1501 carry out the Lichtenstein repair through an incision half the length of the conventional incision is doomed to failure. Effective fixation of the mesh can only be achieved by a wide coverage of the posterior-inguinal-wall/internal oblique/conjoint-tendon with good exposure. Surgeons who add their own "little improvements" or "keystitch" to established operations must publish peer-reviewed data to back their claims before going into print. Finally, the requirement for antibiotic prophylaxis to prevent mesh infection is unnecessary both in our own practice and according to surgeons in the USA with more extensive practice.’,’ A N Kingsnorth Department of Surgery, University of Liverpool, PO Box 147, Liverpool L69 3BX, UK 1 Davies N, Thomas M, McIlroy B, Kingsnorth AN. The Lichtenstein tension free hernia repair: early results from the UK. Br J Surg (in press). 2 Gilbert AI, Feilton OL. Infection in inguinal hernia repair considering biomaterials and antibiotics. Surg Gynecol Obstet 1993; 199: 126-30. Leu106→Val (CTC→GTC) mutation of superoxide dismutase-1 gene in patient with familial amyotrophic lateral sclerosis in Japan SIR—Amyotrophic lateral sclerosis (ALS) is a devastating neurological disease that selectively affects motoneurons. Patients who have a family history are reported to account for 5-10% of ALS cases in whites, which does not grossly differ from the rate in Japan. Deng et all reported point mutations in the gene that encodes superoxide dismutase-1 (SOD-1) in some patients with familial ALS (FALS). They reported that the most common mutation site was Ala4→Val (GCC—>GTC) in exon 1, which was found in eight FALS families. There were 13 other mutation sites in exons 2, 4, and 5, but each mutation site was found in only one or two families. SOD-1 activities associated with these mutations were reduced by about half. In Japan, three FALS families with point mutations of the SOD-1 gene have been reported.2,3 Patients in two FALS families with a novel mutation site His46→Arg (CAT->CGT) showed mild clinical manifestations and about 20% reduced activity of SOD-1. The patients in another family also had a new point mutation Ala4→Thr (GCC->ACC) of the same codon that was previously reported in whites but as a different missense mutation. We have examined the whole sequence of 5 exons of SOD-1 gene in affected patients of five unrelated FALS families with an automated fluorescence DNA sequencer. A mutation Leu106→Val (CTC—>GTC) was found in exon 4 in one family. No mutation was detected in the other families. The patient with this mutation was a 42-year-old woman who 2 years earlier noticed weakness of the right hand and fasciculation of both legs. The following year she also noticed weakness of the left arm and muscular atrophy of both arms. The cranial nerves, coordination, sensation, and autonomic nervous system were spared. Diagnosis of ALS was made by clinical features and electrophysiological studies. 25 years ago, her father died of "muscular atrophy" at the age of 44. Her paternal grandparents had died and no further information could be obtained. She has two normal siblings (brothers) and three daughters (10-17 years old). We have not done gene analysis of her offspring because of ethical dilemmas. The point mutation that we report here has been reported in two white families that were branches of the same origin.1 To our knowledge a Japanese FALS family sharing the same point mutation of SOD-1 gene with white families has not been reported. As for myotonic dystrophy, there is a report suggesting that white and Japanese patients share common ancestral mutation events.4 Thus, we must be cautious of attributing such a coincidence to two independent mutations. Analysis of the haplotype adjacent to the SOD-1 gene and allelic polymorphism of introns of SOD-1 gene between the white and this Japanese family is required to ascertain their relationship. Supported by Grants-in-Aid for Scientific Research on Priority Area (06254207) for General Scientific Research (04404043, 06670652) from the Ministry of Education, Science and Culture, Japan. Jun Kawamata, Hiroshi Hasegawa, Shun Shimohama, Jun Kimura, Seigo Tanaka, Kunihiro Ueda Department of Neurology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan; and Laboratory of Molecular Clinical Chemistry, Institute for Chemical Research, Kyoto University 1 Deng HX, Hentati A, Tainer JA, et al. Amyotrophic lateral sclerosis and structural defects in Cu, Zn superoxide dismutase. Science 1993; 261: 1047-51. 2 Ogasawara M, Matsubara Y, Narisawa K, et al. Mild ALS in Japan associated with novel SOD mutation. Nat Genet 1993; 5: 323-24. 3 Nakano R, Sato S, Inuzuka T, et al. A novel mutation in Cu/Zn superoxide dismutase gene in Japanese familial amyotrophic lateral sclerosis. Biochem Biophys Res Commun (in press). 4 Yamagata H, Miki T, Ogihara T, et al. Expansion of unstable DNA region in Japanese myotonic dystrophy patients. Lancet 1992; 339: 692. Optimum timing for endoscopy in management of dyspepsia SIR—Bytzer and colleagues (April 2, p 811) provide direct evidence that referring dyspeptic patients to endoscopy is beneficial before any drug treatment. They show that the empirical trial of Hz-blocker treatment before allowing endoscopy referral does not improve case selection for endoscopy and is associated with increased costs and reduced patient satisfaction. These data give new information to the physician who is continuously challenged to determine the optimum timing for endoscopy in dyspeptic patients with no obvious signs of organic disease. However, we believe that a more detailed analysis of Bytzer’s results would be beneficial. First, they do not emphasise the importance of patients’ age as a criterion for endoscopic investigation. Since an empirical trial of drug treatment is generally considered useful before endoscopy in patients under 45,2,3 it would have been helpful if they had evaluated endoscopic profile according to age. In our experience the ratio of normal to abnormal endoscopic findings is a function of age. Normal findings progressively declined with age: under 40 years, the most common abnormalities were duodenitis and erosive prepyloric changes, and malignant disease was never seen. Do Bytzer and colleagues’ data lend support to age as a valid criterion for endoscopic examination? Second, we have shown that the clinical classification of dyspepsia can be a valid guideline in the need for endoscopy.’ We found that in dysmotility-like dyspepsia negative findings at endoscopy were seen in as many as 78% of patients under 30 years of age, malignant disease was not seen in patients under 60, and major lesions (ulcer and oesophagitis) were recorded in only 6 of 145 patients. If Bytzer and colleagues had analysed endoscopic findings in relation to the clinical patterns of dyspepsia, they might have provided direct evidence of the relevance of the clinical picture of dyspepsia as a valid guideline for endoscopy. Such analysis might also have confirmed our data indicating that in patients under 60 endoscopy is inappropriate.