Prevalence and Risk Profile Of Unread Messages To Patients In A Patient Web Portal.

BACKGROUND: Excitement around the adoption of electronic communication between physicians and patients is tempered by the possibility of increased clinical and legal risk. If patients do not read messages in a timely fashion, duplicative communication efforts may be required and patient safety may be jeopardized. OBJECTIVE: We sought to assess the prevalence and risk profile of unread messages in a mature patient portal. METHODS: We analyzed six years of messages (2005-2010) from physicians to patients to determine the prevalence and associated characteristics of unread messages in a patient portal. We focused on clinical messages, and excluded announcements. Because some physicians sent clinical messages to groups of patients, we labeled messages sent to more than 5 patients as "outreach" messages and excluded them from general analyses. We performed a chart review of 75 clinical messages to assess for harm. RESULTS: We found that 3% of clinical messages were unread after 21 days. Messages arriving outside of business hours were slightly more likely to go unread (RR 1.15 95% CI 1.11-1.19). Patients who were male (OR 1.14 CI 1.04-1.26) African American (OR 1.69 CI 1.29-2.22) or Hispanic (OR 1.74 CI 1.17-2.59), or in the lowest income group (OR 1.72 CI 1.19-2.49) were more likely to have unread messages. Chart review showed no evidence of harm, but 13% of sampled unread messages were associated with potential delays in care. Incidentally, we found 50% of the physician-initiated outreach messages were unread. CONCLUSIONS: Overall, secure messaging appears a safe form of communication, but systems to notify senders when messages are unread may have value. While most clinical messages were read, many outreach messages were not, providing caution for relying on such systems for information dissemination. Similar to other studies, differences by race and income were observed and require further study.

Training general practitioners in flexible sigmoidoscopy to screen for colorectal cancer.

BACKGROUND: A screening programme to detect polyps or early carcinoma would significantly reduce the mortality and morbidity of colorectal cancer (CRC). The aims of the present study were to evaluate: (i) the feasibility of training general practitioners in flexible sigmoidoscopy (FS) for CRC screening; (ii) the acceptability of screening by faecal occult blood testing (FOBT) and FS in asymptomatic standard risk Australians aged over 50 years; and (iii) the yield of such screening. METHODS: Subjects were recruited by general practitioner (GP) referral, newspaper advertisement or by a direct approach to retirement villages. Participants were mailed a FOBT kit and a prescreening questionnaire. Flexible sigmoidoscopy was performed by a GP supervised by an experienced endoscopist. Subjects then completed a second questionnaire. General practitioners were assessed after 50 unassisted procedures. RESULTS: A total of 264 individuals contacted the study coordinator; 169 were screened. Screening was accepted well by the participants. Fifteen per cent of subjects had polyps and 4% had a positive FOBT. Training in FS was adversely affected by the availability of resources. Three GPs completed 50 unassisted procedures over a 15-month period, but none were able to reliably assess the distal bowel. CONCLUSIONS: Although the three trainees and their supervisors did not consider that the GPs were adequately trained after 50 unassisted procedures, training was adversely affected by limited resources within the Victorian public hospital system. Screening by FOBT and FS was considered to be acceptable by the patients undergoing these procedures. Existing facilities are not adequate if GPs are to be trained in FS as part of a national CRC screening program.

Risk of gastric cancer is not increased after partial gastrectomy.

