eMJA     The Medical Journal of Australia

Home | Issues | eMJA shop | Classifieds | Contact | More... | Topics | Search | Login | Buy full access   

Letters

Anorexia nervosa and senna misuse: nephrocalcinosis, digital clubbing and hypertrophic osteoarthropathy

Andrew F McLaughlin
MJA 2008; 189 (6): 348

To the Editor: I read with interest the letter by Lim and colleagues on anorexia nervosa and senna misuse.1 I have seen abnormal whole body bone scans in patients with severe eating disorders of exactly the same pattern (except for the avid bilateral apical lung and gastric uptake) as the case described.

However, I disagree with the interpretation of the bone scan. There was increased periarticular tracer uptake involving long bones. The pattern was not that of hypertrophic osteoarthropathy (HOA). The pattern in HOA is linear tracer uptake by the periosteum, particularly along the distal ends of long bones.2 The scan in the case reported did not show uptake of this pattern, despite radiological evidence showing periosteal reaction and new bone formation of the tibia and fibula at the ankle. The pattern exhibited in this patient was more consistent with metabolic bone disease (increased tracer uptake by the ends of long bones periarticularly, the axial skeleton, calvaria, mandible, sternum and “beading” of costochondral junctions, with faint, or absent, renal uptake),3 although not all of these features were present in this case.

Metastatic calcification of the gastric wall (not mentioned by the authors) and upper lobes of the lung was present in this patient. Metastatic calcification of the lungs can be diffuse4 or localised (most commonly) to the upper lobes, as in this case.5

With regard to the bone mineral density results in this case, the authors state that the lumbar and femoral neck T scores were elevated (1.2 and 1.3, respectively). The normal range of the T scores is ± 1.0 standard deviation of young adult normal values.6 Elevated bone mineral density measurements are generally not of pathological significance and are therefore clinically not relevant. In my experience they are usually decreased, and are often osteoporotic, in patients with severe eating disorders.

Andrew F McLaughlin, Nuclear Medicine Physician

Burwood Nuclear Medicine, Sydney, NSW.

afmATnucmedburwood.com.au

  1. Lim AKH, Hook PH, Kerr PG. Anorexia nervosa and senna misuse: nephrocalcinosis, digital clubbing and hypertrophic osteoarthropathy [letter]. Med J Aust 2008; 188: 121-122. <eMJA full text> <PubMed>
  2. Ali A, Tetalman MR, Fordham EW, et al. Distribution of hypertrophic pulmonary osteoarthropathy. Am J Roentgenol 1980; 137: 771-780.
  3. Fogelman I, Collier BD, Brown ML. Bone scintigraph. Part 3: bone scanning in metabolic bone disease. J Nucl Med 1993; 34: 2247-2252. <PubMed>
  4. McLaughlin AF. Uptake of 99mTc bone scanning agent by lungs with metastatic calcification. J Nucl Med 1975; 16: 322. <PubMed>
  5. Bloodworth J, Tomashefski RF Jr. Localised pulmonary metastatic calcification associated with pulmonary artery obstruction. Thorax 1992; 47: 174-178. <PubMed>
  6. World Health Organization. An assessment of fracture risk and its application to screening and postmenopausal osteoporosis. Report of a WHO Study Group. (Technical Report Series No. 84.) Geneva: WHO, 1994.

(Received 16 Apr 2008, accepted 26 Jun 2008)

Home | Issues | eMJA shop | Terms of use | Classifieds | More... | Contact | Topics | Search

The Medical Journal of Australia    eMJA  

©The Medical Journal of Australia 2008 www.mja.com.au PRINT ISSN: 0025-729X ONLINE ISSN: 1326-5377