 children, since the first description of this entity by Colletti and Trainer in 1989. This is a histological diagnosis characterised by a dramatically thickened subepithelial collagen band in the gastric mucosa associated with an inflammatory infiltrate. Children with this condition often present with epigastric pain and severe anaemia, with no evidence of extragastric involvement, in contrast to the adult patients, where chronic watery diarrhoea is the main presentation due to associated collagenous colitis. A macroscopic pattern of gastritis with nodularity of gastric mucosa, erythema and erosions are characteristic endoscopic findings in paediatric patients. Specific therapy has not been established and resolution of the abnormalities, either endoscopic or histological, has not been documented. In conclusion, collagenous gastritis is a rare entity of unknown aetiology, pathogenesis and prognosis. Gastroenterologists and pathologists need to be aware of this condition when evaluating a child with epigastric pain, anaemia and upper gastrointestinal bleeding, particularly when endoscopy reveals the nodularity of gastric mucosa. The identification, reporting and long-term follow-up of cases will shed more light on this puzzling condition.
Archives of Disease in Childhood | 2014
M. Cole; Christine Spray; Dharamveer Basude; S Sandmann; Pramila Ramani; Bhupinder Sandhu
Background Inflammatory bowel disease (IBD) is understood to result from the interaction of genetic, immunological and environmental factors. There has been a marked increase in the incidence of IBD over the last 25 years, suggesting environmental factors are important. A previous study found a higher incidence of Coeliac disease in the least deprived socioeconomic groups.1 The objective of this study was to investigate the relationship between IBD and socioeconomic position. Methodology Bristol Children’s Hospital is the single regional centre where all children with suspected IBD from the South-west of England are referred. Data was collected prospectively on all children diagnosed between May 2004–March 2013. Socioeconomic status was determined by quintile rank of Index of multiple deprivation score (IMD-10 score) based on postcode at diagnosis. This has been shown to provide a nationally consistent measure of how deprived an area is. Population data was obtained from the 2011 Census. Data was analysed using Pearson Chi Squared test. Children with a postcode outside of the City of Bristol were excluded from the analysis. Results 384 children aged 0–17 years were diagnosed with IBD over the study period of which 50 had a postcode of residence within the City of Bristol. The incidence of IBS was higher in the three lower socio-economic classes compared to the two highest socio-economic classes (see Figure 1). However, the difference in incidence between the socio-economic classes was not statistically significant. Abstract G81(P) Figure 1 Conclusion Our data suggests a higher incidence of diagnosed IBD in children from lower socioeconomic classes which may favour an environmental aetiology. However this did not reach statistical significance, possibly due to small numbers. A larger study is warranted. Reference Whitburn and Sandhu. Coeliac disease and relationship to socio-economic status. Arch Dis Child 2013;98:A86
Archives of Disease in Childhood | 2014
Nkem Onyeador; N Jennings; Siba Prosad Paul; Pramila Ramani; Bhupinder Sandhu
Background Coeliac disease (CD) is an immune mediated systemic disorder elicited by the ingestion of gluten and related prolamines in genetically susceptible individuals. Diagnosis has been based on small bowel histology as per ESPGHAN guidelines. In 2012 ESPGHAN guidelines1 were modified and recommend that in symptomatic patients a diagnosis of CD can be made without small-bowel biopsy if anti-tissue transglutaminase antibody (TTG) titre is greater than 10 times upper limit of normal (>10ULN), together with presence of HLA-DQ2 and/or DQ8. This study aimed to examine the relationship between TTG levels and the corresponding histological features. Methods Data was collected prospectively at diagnosis of CD from 126 consecutive children between June’ 2011 – May’ 2012. TTG was measured using ELISA technique. Histological samples were obtained from endoscopic small-bowel biopsies and interpreted by paediatric histopathologists. The relationship between the modified Marsh criteria histological findings and contemporaneous TTG levels was analysed. Results Out of 126 children, 13(10.5%) had positive TTG but no documented titres. In 12(10%) histological report did not specify Marsh classification. Complete data of histological report and TTG level were therefore available from 104 children (82%). The data (table) shows an association between TTG level and histological staging of CD. 58 (48%) children had TTG >10ULN (>100U/ml). 57/58 of these patients had biopsy proven CD. The sensitivity of the TTG level >100U/ml alone in correctly diagnosing CD in this cohort was 98.3%. Modified Marsh Criteria identified on histology 3a 3b 3c Mean TTG level (U/ml) (SD) 95.9 110.0 167.4 (95% confidence level) 66.8–124.9 87.5–132.3 143.0–191.7 Conclusion 98.3% of children with TTG >100U/ml had histologically confirmed CD although total villous atrophy was associated more often with TTG level of >200U/ml. It is essential to report TTG titres by all laboratories. This study supports the new ESPGHAN guidelines for the selective use of high TTG levels in diagnosing CD in symptomatic children without a biopsy. Reference Husby S, et al. J Pediatr Gastroenterol Nutr. 2012;54(1):136–60
Journal of Pediatric Surgery | 2008
Yatin Patel; Pramila Ramani; David Grier; Janet McNally
The first case of jejunal phlebectasia in a pediatric patient presenting with life-threatening gastrointestinal bleeding is described. The pathology of vascular anomalies is discussed.
