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Biomedical subjects

D Bjorkman

Publications and source records attributed to D Bjorkman.

13 recordsLinked to original sources
PubMed2004

Systematic review: short-term adverse effects of 5-aminosalicylic acid agents in the treatment of ulcerative colitis.

AIM: To determine whether there is a difference in short-term adverse events in patients with ulcerative colitis treated with mesalazine, olsalazine or balsalazide. METHODS: MEDLINE was searched for articles published until 2002. Randomized trials of oral mesalazine, olsalazine or balsalazide for the treatment of active disease or the maintenance of remission were included. Outcomes of interest were the frequencies of patients experiencing adverse events and those withdrawn due to adverse events. RESULTS: Forty-six trials were included. One study of mesalazine vs. sulfasalazine for active colitis showed significantly fewer patients with adverse events with mesalazine. Both balsalazide vs. sulfasalazine studies for active disease showed significantly fewer withdrawals with balsalazide. One trial of balsalazide vs. sulfasalazine for maintenance showed significantly fewer patients with adverse events with balsalazide. Otherwise, no significant differences in safety outcomes were noted. CONCLUSION: All three 5-aminosalicylic acid agents are safe in the short term. In mesalazine-treated patients, the frequencies of adverse events or withdrawals due to adverse events were comparable with those in placebo-treated patients and lower than those in sulfasalazine-treated patients. Overall, adverse events or withdrawals were not significantly more frequent with olsalazine than with placebo or sulfasalazine. Adverse events and study withdrawals on balsalazide were less frequent than those on sulfasalazine.

Administration, Oral↗
PubMed2003

Systematic review: the economic impact of irritable bowel syndrome.

BACKGROUND: Although little mortality is associated with irritable bowel syndrome, curative therapy does not exist and thus the economic impact of this disorder may be considerable. METHODS: A systematic review of the literature was performed. Studies were included if their focus was irritable bowel syndrome, and direct and/or productivity (indirect) costs were reported. Two investigators abstracted the data independently. RESULTS: One hundred and seventy-four studies were retrieved by the search; 11 fulfilled all criteria for entry into the review. The mean direct costs of irritable bowel syndrome management were reported to be UK pound sterling90, Canadian$259 and US$619 per patient annually, with total annual direct costs related to irritable bowel syndrome of pound sterling45.6 million (UK) and $1.35 billion (USA). Direct resource consumption of all health care for irritable bowel syndrome patients ranged from US$742 to US$3166. Productivity costs ranged from US$335 to US$748, with total annual costs of $205 million estimated in the USA. Annual expenditure for all health care, in addition to expenditure limited to gastrointestinal disorders, was significantly higher in irritable bowel syndrome patients than in control populations. CONCLUSIONS: Despite the lack of significant mortality, irritable bowel syndrome is associated with high direct and productivity costs. Irritable bowel syndrome patients consume more gastrointestinal-related and more total health care resources than non-irritable bowel syndrome controls, and sustain significantly greater productivity losses.

Cost of Illness↗
PubMed2002

Health-related quality of life among persons with irritable bowel syndrome: a systematic review.

AIM: To perform a systematic review of the literature with three objectives: (1) to compare the health related quality of life (HRQoL) of patients with irritable bowel syndrome with that of healthy controls; (2) to compare the HRQoL of irritable bowel syndrome patients to those with other diseases; and (3) to examine therapy-associated changes in HRQoL of irritable bowel syndrome patients. METHODS: Searches of all English and non-English articles from 1980 to 2001 were performed in Medline and Embase, and two investigators performed independent data abstraction. RESULTS: Seventeen articles met our selection criteria. 13 studies addressed objective no. 1; 11 showed a significant reduction in HRQoL among irritable bowel syndrome patients. Of these, only one study was considered of high quality. Four studies addressed objective no. 2, none of which was considered to be high quality in addressing this objective. Four trials (three of high quality) addressed objective no. 3. One showed that symptomatic improvement with Leupron compared to placebo was accompanied an improvement only in the comparative health domain of the HRQoL. The second study reported significant positive changes in HRQoL after 12 weeks of cognitive behavioural therapy. The third report of two placebo-controlled studies indicated significant improvement with alosetron on most domains of Irritable Bowel Syndrome Quality of Life Questionnaire. CONCLUSIONS: (i) There is reasonable evidence for a decrease in HRQoL in patients with moderate to severe irritable bowel syndrome; however, the data are conflicting regarding the impact of irritable bowel syndrome on HRQoL in population-based studies of nonconsulters. (ii) HRQoL in irritable bowel syndrome patients is impaired to a degree comparable to other chronic disorders such as GERD and depression. (iii) A therapeutic response in irritable bowel syndrome-related pain has a corresponding improvement in HRQoL. (iv) Limitations of the literature include focusing on moderate-severe irritable bowel syndrome in referral centres, and lack of appropriate controls

Colonic Diseases, Functional↗
PubMed2001

A critical approach to noncardiac chest pain: pathophysiology, diagnosis, and treatment.

