Pathology

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Markers of bone turnover, measured in blood or urine, correlate with changes in the metabolic activity of bone.The rate of bone remodelling is important. With ageing, the quantum of bone removed/ resorbed and the amount replaced/ formed becomes increasingly imbalanced. Consequently, the more bone remodelling units that are active at any one time, or the greater the activity of individual units, the greater the overall rate of bone loss.Bone turnover markers are probably predictive of the rate of bone loss and could help determine the efficacy of treatment.

Bone turnover markers:

  • May predict fracture risk independently of bone mineral density, according to some studies.
  • A drop in bone resorption is an early predictor of response to all anti-resorptive osteoporosis treatments initiated in general practice (bisphosphonates, denosumab or raloxifene), with these markers changing earlier than comparable markers of bone formation.
  • They may be predictive of later changes in bone mineral density (BMD), and can be measured before BMD changes can be evaluated.

Which bone resorption marker?

Markers measuring the rate of bone loss are degradation products of type 1 collagen cleaved during bone resorption. Cross-linking telopeptides of collagen can be measured by immunoassays that are specific for the beginning (N terminal- called NTX) or end (C terminal- called CTX) of type 1 collagen. While measuring urinary NTX and serum CTX provide comparable information there are some advantages of CTX over NTX. Consequently, serum CTX has been proposed as a reference method.The measurand in the CTX assay is clearly defined, allowing this 8 amino acid oligopeptide to become the reference method.
  • Most serum CTX is from osteoclastic bone resorption (indicating high specificity).
  • The assay can be performed manually or by automated methods and is only provided by one manufacturer (obviating the need for harmonisation)
  • The biological and analytical variability for CTX is well documented in the literature.

Uses and limitations

Serum CTX is a potentially useful test when investigating the cause of increased alkaline phosphatase, verifying compliance with osteoporosis treatment, improving persistence with that treatment or identifying occult secondary causes of osteoporosis such as apathetic hyperthyroidism or other metabolic bone disorders such as Paget’s disease.Samples collected fasting in the morning minimise intra-individual variation and requests ideally should include the reason for testing.Medicare currently provides a rebate for tests of bone resorption in patients with known bone disease taking treatment.
  1. Not all anti-resorptive treatments suppress bone resorption to the same degree. Provision of the type of anti-resorptive agent used and the duration of treatment is not only helpful for billing but allows us to report more specifically - whether the rate of bone resorption is typical or higher than expected for a particular anti-resorptive agent. For example, denosumab suppresses bone resorption earlier and to a greater degree than a bisphosphonate.
  2. Bone resorption is not predictive of future fracture risk in individuals. CTX can provide complementary information to bone mineral density in subpopulations but this measurement has not been currently adopted into fracture risk alogrithm calculators such as FRAX or the Garvan risk calculator for individuals.
  3. The measurement of serum CTX cannot be used to select treatment. This is because the baseline rate of bone remodelling is not predictive of the rate of change of bone remodelling or rate of change of bone density while on treatment.
  4. Measurement of bone formation and bone resorption do not provide additive information. While bone remodelling is a coupled process wherein bone formation and bone resorption are linked, the measurement of bone resorption or bone formation markers provide comparable information regarding the rate of bone remodelling. Measurements of both bone formation and bone resorption markers in individual patients do not help determine the degree of imbalance in bone remodelling and is therefore unnecessary. Understanding these limitations and the potential value of measuring bone remodelling markers can be useful when making decisions regarding individual patient management in those taking treatment for osteoporosis.
Reproduced with permission from Medical Forum magazine Oct 2017 edition
General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs.The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.
Clinical Articles iconClinical Articles

Identified in 1983 by Australian Nobel prize winners Marshall and Warren, H. pylori is linked to a spectrum of disease including non-ulcer dyspepsia, peptic ulcer, gastric cancer and mucosa-associated lymphoid tissue lymphoma.Infection is estimated to be present in about 30% of adult Australians, though not uniformly distributed in the population. Prevalence is higher in immigrants, those of lower socioeconomic status and the institutionalised.It has been conventionally treated with a standard first-line triple therapy including a proton pump inhibitor (PPI), clarithromycin and amoxicillin or metronidazole administered for seven days.However, in the past decade the effectiveness of this triple therapy, although still recommended in Therapeutic Guidelines, has declined mainly due to the development of antibiotic resistance.A recent meta-analysis1 of treatment, which reviewed 15,565 studies worldwide, highlighted the geographically localised nature of resistance profiles. It concluded that one single ‘most effective’ treatment was unlikely to be identified across the world, as the treatments needed to be tailored to regional resistance profiles.The range of tests, both non-invasive and invasive, following endoscopy are outlined below.

