553
After 2-11 months, the drug was withdrawn for 1-5 weeks, any concomitant systemic or local treatment being kept constant. Before withdrawal of fusidin, the absence of active intraocular inflammation was confirmed by consecutive ocular assessments. A flare-up in ocular inflammation occurred within 4 weeks in all ten patients. This was ascertained by biomicroscopy and
ophthalmoscopy combined with subjective (ten patients) and objective (eight) reduction in visual acuity. Visual acuity was measured by a nurse who had no knowledge of the study’s purpose.
Fusidin, again without change in concomitant therapy, was then reinstituted at the previous dosage. Remission was achieved again in all patients in 1-3 weeks. On morphological criteria ocular inflammation had subsided in all ten patients. In seven visual acuity had improved to the level previously achieved under fusidin therapy whereas in the remaining three, vision was slightly and transiently impaired by intraocular haze. Apart from slight and transient abdominal discomfort, there were no side-effects. These preliminary observations, with the results of in-vitro studies,9 make fusidin an interesting alternative to conventional therapy of uveitis. Uveitis recurred when the drug was stopped and remissions were achieved again when fusidin was restored. We thank Leo Pharmaceutical Products for
Departments of Medicine TTA and
Ophthalmology E, Rigshosprtalet University Hospital, DK-2200 Copenhagen N, Denmark
incubator or cot depending on size and state of maturity.3 Feeding is orally or via a nasogastric tube with expressed breast milk or glucose-electrolyte solution, as dictated by the baby’s weight. Other aspects of care in the unit include prevention and treatment of infection and jaundice and correction of hypoglycaemia and metabolic acidosis. Having come into being at a time when finances in the country have plummeted, the hospital does not possess many of the high technology obstetric gadgets found in university centres. There are no fetal monitoring machines and no cardiotocographs, and fetal blood is not sampled, nor can chorionic villus biopsy be done. Even so, analysis of all deliveries between January, 1987, andDecember, 1989 shows that a fit, literate woman who has simple but professional antenatal care as offered here, has an obstetric outcome comparable with that of a woman who delivers in the most advanced unit in Europe or the USA with all the benefits of modern
technology:
providing fusidin. KLAUS BENDTZEN NIELS VESTI-NIELSEN JØRGEN PETERSEN VAGN ANDERSEN GUNNAR BENDIXEN
1 Bienfang DC, Kelly LD, Nicholson DH, Nussenblatt Ophthalmology N Engl J Med 1990; 323: 956-67.
RB
Despite the limitations of our special-care baby unit, weightspecific mortality patterns for low birthweight babies are reasonably similar to those reported earlier from better-equipped centres:3,4
Medical progress.
2. Nussenblatt RB, Rook AH, Wacker WB, Palestine AG, Scher I, Gery I Treatment of intraocular inflammatory disease with cyclosporin A. Lancet 1983; ii: 235-38. 3 Bendtzen K, Nissen C, Tvede N, Anderson V. Ciclosporin treatment of autoimmune inflammatory disorders of the eye In. Schindler R, ed Ciclosporin in autoimmune diseases Berlin: Springer-Verlag, 1983: 143-46. 4. Masuda K, Nakajima A, Urayama A, Nakae K, Kogure M, Inaba G Double-masked trial of cyclosporin versus colchicine and long-term open study of cyclosporin in Bechet’s disease. Lancet 1989, i: 1093-96 5 Bendtzen K Ciclosporin (cyclosporin A) prototype of a new generation of immunosuppressive drugs Allergy 1984; 39: 565-71. 6. Palestine AG, Austin HA, Balow JE, et al Renal histopathologic alterations in patients treated with cydosporine for uveitis N Engl J Med 1986; 314: 1293-98 7 von Daehne W, Godtfredsen WO, Rasmussen PR. Structure-activity relationships in fusidic acid-type antibiotics. Adv Appl Microbiol 1979; 25: 95-146 8 Garrod LP, Lambert HP, O’Grady F, Waterworth PM Fusidic acid. In. Antibiotic and chemotherapy, 5th edn Edinburgh: Churchill Livingstone, 1981. 220-25. 9 Bendtzen K, Diamant M, Faber V Fusidic acid, an immunosuppressive drug with functions similar to cyclosporin A Cytokine (in press).