Approximately 30% of coronary angiograms performed in this country are negative for significant coronary artery disease. These patients are classified as having noncardiac or unexplained chest pain (UCP). Despite the good overall prognosis, this condition has significant morbidity and costs. The pathophysiology of this condition is likely caused by overlapping cardiac, esophageal, and psychiatric abnormalities with visceral hyperalgesia playing a central role. Gastroenterologists are often consulted in the evaluation of these patients because esophageal disorders are among the most common conditions associated with UCP. However, clinical symptoms are unreliable in differentiating between esophageal and cardiac causes of UCP. Gastroesophageal reflux disease, not esophageal motility disorders, is the most common esophageal disorder present in patients with UCP. The most useful diagnostic test in the evaluation of UCP is 24-h pH monitoring. An initial empiric trial of high-dose acid suppression is the most cost-effective intervention in the management of these patients. A clinical algorithm is suggested for the evaluation and treatment of UCP.

Algorithms↗
PubMed1999

Prospective determination of distal colon findings in average-risk patients with proximal colon cancer.

BACKGROUND: Recent guidelines indicate that colonoscopy and sigmoidoscopy are both acceptable options for screening average-risk patients for colorectal cancer. Retrospective studies have found that a majority of patients with cancer proximal to the splenic flexure have a normal screening flexible sigmoidoscopy. METHODS: This was a multicenter, prospective description of colonoscopic findings and family history in consecutive patients with proximal colon cancer. RESULTS: Among 116 prospectively identified average-risk patients with cancer proximal to the splenic flexure, 40 (34.5%) had neoplasia distal to the splenic flexure. The prevalence of patients with adenomas greater than or equal to 1 cm, with only one tubular adenoma less than 1 cm, and with only hyperplastic polyps were 16.4%, 8.6%, and 6.9%, respectively. CONCLUSIONS: Most average-risk patients with cancer proximal to the splenic flexure will have a normal screening flexible sigmoidoscopy. These patients have an unexpectedly high prevalence of large distal adenomas, but the prevalence of both single small tubular adenomas and hyperplastic polyps alone is similar to that expected during screening of the general population. Clinicians and payers should continue to seek methods to improve the cost-effectiveness and availability of screening colonoscopy in average-risk persons.

Adenocarcinoma↗
PubMed1999

Review article: nonsteroidal anti-inflammatory drug-associated gastrointestinal complications--guidelines for prevention and treatment.

Chronic ingestion of NSAIDs increases the risk for gastrointestinal complications, which range from dyspepsia to gastrointestinal bleeding, obstruction, and perforation. Among patients using NSAIDs, 0.1 to 2.0% per year suffer serious gastrointestinal complications. Patients who require analgesic therapy should be carefully assessed for the lowest possible dosage and shortest duration of NSAID use and for the potential of treatment with a non-NSAID pain reliever. These patients should also be assessed for factors that increase their risk of gastrointestinal complications, including increased age, concomitant anticoagulant or corticosteroid use, and past history of NSAID-associated gastrointestinal complications. The exact association between Helicobacter pylori infection and NSAID-related ulcer disease is unclear, and the routine testing and treatment of all NSAID using patients for H. pylori infection is not recommended at this time. NSAID-using patients who suffer from dyspepsia should have NSAIDs discontinued, the dosage changed, or be changed to a different class of NSAID. If NSAIDs cannot be discontinued, then an antisecretory agent should be initiated. Misoprostol prevents NSAID-associated gastrointestinal complications. Proton pump inhibitors are the most effective at healing NSAID-associated ulcers among patients who cannot discontinue NSAID therapy.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Nonsteroidal anti-inflammatory drug-associated toxicity of the liver, lower gastrointestinal tract, and esophagus.

Although upper gastrointestinal (GI) adverse events are the most common consequences of nonsteroidal anti-inflammatory drug (NSAID) use, there are other GI side effects that can contribute to the morbidity and mortality associated with these drugs. NSAID-associated toxicity of the large and small bowel is increasingly recognized in clinical practice, as enteroscopic procedures become more frequently used. This lower GI toxicity may have several different manifestations: ulcerations, strictures, colitis, or exacerbation of inflammatory bowel disease. Hepatic injury, most likely due to an idiosyncratic reaction resulting from an immunologic response or altered metabolic pathways, is another sequela of NSAID use that is usually reversible. Although hepatotoxicity is listed as a class warning for NSAIDs, aspirin, diclofenac, and sulindac are most commonly associated with this problem. Surveillance for hepatic injury is not always reliable, and the low frequency of both hepatic and lower GI toxicity in NSAID users renders these events difficult to characterize. An increase in awareness, surveillance, and reporting of these events can lead to a better understanding of the risk factors and etiology associated with NSAID toxicity.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Protoporphyrin overload in unrestrained rats: biochemical and histopathologic characterization of a new model of protoporphyric hepatopathy.

