The primary care of children with autism.
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Biomedical subjects
Publications and source records attributed to Ashley Price.
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BACKGROUND & AIMS: Patients with ulcerative colitis are at increased risk of colorectal cancer. It is widely believed that this is secondary to colonic inflammation. However, the severity of colonic inflammation has never been shown to be a risk factor. METHODS: We devised a case-control study of patients with long-standing extensive ulcerative colitis to examine various potential risk factors for neoplasia. All cases of colorectal neoplasia detected from our surveillance program between January 1, 1988, and January 1, 2002, were studied (n = 68). Each patient was matched with 2 control patients from the same surveillance population (n = 136). Matching was for sex, colitis extent, age at onset, duration of colitis, and year of index surveillance colonoscopy. Segmental colonoscopic and histological inflammation was recorded by using a simple score (0, normal; 1, quiescent/chronic inflammation; and 2, 3, and 4, mild, moderate, and severe active inflammation, respectively). Other data collected included history of primary sclerosing cholangitis, family history of colorectal cancer, and smoking and drug history (mesalamine 5-aminosalicylic acid, azathioprine, and folate). RESULTS: Univariate analysis showed a highly significant correlation between the colonoscopic (odds ratio, 2.5; P = 0.001) and histological (odds ratio, 5.1; P < 0.001) inflammation scores and the risk of colorectal neoplasia. No other factors reached statistical significance. On multivariate analysis, only the histological inflammation score remained significant (odds ratio, 4.7; P < 0.001). CONCLUSIONS: In long-standing extensive ulcerative colitis, the severity of colonic inflammation is an important determinant of the risk of colorectal neoplasia. Endoscopic and histological grading of inflammation could allow better risk stratification for surveillance programs.
A 33-year-old African woman who was HIV positive and being treated with zidovudine and zalcitabine presented with a 4-week history of a generalized pruritic rash superficially resembling molluscum contagiosum. The appearance of the lesions appeared to coincide with a dramatic decrease in her peripheral CD8+, and to a lesser extent, CD4+ T-lymphocyte count. Hematologic investigations revealed anemia with eosinophilia and she had a strongly positive Strongyloides antibody test. The eruption persisted despite appropriate antihelminthic treatment and temporary withdrawal of antiretroviral therapy. Histologic examination showed ill-defined nodules of necrobiotic collagen with surrounding palisading mononuclear cell infiltrate consistent with granuloma annulare. The rash disappeared spontaneously over several weeks.
The bacterium Helicobacter pylori is found in c. 40% of the population and is responsible for the development of duodenal disease. Triple treatment with a proton-pump inhibitor or bismuth salt plus two antibiotics is now commonplace in all patients diagnosed. As antibiotic resistance reduces treatment efficacy, it is time to consider routine susceptibility testing to guide individual patient treatment and surveillance of antibiotic resistance. There are no published nationally agreed standards for disc diffusion testing of H. pylori. After reviewing the literature, we recommend the following method for disc diffusion tests. A suspension of cultures < or = 4 days old equivalent to McFarland Standard no. 4 (10(8) cfu/mL) should be used on Mueller-Hinton or Columbia agar base with 5-10% blood, using a metronidazole disc strength of 5 Ig and a clarithromycin disc strength of 2 microg. Anaerobic pre-incubation of plates is unnecessary. A H. pylori control susceptible to metronidazole (e.g. NCTC 12822) should be used. Zone sizes with the Mueller-Hinton agar base for metronidazole testing are <16 mm resistant, 16-21 mm intermediate and >21 mm susceptible. We suggest that isolates in the intermediate zone should be re-tested by Etest. Zone sizes with the Columbia agar base for metronidazole testing are <10 mm resistant and > or = 10 mm susceptible. Co-infection with two strains, which may be a mixture of isolates susceptible and resistant to metronidazole leading to conflicting susceptibility results, occurs in 5-10% of patients. Zone sizes with Mueller-Hinton agar and Columbia blood agar for clarithromycin testing are resistant no zone and susceptible any zone.
Small bowel Crohn's disease has been related to an increased incidence of small bowel adenocarcinoma, but the total number of reported cases is small. We present an interesting case of a young male patient with nephrolithiasis in childhood, an atypical intermittent history of diarrhoea also since his childhood, who developed obstructive ileus and underwent an urgent operation. The operation revealed a stenosis of the ileum owing to a mass, which proved to be a small bowel adenocarcinoma. One month later, the patient underwent a curative surgical resection of the tumour with additional lymphadenectomy, followed by chemotherapy for 6 months. Since then, the patient had mild diarrhoea but enteroclysis was normal. Approximately 2 years after the resection of the tumour, a new ileocolonoscopy demonstrated deep ulcerations of the terminal ileum and the adjacent area of the colon as well as anal ulcerations. The new biopsy specimens were convincing for Crohn's disease. There were no signs of residual or relapsing cancer. There is growing evidence that Crohn's disease is one of the triggering factors for the development of small bowel adenocarcinoma. Underlying Crohn's disease should be suspected in a young patient with an atypical history of diarrhoea and small bowel adenocarcinoma.