Ultrasound measurements of the vocal folds were taken for a number of boys passing through puberty. The boys were grouped according to their pubertal stage as defined by Tanner and there was a gradual increase in the length of the vocal folds as puberty progressed. The fundamental frequency of the boys' speaking voice was recorded via laryngography and a good correlation between the length of the vocal folds and the frequency of the voice was seen. The sudden drop in frequency seen between Tanner stages 3 and 4 did not correlate with similar changes in the length of the vocal folds at this time but stroboscopic findings suggest a change in the structure and mass of the vocal folds at this time of maximum frequency change.

Diaphragm-like strictures of the terminal ileum have been described in association with non-steroidal anti-inflammatory drugs (NSAIDs)'. The first description of a patient with similar strictures in the colon is presented. Case reportA 61-year-old woman presented with a 6-month history of intermittent colic, weight loss, diarrhoea and vomiting related to meals. She had a long history of osteoarthritis of the knees and lumbar spine, and had been treated with slow-release indomethacin for the previous 9 years.On examination the patient was pale; the haemoglobin concentration was 8.5 g/dl and serum albumin level 26 g/l. Gastroscopy revealed both gastric and duodenal ulcers. The indomethacin was stopped and the patient treated with omeprazole and ferrous sulphate. Nevertheless symptoms persisted. A barium enema showed an unusual series of smooth contoured strictures in the proximal ascending colon (Figure 1 ).At laparotomy the terminal ileum was found to be thickened and the ascending colon nodular; the serosa appeared unremarkable. A provisional diagnosis of Crohn's disease was made, and the terminal ileum and ascending colon were resected. Macroscopically the terminal ileum had a uniformly thickened wall and narrowed lumen. There were tight strictures with superficial ulceration both at the ileocaecal valve and in the ascending colon at 10 cm from the valve, with a few thin diaphragms in the caecum (Figure 2). Microscopically the prominent finding at sites of constriction in both the ileum and colon and at the diaphragms in the caecum was thickening of the bowel wall by submucosal fibrosis. The muscularis mucosa and muscularis propria showed focal fibrous replacement; the former had focal muscular hyperplasia. The serosa had mild fibrous thickening. There was some superficial mucosal ulceration with granulation tissue at the sites of constriction. The intact mucosa showed a moderate excess of chronic inflammatory cells with scanty focal lymphoid infiltrates through the bowel wall. No granulomas or definite evidence of Crohn's disease were seen. The lymph nodes showed follicular hyperplasia; the mesenteric vessels were unremarkable.A diagnosis of diaphragm disease caused by NSAIDs was made after considering descriptions of similar lesions in the ileum'. DiscussionIt is well recognized that NSAIDs can injure the stomach and duodenum. As early as 1966, caecal ulceration associated with indomethacin and oxyphenbutazone was reported'. Since then many other lower-tract complications of NSAID use have been described. Although colonic strictures in this setting have been mentioned previously3, we believe this is the first description in a colectomy specimen of diaphragm-like strictures as detailed by Lang a/.' in the terminal ileum. The main histological feature is extensive submucosal fibrosis. The diaphragms, which resemble exaggerations of the plicae circulares, eventually progress to broad-based strictures'. NSAIDs appear to produce intestinal injury by inhibiting cyclo-oxygenase, thereby resulting in diminished levels...

Causes and investigation of increasing dyspnoea in rheumatoid arthritis J C Hacking, C D R Flower Rheumatoid arthritis (RA) is the most common inflammatory arthropathy in the United Kingdom. The exact level of thoracic involvement in this systemic disorder is unknown but postmortem studies show pleural involvement in up to 40% of cases.' While the

Sacral edema is a widely recognized clinical sign. Hitherto there has been no method of radiological confirmation, nor has the anatomy of this sign been well described. In a prospective study of 100 patients referred for abdominopelvic computed tomography (CT), 17 showed radiological evidence of sacral edema. It was demonstrated clinically in 12 of these 17 patients, leaving five patients with apparent CT evidence of sacral edema in whom this was not demonstrated clinically. In two patients with clinical evidence of sacral edema, their tissue planes in this region appeared normal on CT. The edema fluid accumulates in an intermediate plane of fibrous tissue within the subcutaneous fatty layer of the trunk. In those 17 patients with CT evidence of edema, the center of the fluid accumulation was situated over the lumbar rather than the sacral spine, suggesting that the term "sacral" edema is something of a misnomer.

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