Pylori serology

This detects organism-specific IgG. It requires the collection of 5 mL of serum. No special preparation of the patient is required. Antibodies may take 5–10 weeks to develop after infection and may remain positive long term. A positive result may indicate present or past infection.Epidemiologic evidence now indicates that most infections are acquired during childhood, even in developed countries, and the frequency of H. pylori infection for any age group in any locality reflects that particular cohort's rate of bacterial acquisition during childhood years.

Urea breath test (UBT)

The UBT requires the patient to drink 13C-labelled or 14C-labelled urea, which is converted to labelled CO2 by the urease in H. pylori. The labelled gas is measured in a breath sample. Sullivan Nicolaides Pathology currently utilises the nonradioactive 13C-labelled isotope.The test has a sensitivity of 95% and a specificity of 98%. It is generally not suitable for children under five years because of the difficulty in following test instructions. This test has an out-of-pocket fee to the patient of $60.

Faecal antigen test

Active H. pylori infection can be detected by identifying H. pylori–specific antigens in a stool sample with the use of monoclonal antibodies. This assay has similar sensitivity and specificity to the UBT and has no additional out-of-pocket expenses for the patient.

Rapid urease test (CLO test)

If endoscopy is indicated, a biopsy specimen can be placed into a CLO tube containing urea and a pH indicator. If H. pylori is present, the urease will convert the urea to ammonia, leading to a colour change in the pH indicator. This is a reliable and cheap method for identifying H. pylori infection with reported excellent sensitivity and specificity in excess of 90%. The colour change usually occurs within minutes and the clinician can record the results the same day. If the inoculated CLO tube is forwarded to the laboratory the results can be recorded in the pathology Laboratory Information System, but must be read within 72 hours of the tube being inoculated for the result to be valid.

Histology

Histology is slightly more sensitive and specific than the rapid urease test and provides additional information on the type of gastritis, atrophy, intestinal metaplasia and malignancy. If proton pump inhibitors (PPIs) have been taken, biopsies from the gastric body in addition to the antrum can improve the diagnostic yield. The organism can be identified with conventional stains including haematoxylin and eosin and Giemsa. Immunohistochemistry increases sensitivity and specificity further and is of most use in cases of assumed low density colonisation.

Culture and susceptibility testing

Culturing of the organism is available for those who fail therapy. This is done from a gastric biopsy and permits testing for sensitivity to antimicrobial agents. Specialised transport media Portagerm pylori (PORT-PYL – Item 25016) is available to improve organism viability.Susceptibility guided versus empirical antibiotic treatment for H. pylori infection has been shown to be superior to empirical 7–10 day triple therapy for first line treatment. The recent meta-analysis showed that the worst-ranking treatment is standard triple therapy (proton pump inhibitor, clarithromycin and amoxycillin or metronidazole) administered for seven days.Over the past 10 years our microbiology laboratory has cultured H. pylori from 108 endoscopic biopsies and 102 patients. Most of these cultures were performed because patients had failed therapy, introducing significant sample bias. For 24% of episodes, despite the organism being cultured, it did not remain viable to complete susceptibility testing. Susceptibility results for 76 isolates that remained viable for testing indicate that antibiotic resistance (clarithromycin – 59.7%; metronidazole – 51.3%; ampicillin – 22.4%) is a significant cause of treatment failure.Ref:
  1. Li Bao-Zhu, Threapleton DE et al Comparative effectiveness and tolerance of treatments for Helicobacter pylori: systematic review and network meta-analysis. BMJ 2015;351:h4052 http://www.bmj.com/content/351/bmj.h4052

General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs.The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

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