BACKGROUND: It has been suggested that there is an increased risk of gastric cancer following partial gastrectomy. This question has not been studied in an Australian population. METHODS: The records of a total of 569 patients who had a partial gastrectomy for peptic ulcer disease at Repatriation General Hospital, Heidelberg, between 1957 and 1976 were reviewed. All were followed to date of death or 31 December 1996. The expected rate of gastric cancer for this population was estimated from published Australian age-and sex-specific gastric cancer mortality rates over this period, and a standardized incidence ratio was calculated. RESULTS: The mean age at surgery was 53.5 years (range 27-83 years). There were 547 male (96.4%) and 22 female (3.6%) patients. Five hundred and seven (83.5%) had a Billroth II procedure. Thirty-eight patients (6.3%) were lost to follow up and were not included in the analysis. From the records of the Department of Veterans' Affairs, it was established that 125 (20.6%) were alive in December 1996, a mean survival after surgery of 18.8 years. The mean documented duration of follow up was 17.3 years (range 1-41 years). Nine patients developed cancer in the gastric remnant. The expected number of cancers in this population was 6.5. Assuming all survivors were free of gastric cancer, the standardized incidence ratio was 1.39 (95% confidence intervals 0.64-2.65, P=0.313). CONCLUSION: The risk of gastric cancer was not increased after partial gastrectomy in this Australian population.

Percutaneous endoscopic gastrostomy feeding in AIDS.

Reduced energy intake is the most important reason for weight loss in advanced human immunodeficiency virus (HIV) infection. From January 1989 to August 1995 enteral feeding via a percutaneous endoscopic gastrostomy tube (PEG) was offered to all human immunodeficiency virus(HIV)/AIDS patients attending Fairfield Hospital, Melbourne who were unable to maintain 85% ideal body weight. A total of 71 patients received enteral feeding (1000-2000 kcal/day) for a median period of 161 days (range 4-644 days). Fifty-one (72%) patients gained 5.8 +/- 4.4kg (range 0.4-19.2 kg). Nine gained 10 kg or more. The median time to maximum weight was 74 days after PEG insertion. Those who gained weight had a longer median survival, but this difference was not statistically significant (210 vs 109 days, P = 0.07). The only predictor of weight gain was a CD4 count greater than 100/microL. Patients who gained weight reported improved quality of life and increased independence. However, early complications, especially wound infection, were common. Although these data have been gathered retrospectively, our experience suggests that enteral feeding can maintain or improve nutritional status and may improve quality of life in advanced HIV infection.

Bowel preparation for colonoscopy: a randomized prospective trail comparing sodium phosphate and polyethylene glycol in a predominantly elderly population.

Many patients find polyethylene glycol-based preparations (PEG) difficult to take because of the large volume of fluid they are required to consume. One hundred and sixteen predominantly elderly patients were randomized to receive either sodium phosphate (n = 61) or PEG (n = 55) bowel preparations before colonoscopy. Patients with a history of symptomatic ischaemic heart disease or cerebrovascular disease in the preceding 6 months, severe liver disease or heart failure, or serum creatinine above 200 micrograms/L were excluded from the study. Each patient filled in a questionnaire about the bowel preparation prior to the procedure. The colonoscopists, who were not aware which preparation had been used, were asked to complete a questionnaire about the quality of the bowel preparation after the procedure. The patients found the sodium phosphate preparation slightly more tolerable than PEG. Side effects were slightly more common with sodium phosphate. Neither difference was statistically significant. However, 91% of patients who had previously had PEG found sodium phosphate easier to take. Approximately 25% of patients in each group experienced at least one episode of incontinence. The colonoscopists found no difference in the overall quality of the bowel preparation. The amount of fluid in the colon was greater in patients prepared with PEG. As expected, patients taking sodium phosphate developed hyperphosphataemia (mean phosphate level before colonoscopy 1.56 mmol/L, normal 0.8 -1.3). They also had a lower mean serum potassium level (3.8 mmol/L) than the PEG group (4.2 mmol/L). However, there were no clinically significant consequences. Sodium phosphate was a safe and effective bowel preparation for colonoscopy in this carefully selected group of patients. It was preferred by patients who had previously had PEG. Many elderly patients were found to develop faecal incontinence, irrespective of the type of bowel preparation used.

5-Aminosalicylic acid inhibits the impaired epithelial barrier function induced by gamma interferon.