Archives of Disease in Childhood | 2014
D Vieten; Richard Spicer; Pramila Ramani; Ap Corfield
Background The aetiology of necrotizing enterocolitis (NEC) is multifactorial and its pathogenesis poorly understood. The trefoil factor peptides (TFF1–3) contribute to protective mechanisms operating in the gastro-intestinal (GI) mucosa and play a fundamental role in epithelial protection, restitution and repair. The role of TFF1–3 in neonatal mucosal protection has not been well investigated. Aims This study aims to investigate alterations in TFF 13 mRNA and protein expression in the GI tract of infants with NEC compared to normal neonatal controls. Methods Bowel resection specimens were collected with parental consent from neonates undergoing laparotomy. In situ hybridisation, real time PCR and immunohistochemistry were performed to examine trefoil mRNA and peptide expression in the neonatal GI tract. Results 77 neonatal bowel specimens were examined (NEC n = 27, recovering from NEC n = 16, normal neonatal controls n = 29). There was no upregulation of TFF 1 and 2 mRNA and protein expression in acute NEC and there was significant down-regulation of TFF3 protein and mRNA expression. Adjacent to areas of mucosal necrosis there was an inverse relationship in the number of TFF3-positive goblet cells and proximity to the ulceration. Conclusions A number of studies have shown up-regulation of TFF 1–3 in the acute phase response to GI mucosal injury, promotion of epithelial cell migration and protection against apoptosis. Our results suggest a lack of TFF expression in response to NEC in the premature gut. This may lead to impaired restitution of the mucosa and contribute to the cascade of bowel necrosis and generalised sepsis characteristic of NEC.
Archives of Disease in Childhood | 2014
Siba Prosad Paul; Christine Spray; Dharamveer Basude; S Sandmann; Pramila Ramani; Bhupinder Sandhu
Background In 5–15% of children diagnosed with inflammatory bowel disease (IBD), the histological picture at diagnosis doesn’t fit in with either ulcerative colitis (UC) or Crohns disease (CD) and is classified as unclassified-IBD (IBDU) or indeterminate colitis.1 The aim of this prospective study is to determine whether IBDU evolves into UC or CD. Methods Prospective data has been collected on all the newly diagnosed children with IBD at the only regional paediatric gastroenterology centre covering southwest of England. All patients suspected of IBD had upper and lower gastrointestinal endoscopy and MRE scan or barium meal as recommended by BSPGHAN.2 Patients diagnosed with IBDU during 2004–2011 were included in the study and followed up for a minimum of 2 years (range 2–9 years). The patient notes were reviewed in 2013 and any changes in diagnosis recorded. Results 333 children were diagnosed with IBD between 2004–2011: 193 (58%) had CD, 115 (34.5%) UC and 25 (7.5%) IBDU. Age (mean) at diagnosis: 10.2 years (IBDU), 11.5 years (CD) and 11.6 years (UC). 7/26 (27%) IBDU had pan-colitis and 19/26 (63%) had patchy or left-sided colitis on lower gastrointestinal endoscopy. After 2 to 9 years, IBDU evolved into CD in 5 patients (22.8%), UC in 3 (13.6%) and remained IBDU in 14 patients (63.6%). Latest data was unavailable for 3 (11.6%) because of transfer to distant adult services. ANCA was positive in 3 out of 4 patients whose diagnosis was revised as CD. Conclusion This large prospective study has documented that over 2–9 years, 22.8% IBDU evolved into CD, 13.6% into UC and 63.6% remained IBDU. IBDU patients tended to be younger at diagnosis. Positive ANCA was not an useful predictive marker. This has implications for management of IBDU patients especially where surgical treatment is considered. References De Bie CL, et al. (2012). J Pediatr Gastroenterol Nutr. 54(3):374-80 Sandhu BK, et al. (2010). J Pediatr Gastroenterol Nutr. 50:S1-S13
Journal of Pediatric Surgery | 2007
Yatin Patel; Janet McNally; Pramila Ramani
Journal of Pediatric Hematology Oncology | 2007
Nicola J. Matcham; Savvas Andronikou; Keith Sibson; Pramila Ramani; David Grier
Journal of Pediatric Gastroenterology and Nutrition | 2017
Siba Prosad Paul; Bhupinder Sandhu; Christine Spray; Dharamveer Basude; Pramila Ramani
Journal of Pediatric Gastroenterology and Nutrition | 2018
Ian Jones; Pramila Ramani; Christine Spray; Eleri Cusick