HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pavlu, J Articles by Winer, J B Search for Related Content PubMed PubMed Citation Articles by Pavlu, J Articles by Winer, J B

Hypothyroidism and nemaline myopathy in an adult

¹ Catherine Lewis Centre, Hammersmith Hospital, London, UK
² Department of Neuropathology, Neuroscience Centre, University Hospital Birmingham, Birmingham, UK
³ Department of Neurology, Neuroscience Centre, University Hospital Birmingham

Correspondence to:
Correspondence to:
Dr John B Winer
Neuroscience Centre, University Hospital Birmingham, Queen Elizabeth Hospital, Birmingham B15 2TH, UK; j.b.winer@bham.ac.uk

Keywords: autoimmune hypothyroidism; nemaline myopathy

The first 150 words of the full text of this article appear below.

A significant proportion of patients with myopathy attributed to hypothyroidism remain symptomatic after long term thyroxine treatment, but muscle biopsies are rarely undertaken. Systemic review of published reports revealed only one case of typical nemaline myopathy associated with the condition. We hypothesise that hypothyroidism may not directly cause nemaline changes in muscles but it may unmask asymptomatic muscle disorders.

Case report
A 65 year old white man presented with bilateral lower limb oedema extending to the abdomen, and shortness of breath on exertion. The oedema improved on diuretics but he was noted to have muscle tenderness and weakness. He was unable to stand up from sitting. Physical examination showed proximal muscle weakness of grade 3/5. There was no previous history of an autoimmune disease and no relevant family history of muscle disease or weakness. There was no consanguinity in his family. His creatine kinase was found to be raised at 912 U/l . . . [Full text of this article]