Gamma interferon (IFN gamma) impairs epithelial barrier function and induces HLA-DR expression on colonic cancer cell lines. Salicylates have been shown to reduce IFN gamma induced HLA-DR expression. The effect of 5-aminosalicylic acid (5-ASA) on IFN gamma induced changes in transepithelial resistance and permeability was investigated in HT29 clone 19A and Caco 2 monolayers. Monolayers were incubated with different concentrations of IFN gamma (100, 500, 1000, and 3000 U/ml) and 5-ASA. IFN gamma induced class II expression in a time and dose dependent manner in HT29:19A but not Caco 2 cells. HT29:19A monolayers incubated with both IFN gamma and 5-ASA showed lower HLA-DR expression compared with monolayers incubated with IFN gamma alone. Electrical resistance and 14C-mannitol flux across HT29:19A monolayers were significantly changed by IFN gamma. Addition of both IFN gamma and 5-ASA to the basolateral surface of the monolayers significantly reduced paracellular permeability compared with addition of IFN gamma alone. These data show that IFN gamma is able to induce HLA-DR expression and to impair the barrier function of HT29:19A monolayers, and that 5-ASA reduces IFN gamma induced HLA-DR expression and inhibits the effects of IFN gamma on epithelial barrier function.

Site of action of platelet-activating factor within the mucosa of rabbit distal colon.

1. To determine how platelet-activating factor stimulates colonic anion secretion and increases epithelial permeability, epithelial sheets of rabbit distal colon excluding the submucosal neural plexus were mounted in Ussing chambers. The influence of specific inhibitors and 50 nmol/l platelet-activating factor on short-circuit current and transepithelial resistance was then investigated. 2. Pretreatment with 1 mumol/l indomethacin or 1 mumol/l doxantrazole abolished the biphasic stimulation of the short-circuit current and decrease in transepithelial resistance induced by platelet-activating factor. Addition of 10 mumol/l mepyramine attenuated the early phase and completely inhibited the late phase. Pretreatment with 1 mumol/l ranitidine, 0.1 mumol/l tetrodotoxin, 0.1 mumol/l ritanserin or a 5-lipoxygenase inhibitor (1 mumol/l MK886) had no effect. 3. To assess the influence of platelet-activating factor on epithelial function isolated from lamina propria elements, monolayers were cultured from a human colonic epithelial cell line (T-84). 4. The short-circuit current across monolayers mounted in Ussing chambers stimulated by 10 mumol/l ionomycin could be inhibited by pretreatment with ouabain or frusemide, consistent with the capacity for chloride secretion. Addition of platelet-activating factor (up to 500 nmol/l) had no effect on short-circuit current or transepithelial resistance. Receptor expression was examined with [3H] platelet-activating factor in isolated T-84 and HT-29 cells and found to be absent. 5. The influence of physiological concentrations of platelet-activating factor on colonic epithelial anion secretion and increased permeability in rabbit distal colon is indirect and consistent with mediation by prostaglandins released from mucosal mast cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Upper gastrointestinal tract.

Drug therapy for upper gastrointestinal disease in the elderly must be moderated by the likelihood of increased sensitivity to the side effects of drugs. For example, in the frail elderly with helicobacter-associated duodenal ulcers, maintenance therapy with an H2-receptor antagonist or omeprazole may be preferable to attempting to eradicate Helicobacter pylori with the current antimicrobial regimens.

Gastrointestinal bleeding from hepatocellular carcinoma invading the stomach.

Bleeding from hepatocellular carcinoma (HCC) invading the gastrointestinal tract is very uncommon. We report the case of a 61 year old man who had a large bleed from HCC invading the fundus of the stomach. Diagnosis was eventually made at laparotomy and he is still alive 7 months after local resection.

Ulcerative colitis and xenobiotic metabolism.

