Rheumatology Advance Access originally published online on March 23, 2007
Rheumatology 2007 46(5):894; doi:10.1093/rheumatology/kem036
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
An unusual association with Raynaud's phenomenon: reply
Rheumatology Department, Derbyshire Royal Infirmary, Derby, DE1 2QY, 1Department of Medicine, Burton Hospitals NHS Trust, Burton-on-Trent, Staffordshire DE13 0RB, UK
Correspondence to: Dr C. M. Deighton. E-mail: chris.deighton{at}derbyhospitals.nhs.uk
SIR, Dr Binymin is clearly not aware of the challenging 200-word limit placed on Clinical Vignettes. We thank him for his interest, and for giving us an opportunity to expand on the details. The patient gave a good history for secondary Raynaud's phenomenon. We do not possess a capillaroscope in Derby, but the nail folds did not demonstrate any abnormalities using an ophthalmoscope (poor man's capillaroscopy).
Dr Binymin is correct to say that pituitary insufficiency is a biochemical diagnosis and does not rest on the pituitary anatomy. We disagree however that in this case further dynamic testing was necessary in order to make a firm diagnosis of hypopituitarism. At the time of diagnosis of her hypopituitarism she had marked hyponatraemia with sodium at 122 mmol/l. Endocrine testing revealed abnormalities of all her anterior pituitary hormonal axes (normal ranges are given in brackets). She had secondary thyroid deficiency with a TSH 2.37 mu/l (0.3–5.5), Free T4 6.0 pmol/l (11.0–23.0) and Free T3 1.5 pmol/l (3.5–6.5). These results are not compatible with primary hypothyroidism as suggested by Dr Binymin. She had gonadotrophin deficiency with an LH 0.1 Iu/l (1–17), FSH 0.7 Iu/l (2.5–10.2) and a previous test showing a low oestradiol of 33 pmol/l (95–800). She had cortisol deficiency with a short synacthen test at 9am that showed a basal cortisol of 128 nmol/l, rising to 216 nmol/l at 30 min and 289 nmol/l at 60 min. This is the typical response seen in hypopituitarism with a low basal and a delayed and inadequate response. ACTH was not measured because of a problem with sample collection. She had an undetectable growth hormone (<0.13 mu/l) and an undetectable IGF1 [<1 µg/l (114–492)], although dynamic testing would be needed to formally document growth hormone deficiency.
Given her clinical state and marked hyponatraemia, it was necessary to start steroid treatment immediately after sending off these initial samples. The clear abnormalities of all the anterior pituitary hormonal axes can only be explained by a central cause and made further dynamic testing unnecessary for the diagnosis of hypopituitarism in this case. We thank Dr Binymin once again for converting our Clinical Vignette into a fuller case report.
The authors have declared no conflicts of interest.
Accepted 24 January 2007
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||