We determined the feasibility of producing protoporphyric hepatopathy in unrestrained rats by infusing protoporphyrin into their portal circulation via chronic indwelling catheters. Sprague-Dawley rats, 200-300 g, received single (8.5-27.8 mumol) or multiple (64.1-208.7 mumol) infusions of protoporphyrin over 3-240 h. Single protoporphyrin infusions increased the hepatic protoporphyrin concentration from < 1 nmol/g up to 1368 nmol/g; multiple infusions up to 3908 nmol/g. The maximal non-hepatic tissue concentrations averaged 243 nmol/g in the spleen. Hepatocanalicular and ductular birefringent pigmented deposits were found in all livers, generally proportional to the protoporphyrin load. Aggregates of crystalline protoporphyrin were detected in biliary ductules, canaliculi, hepatocytes, Kupffer cells and fat-storage cells by electron microscopy. Laboratory abnormalities included elevations of the transaminases, LDH, GGTP and bilirubin and a modest fall in the haematocrit suggesting a mixture of red blood cell and hepatic injury. Thus, protoporphyric hepatopathy was produced by infusions of protoporphyrin into the portal circulation. This model may aid in understanding the pathogenesis and pathophysiology of liver disease in protoporphyria.

Animals↗
PubMed1991

Alteration of gastric surface cell pH regulation by sodium taurocholate.

Gastric mucosal cells from guinea pigs were grown in cell culture. Acridine orange fluorescence at 624 nm was used as an qualitative indicator of intracellular pH. The cultured cells were exposed to Hank's solution at pH 7.4, 6.0, 5.0, 4.0, 3.0, and 1.8 for 30 min. After removal of the acid, the cells were loaded with acridine orange for qualitative pH assessment. The cells developed alkaline shifts in the cytoplasmic pH in direct proportion to the acid load. This alkaline overcorrection after exposure to acid was blocked by amiloride and blunted by taurocholic acid in a dose-dependent fashion. These results suggest that gastric surface cells may regulate their cytoplasmic pH with a sodium-hydrogen antiporter. These results also suggest that this antiport system may be adversely affected by bile salts.

Acid-Base Equilibrium↗
PubMed1990

Ultrastructural changes in gastric epithelium caused by bile salt.

We assessed the influence of bile salt in neutral solution on the morphology and function of the Ussing-chambered stomach mucosa. Guinea pig gastric mucosa was exposed to 5, 10, and 20 mM taurocholic acid in balanced salt solution with glucose. Control tissues were exposed to salt solution without taurocholic acid. During exposure to the bile salt, the pH of the bathing solutions was maintained at 7.0-7.4 with 0.1 M sodium hydroxide. Potential difference, short-circuit current, and resistance of the tissues were recorded every 15 min. The morphologic effects of the bile salt were determined with light and electron microscopy. The 10 and 20 mM concentrations caused significant deterioration of the electrophysiologic measurements and major morphologic alteration on both light and electron microscopic evaluations. The 5 mM concentration of taurocholic acid did not affect the electrophysiologic measurements or the light microscopic appearance of the surface cells. Electron microscopy, however, revealed morphologic changes in over 50% of the specimens examined. These findings demonstrate that in vitro, mammalian gastric mucosa shows significant ultrastructural changes when exposed to physiological concentrations of bile salt in a neutral solution. These changes appear to be subtle in that they are evident on transmission electron microscopy even before significant change can be demonstrated by light microscopy or by standard electrophysiologic measurements.

Animals↗
PubMed1987

Endotoxin: a twofold effect on bone marrow ultrastructure.

Ultrastructural studies of mouse bone marrow reveal that reduction of the marrow-blood barrier precedes the two waves of leukocytosis which follow endotoxin administration. These ultrastructural changes include a decrease in adventitial cover of the marrow sinus wall, an increase in sinus circumference, and a decrease in endothelial cell overlap. The marrow-blood barrier changes which precede the first wave of leukocytosis are transient and are associated with depletion of marrow granulocytes. The changes that precede the second wave of leukocytosis 5 to 6 days later are more sustained and are associated with marked granulocyte hyperplasia. We suggest that endotoxin has two effects on marrow ultrastructure: (1) an early, direct effect on the sinus wall and (2) a later, indirect effect associated with granulocyte proliferation. The late effect may be mediated through endotoxin induced release of colony stimulating factor. Both effects diminish the normal marrow-blood barrier and appear to facilitate cell release from the marrow.

Animals↗