Biomedical subjects

Sybrand Y de Boer

Publications and source records attributed to Sybrand Y de Boer.

4 recordsLinked to original sources

PubMed2006

Prevention of NSAID-associated gastrointestinal lesions: a comparison study pantoprazole versus omeprazole.

AIM: To investigate tolerability and efficacy of pantoprazole 20 mg, once daily (o.d.), pantoprazole 40 mg o.d., and omeprazole 20 mg o.d., in patients taking nonsteroidal anti-inflammatory drug(s) (NSAIDs). METHODS: Included in this randomized, double-blind, multicenter, parallel-group study were rheumatic patients (>55 yr) on continual NSAIDs and with at least one more recognized risk factor that contributes to the development of gastrointestinal (GI) injury. Study duration was 6 months, and the treatment consisted of pantoprazole 20 mg o.d. (N = 196), pantoprazole 40 mg o.d. (N = 199), or omeprazole 20 mg o.d. (N = 200). Patients took NSAID(s) (except COX-2 inhibitors), had no more than five erosions/petechiae in the upper GI tract, no current peptic ulcers or reflux esophagitis, and had at most moderate intensity GI symptoms. Endoscopy was performed at baseline, 3, and 6 months. The primary end points were lack of "therapeutic failure" and lack of "endoscopic failure" at 6 months. RESULTS: After 6 months, the probabilities to remain in remission were 90% pantoprazole 20 mg o.d., 93% pantoprazole 40 mg o.d., and 89% omeprazole 20 mg o.d. for lack of "therapeutic failure;" 91% pantoprazole 20 mg o.d., 95% pantoprazole 40 mg o.d., and 93% omeprazole 20 mg o.d. for lack of "endoscopic failure." CONCLUSIONS: For patients taking NSAIDs continually, pantoprazole 20 mg o.d., pantoprazole 40 mg o.d., or omeprazole 20 mg o.d. provide equivalent, effective, and well-tolerated prophylaxis against GI lesions, including peptic ulcers.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed2006

Decrease in mortality in Lynch syndrome families because of surveillance.

BACKGROUND & AIMS: Lynch syndrome family members have a high risk of developing colorectal (CRC), endometrial (EC), and other cancers. A large-scale surveillance program was introduced in The Netherlands in the late 1980s. The aims of the study were to evaluate the effectiveness of this program by assessing mortality because of CRC and EC before and after 1990 and to compare mortality because of all cancers (except CRC/EC) with mortality in the general population. METHODS: Family members with at least 50% probability of being a carrier were selected for the study. The standardized mortality ratio (SMR) because of cancer and the absolute excess risk of death (AER) were calculated. RESULTS: In the total cohort (N = 2788), 445 subjects had died because of cancer. The 3 most frequent causes of cancer-related deaths were CRC (50.3%), EC (6.7%), and brain tumors (6.7%). A significant decrease (70%) in SMR for CRC over time was observed (P < .001); the SMR for EC showed no decreasing trend over time. A significantly increased SMR was found for cancer of the small bowel (SMR = 18.3), brain (SMR = 9.1), kidney/ureter (SMR = 5.9), ovarium (SMR = 2.3), pancreas (SMR = 2.2), and stomach (SMR = 2.1). The AER was significantly increased for brain tumors only. CONCLUSIONS: Since the introduction of surveillance, the mortality because of CRC has decreased. Except for brain tumors, we did not find a significantly increased AER for tumors other than CRC/EC.

Adult↗

PubMed2005

Promising treatment of autoimmune hepatitis with 6-thioguanine after adverse events on azathioprine.

The use of corticosteroids in autoimmune hepatitis is an established therapy. To avoid the possible serious side effects of corticosteroids, immunosuppression with azathioprine is often warranted. Azathioprine, a purine analogue, is frequently used to taper or replace corticosteroids. However, approximately 10% of the patients are intolerant to azathioprine. Alternative therapies using mycophenolate, tacrolimus, budesonide, cyclosporine and 6-mercaptopurine have been studied, with variable results. The use of 6-thioguanine, an agent more directly leading to the down-stream active metabolites of azathioprine (6-thioguanine nucleotides) in inflammatory bowel disease patients intolerant to azathioprine or 6-mercaptopurine showed conflicting results. We report three patients with autoimmune hepatitis who could not tolerate azathioprine but tolerated 6-thioguanine 0.3 milligram per kilogram daily well. All three patients improved clinically. Therapeutic drug monitoring was performed. The prospective evaluation of 6-thioguanine as a possible immunosuppressive drug in autoimmune hepatitis patients is warranted.

Aged↗

PubMed2004

Effect of SULT1A1 and NAT2 genetic polymorphism on the association between cigarette smoking and colorectal adenomas.

Cigarette smoke contains polycyclic hydrocarbons and arylamines that may both be activated by sulfotransferase, encoded by SULT1A1. A genetic polymorphism leads to an Arg213His substitution, thereby decreasing enzyme activity and stability and might thus modify the association between smoking and colorectal adenomas. We investigated this in a Dutch case-control study. Additionally, we evaluated potential roles of epoxide hydrolase (EPHX), N-acetyltransferases (NAT1 and NAT2) and glutathione S-transferases (GSTM1 and GSTT1). The data analysis included 431 adenoma cases and 432 polyp-free controls (54% women; mean age, 54.6 years) enrolled at endoscopy in 8 Dutch hospitals between 1997 and 2000. All participants provided data on smoking habits and blood for DNA isolation. Genotyping was performed using appropriate polymerase chain reaction-restriction fragment length polymorphism procedures. Multivariate models included age, sex, endoscopy indication, consumption of snacks and alcohol and, if appropriate, daily smoking dose or smoking duration. Smoking increased colorectal adenoma risk, most importantly by duration. Smoking for more than 25 years more than doubled adenoma risk (OR = 2.4, 95% CI = 1.4-4.1) compared to never smoking. Combinations of SULT1A1 fast sulfation (*1/*1) and of NAT2 slow acetylation with smoking resulted in a 4 times higher risk of adenomas compared to never smokers with other inherited gene variants, although there was no statistically significant effect modification. We found no clear effects of the other genetic polymorphisms on the association between smoking and adenomas. We conclude that smoking increases risk of colorectal adenomas and that SULT1A1 and NAT2 only modestly modify this association.

Acetyltransferases↗