Any hypothesis on the cause of ulcerative colitis must account for genetic influences, geographic and ethnic variations, effects of smoking and oral contraception, anatomical distribution, the relapsing and remitting nature of the disease, and association with primary sclerosing cholangitis. This hypothesis proposes that ulcerative colitis is caused by a reactive xenobiotic metabolite which is conjugated before excretion into bile. The amount of metabolite produced is determined by exposure to its parent compound, by the inherited pattern of metabolism, and by inhibition and induction of enzymes catalysing alternative pathways. Deconjugation by bacteria within the colonic lumen releases the reactive metabolite, damaging the colonic epithelial barrier and exposing the mucosal immune system to luminal contents. Biliary epithelial damage by the metabolite leads to an immune response in those individuals carrying appropriate HLA molecules, thereby initiating an inflammatory process within the biliary tree.

Human colonic intraepithelial lymphocytes from patients with inflammatory bowel disease fail to down-regulate proliferative responses of primed allogeneic peripheral blood mononuclear cells after rechallenge with antigens.

Human colonic intraepithelial lymphocytes from control subjects down-regulate the proliferative responses of primed allogeneic peripheral blood mononuclear cells on rechallenge with antigens or phytohaemagglutinin (PHA). In contrast, human colonic intraepithelial lymphocytes from patients with inflammatory bowel disease fail to down-regulate the proliferative responses of primed allogeneic peripheral blood mononuclear cells on rechallenge with antigens. These findings may be important in the development and maintenance of the mucosal immunological activation of inflammatory bowel disease.

Human colonic intraepithelial lymphocytes suppress in vitro immunoglobulin synthesis by autologous peripheral blood lymphocytes and lamina propria lymphocytes.

Human colonic intraepithelial lymphocytes have been shown to suppress the proliferation of autologous lamina propria lymphocytes and allogeneic peripheral blood mononuclear cells. This study has shown that, in vitro, intraepithelial lymphocytes suppress IgA and total immunoglobulin synthesis (but not IgG or IgM production) by autologous peripheral blood and lamina propria lymphocytes. This down regulation of IgA production is mediated by a soluble factor secreted by the intraepithelial lymphocytes. There is no difference in immunoglobulin down regulation by intraepithelial lymphocytes of control subjects and patients with inflammatory bowel disease.

Inhibition of binding of interferon-gamma to its receptor by salicylates used in inflammatory bowel disease.

5-Aminosalicylic acid (5ASA), 4ASA, their N-acetylated metabolites N-acetyl-5ASA and N-acetyl-4ASA, olsalazine, and colchicine impair interferon-gamma (IFN gamma) induced HLA-DR expression on a colonic cell line, HT-29. The mechanism of this effect is now reported. HT-29 cells were cultured with 50 U/ml IFN gamma with or without drug, and northern blot analysis was performed using a probe for the beta chain of the DR molecule. IFN gamma led to a noticeable increase in HLA-DR mRNA which was attenuated by the drugs. Analysis of the specific binding of increasing concentrations of 125I-IFN gamma by non-linear regression showed a Kd of 1.35 x 10(-10) M and 2.3 x 10(5) binding sites per HT-29 cell. Binding of 125I-IFN gamma was reduced by incubation with increasing concentrations of unlabelled IFN gamma but not with IFN alpha. Incubation with therapeutic concentrations of drugs led to the following reductions in binding: 10 mM 5ASA, 20% (p < 0.001); 10 mM N-acetyl-5ASA, 24% (p < 0.01); 10 mM 4ASA, 21% (p < 0.005); 10 mM N-acetyl-4ASA, 29% (p < 0.001); and 1 mM olsalazine, 29% (p < 0.001). Colchicine (10(-7) M) and 10(-5) M prednisolone had no effect. Incubation with higher concentrations of the drugs revealed a dose-response effect on binding with complete inhibition by 100 mM 4ASA and 10 mM olsalazine, and lesser degrees of inhibition by 100 mM 5ASA, N-acetyl-5ASA, and N-acetyl-4ASA. At concentrations found in the rectal lumen, the salicylates used in inflammatory bowel disease impair the binding of IFN gamma to its receptor on colonic epithelial cells.