RESULTS BY PHONE

In order to support our privacy and confidentiality policy, all patient result inquiries will be handled by our Client Information Centre. We will continue to maintain our existing high level of service to you and your patients.

Please direct your inquiries for patient results to:

Mainland: 

 (604) 431-7206 
 1-800-431-7206 
 (604) 412-4445 Fax 

Island: 

 (250) 881-3112 
 1-800-297-7747 
 (250) 881-3117 Fax 

Client Information Services Centre hours:

Monday - Friday: 7:00 a.m. to 10:00 p.m.
Saturday: 9:00 a.m. to 5:00 p.m.
Sunday and Holidays: Closed

After hours please call the appropriate 1-800 number above and follow the recorded instructions.

NEW UREA BREATH TEST (UBT) FOR HELICOBACTER PYLORI

Effective October 1, 1998, MDS Metro Laboratory Services will be offering a UBT for the laboratory diagnosis of H. pylori infection. The UBT is considered to be one of the most effective tests for detection of H. pylori and is considered to be one of the gold standard tests for both diagnosis and assessment of eradication after therapy. The test is based on detection of non-radioactive labeled ¹³CO₂ 30 minutes after the patient consumes a urea drink. H. pylori produces large amounts of urease. If the organism is present, the ingested urea will be split by the urease, resulting in the release of labeled CO₂. The patient is asked to exhale into a collection device to trap the labeled CO₂, and the amount present is measured by a mass spectrometer. Instructions for the test can be obtained from any MDS Metro Specimen Collection Centre, and a copy is enclosed.

H. pylori is now well established as the main cause of peptic ulcer disease and gastritis, and eradication of H. pylori infection has dramatically improved the management of peptic ulcer disease. H. pylori has also been associated with gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma. The organism is found in 20-40% of Canadians and the prevalence increases with age.

The UBT can be used as an alternative or as an adjunct to serology. Studies have shown the UBT to be both more sensitive and more specific than serology for detection of H. pylori. The UBT is also more effective as a test for eradication of the organism after treatment. These features of the UBT may lead to avoidance of unnecessary antibiotic treatment and possibly fewer endoscopies. To confirm the successful eradication of H. pylori, it is suggested that the UBT be repeated six weeks after completion of a course of therapy. In patients over age 50, or in any patient with alarm symptoms (weight loss, anemia), gastroscopy should be used in place of or in addition to the UBT because of the increased risk of cancer.1 The UBT is not covered by MSP at this time, and patients will be billed $95 for the test.

Questions about the UBT can be referred to MDS Metro Medical Microbiologists.

Reference:

Canadian Helicobacter Consensus Conference. 1998. Canadian J. of Gastroenterology 12: 31-41.

HOMOCYSTEINE METHOD CHANGE

Homocysteine (Hcy) is an amino acid produced from the metabolism of methionine. Normally it is either: (1) remethylated to methionine by one of two pathways requiring either Vitamin B12 and folate or betaine, or (2) metabolized to cystathionine with pyridoxal phosphate (Vitamin B6) as a cofactor.

Epidemiologic evidence suggests that hyperhomocysteinemia is a graded, independent risk factor for coronary artery disease (CAD). The etiology of hyperhomocysteinemia is usually vitamin deficiency (folic acid, B12, or B6) or genetic (abnormal enzyme for remethylation or cystathionine pathway), although elevation may also occur in renal insufficiency or acute stress. ^{1, 2, 3} Plasma Hcy measurement is useful 1) in individuals with premature and/or symptomatic CAD whose other risk factors are near-normal or negative or 2) in those with a strong family history, but no usual risk factors in affected family members. Associations have also been reported with repeated deep vein thrombosis (DVT) and pulmonary embolus, stroke and transient ischemic attacks (TIA), or repeat thromboembolic events that occur at an early age, after trivial provocation, and/or at unusual sites, such that plasma Hcy may be indicated in select patients.

Although a prospective, double-blind, placebo-controlled trial is needed to definitively demonstrate the efficacy of vitamin supplements in reducing morbidity and mortality, vitamin treatment to lower elevated Hcy is both inexpensive and nontoxic and is supported by epidemiologic evidence and atherothrombogenic effects of elevated Hcy in vitro. The Healthy Heart Program treatment algorithm for elevated plasma Hcy is available in the September 1997 BCMJ. ⁴

The preferred specimen for Hcy is fasting plasma. Greater day-to-day variability may be seen with serum and non-fasting specimens. Hcy tends to be higher in serum: slight increased or decreased Hcy concentration, which may last several hours, has been observed following meals, possibly related to protein content. To maximize consistency with repeat testing, fasting Hcy is recommended. Drugs such as phenytoin and carbamazepine may increase plasma Hcy in vivo.

A new immunoassay methodology will be introduced within the next month. Results may be 15 to 20 % lower than by the previous high pressure liquid chromatography (HPLC) procedure and should be evaluated relative to the new, lower reference ranges on the report form. Minor reference range adjustments may occur during the next few months as additional experience is gained with the new assay.

For comments or additional information, please call:

Mainland: 

 Dr. Margaret Kelly 
 604-412-4426 
 1-800-431-7206  

 Dr. David Aitken 
 604-412-4412  
 1-800-431-7206 

Island:

 Dr. Michael McNeely
 250-881-3109  
 1-800-304-4011 

References:

1. Boushey C., et.al. "A Quantitative Assessment of Plasma Homocysteine as a Risk Factor for Vascular Disease." Journal of the American Medical Association Oct 4, 1995; 274: 1049-57.
2. Selhub J. and D’Angelo A. "Relationship Between Homocysteine and Thrombotic Disease." American Journal of Medical Science 1998; 316: 129-41.
3. Welch G. and Loscalzo J. "Homocysteine and Atherothrombosis." New England Journal of Medicine 1998; 338: 1042-1050. (See also correspondence for comments and corrections NEJM 1998; 339: 477-79.)
4. Frohlich J. "Homocysteine and Vascular Disease." British Columbia Medical Journal 1997; 39:9: 488.