679 FREQUENCY
OF ANTI-Y.E.
ANTIBODIES
SEROTYPES
3
AND
9
IN
PATIENTS WITH THYROID DISEASES AND IN CONTROLS
90
plasma-exchange all).
sessions each
lasting about
3 h
(270
h in
Our data suggest, however, that if plasmapheresis were restricted to patients with biopsy evidence of some relatively normal glomeruli, the demands on the unit would be much reduced and the success-rate would be significantly higher. If our conclusion that plasmapheresis is worthless in cases where all the glomeruli are badly affected is confirmed by other workers this would have implications for the provision of plasmapheresis on renal units for routine as opposed to research purposes.
had agglutinin titres to brucella, and none of these patients had any symptoms compatible with yersiniosis. The presence of anti-Y.E. antibodies in different thyroid diseases and the improbability of a single xtiology, suggest that the association reported by others is only an incidental finding. Division
If our experience is typical, a regional unit serving a population of 2 million would expect to use plasmapheresis only about five times per year, which is not adequate to maintain the high level of clinical experience in what is a potentially hazardous procedure. It would, therefore, seem preferable that each region should have a central plasmapheresis unit to deal with renal problems, myasthenia gravis, disseminated lupus, and the various hsematological conditions which can be helped
by plasma exchange. D. HARMER R. FINN
of Endocrinology
Department of Medicine, and Division of Microbiology, Ciudad Sanitaria de la Seguridad Social,
Hospitalet de Llobregat, Barcelona, Spain
T. M. GÓMEZ SÁEZ J. SOLER RAMÓN
A. CASANOVA
PLASMAPHERESIS IN FULMINATING CRESCENTIC NEPHRITIS
SiR,-Plasmapheresis has proved very effective in the treatof Goodpasture’s syndrome’ and myasthenia gravis2-4 and it may also be valuable in fulminating glomerulonephritis
epithelial crescents. of ten cases recovered (plasma-creatinine 100-300 1.13-3-39 mg/dl). We retrospectively reviewed the biopsy material to see whether there were any features which correlated with a successful outcome. The main finding was that the four patients who recovered all showed some normal or near normal glomeruli, in addition to the severely damaged glomeruli. Relatively normjl glomeruli were not seen in the six cases who did not respond. There was no control series and we cannot be certain that Four
out
PLEXUS DAMAGE
SIR,-Chronic idiopathic intestinal pseudo-obstruction (c.i.i.p.) is a rare syndrome with an obscure pathogenesis.’ At surgery, there is no identifiable organic lesion obstructing the bowel lumen, and conventional histological examination of resected specimens is unhelpful. However, detailed study of myenteric plexus with silver preparations has revealed significant damage to the neurones in the five published case-reports in which this specialised neuropathological technique has been done.2-s We have demonstrated damage to the myenteric plexus in a resected specimen of small bowel from an 18-month-old child with the C.I.I.p. syndrome.
mol/1,
these were not spontaneous recoveries; we have seen a patient with extensive crescent formation who recovered without any treatment. However, a 40% recovery-rate in patients presenting in acute renal failure with extensive epithelial crescents is quite contrary to our previous experience, particularly since several of these patients had a marked diuresis within a few days of starting plasmapheresis. Our findings, therefore, support those of Lockwood et al. who concluded that plasmapheresis is valuable in this condition. Plasmapheresis, however, is costly and time-consuming. We normally treat our patients with nine 3 litre exchanges within 20 days, so the treatment of these patients over a year required 1. Lockwood, C. M., Rees, A. J., Pearson, T. A., Evans, D. J., Peters, D. K., Wilson, C. B. Lancet, 1976, i, 711. 2. Pinching, A. J., Peters, D. K., Davis, J. N ibid. 1976, ii, 1373. 3. Finn, R., Coates, P. M. ibid. i, 190 4. Dan, P. C., Lindsboun, J. M., Cassel, C. K., Denys, E. H., Shev, E. E., Spitler, L. E. NewEngl. J. Med. 1977, 297, 1134. 5 Lockwood, C. M., Pinching, A. J., Sweny, P., Rees, A. J., Pussell, B., Uff, J.,Peters, D. K. Lancet, 1977, i, 63.
A. W. FORBES
CHRONIC IDIOPATHIC INTESTINAL PSEUDO-OBSTRUCTION WITH MYENTERIC
ment
with crescent formation in the absence of anti-basement membrane antibody.5 We wish to report our experience over a period of one year of treating ten such cases with plasmapheresis combined with prednisolone, azathioprine, and cyclophosphamide. Every patient presented with acute renal failure requiring urgent dialysis, but with no evidence of previous renal disorder, and biopsy revealed severe proliferative changes with marked
H. J. GOLDSMITH J. M. BONE
Renal Unit, Sefton General Hospital, Liverpool L15 2HE
A male child
was
admitted
at
the age of 2 months for vomit-
ing and chronic diarrhoea with steatorrhoea and poor weight gain. A barium meal demonstrated spontaneous gastro-cesophageal reflux with abnormal gastric folds in the cardia and distended coils of proximal small bowel. Jejunal biopsy was normal. Pancreatic insufficiency was excluded by pancreaticfunction studies, and sweat tests were normal. There was no evidence of anaemia or thrombocytopenia. Despite medical treatment, vomiting persisted with no significant weight gain, but steatorrhoea ceased. The child was readmitted at 16 months. A further barium meal showed distension of the proximal jejunal coils followed by an obstruction which severely reduced the barium flow. At operation, a narrowed segment of small bowel 7 cm long was found at 20 cm from the duodenojejunal junction and resected with an end-toend anastomosis. Postoperative recovery was uneventful. Since his operation, the child has gained weight and he is clinically well. Macroscopically, the mucosa appeared normal with no evidence of ulceration or obstruction and the muscle coat was not 1. 2.
Faulk, D. L., Anuras, S., Christensen, J. Gastroenterology, 1978, 74, 922. Dyer, N. H., Dawson, A. M., Smith, B F., Todd, I. P. Br. med. J. 1969, i, 686. 3. Coste, T., Bernardes, P., Molas, P. Nouv. Presse méd. 1972, 1, 447. 4. Phat, V. N., Chousterman, M., Bloch, F., Petite, J. P., Camilleri, J. P. Ann. Anat. Path. 1978, 23, 131. 5. Schuffler, M. D., Bird, T. D., Sumi, S. M., Cook, A. Gastroenterology, 1978, 75, 889.