Technology-free obstetrics SIR,-One important way by which third world countries acquired their mountains of debt, for which draconian adjustments are now being instituted, was the importation of high-technology equipment. In most instances, scant effort was made to understand the workings of this equipment before it was purchased, let alone to ascertain its relevance to the special problems of the third world. The story happened in medicine and agriculture, aviation and communications, and it was against this backdrop that we took interest in a Lancet letter from the Ignaz Semmelweis Frauenklinik maternity unit,’ where obstetric practice resembles that at the University of Port Harcourt Teaching Hospital (UPTH) obstetrics department. Established in 1980, the department now handles about 2500 deliveries a year. Antenatal surveillance, supported by a fairly well-organised mothercraft class, is very basic, as described in the Zaria studiesManagement in labour is simple too, being conducted essentially through the medium of a 24-hour partogram. There is little interference, assistance usually being limited to artificial rupture of membranes, oxytocin augmentation, and mediolateral episiotomy. Problems associated with cephalopelvic disproportion constitute the commonest indications for caesarean section, while assisted vaginal deliveries are more often carried out for fetal heart rate irregularities. Management in the special-care baby unit is not intensive but consists of keeping the baby warm, in
To improve the dismal obstetric performance of women in most third-world countries what is required is a more serious commitment to improving the lot of the people-their education, health, feeding, and housing. Importation of high-technology equipment should take second price of place. University of Port Harcourt Teaching Hospital, Port Harcourt,
Nigeria
N. D. BRIGGS R. S. ORUAMABO
Technology-free obstetrics at the Semmelweis Clinic. Lancet 1990; 335: 977-78. 2. Harrison KA. Childbearing, health and social priorities: a survey of 22 774 consecutive hospital births in Zaria, Northern Nigeria. Br J Obstet Gynaecol 1985, (suppl 5). 3 Oruamabo RS, Ogunremi OA. Mortality in infants less than 2500 gram birthweight admitted into a special care baby unit in Port Harcourt, Nigeria. East Afr Med J 1. Rockenschaub A
1988; 65: 197-202. AH, Effiong CE. Neonatal mortality: effects of selective pediatric interventions. Pediatrics 1985; 75: 51-57.
4 Dawodu
Interstitial
lymphocytic myocarditis in Whipple’s disease
SIR,-Whipple’s disease is a rare systemic disorder caused by a microbe which still remains undefined. Cardiac involvement with changes specific for the disease (SPC-cells, microbial bodies) is common.1 The microbe is a poor immunogen, however, and an inflammatory response in the affected tissues is lacking. Lymphocytic myocarditis in Whipple’s disease has been reported only once before.2 We have observed another such case. A 53-year-old woman presented with migratory arthralgia in 1982. X-ray of affected joints and tests for rheumatoid factor and HLA-B27 were negative. She responded to non-steroidal antiinflammatory drugs. In 1987 she was seen because of weight loss, fatigue, dyspnoea, and chest pain but clinical and laboratory examinations were inconclusive. In 1989 her condition was complicated by fever, non-productive cough, and diarrhoea. She was dyspnoeic with diffuse grey pigmentation of the skin, tachycardia, crackling on inspiration, and lower limb oedema. The
554
erythrocyte sedimentation rate was raised and she had microcytic anaemia, increased serum alkaline phosphatase, and a positive faecal occult blood test. Osteoporosis of the axial skeleton was present. Ultrasonography demonstrated steatosis of the liver and cholecystolithiasis. Liver biopsy revealed steatosis. Activated megakaryopoiesis was seen on bone marrow biopsy. Other investigations were non-contributory, except that lung function tests suggested fibrosis. She refused jejunal biopsy and bronchoscopy. At the end of 1989 frequent vomiting developed with hypoproteinaemia, hypoalbuminaemia, and a low serum carotene. Electrocardiography revealed non-specific ST-T changes. Endoscopy revealed erythematous lesions in the descending duodenum. Biopsy demonstrated infiltration with foamy periodicacid/Schiff (PAS) positive macrophages and Whipple’s disease was suspected. The patient died suddenly in an attack of arrhythmia. Necropsy revealed infiltration of the gut mucosa, mesenteric lymph nodes, and myocardium with PAS-positive macrophages. On electronmicroscopy there were typical microbial bodies in the endothelium of myocardial capillaries. An unexpected observation was dense infiltration of the myocardial interstitium with lymphocytes mixed with some eosinophils. This finding was compatible with the histological diagnosis of interstitial lymphocytic myocarditis. Department of Medicine, University Clinics, Institute of Pathology I, Charles University, Prague 2, Czechoslovakia
TOMÀŠ PELECH PŘEMYSL FRIC ALENA HUSLAROVÁ ADAM JIRÁSEK
1. McAllister HA Jr, Fenoglio JJ Jr. Cardiac involvement in Whipple’s disease. Circulation 1975; 52: 152-56. 2. Southern JF, Moscicki RA, Margo C, Dickersin GR, Fallot JT, Bloch KJ. Lymphedema, lymphocytic myocardins, and sarcoid-like granulomatosis: manifestation of Whipple’s disease. JAMA 1989; 261: 1467-70.
Aluminosilicate in
synovial fluid
of
a
dialysed patient.
(A) Scanning electron micrograph of aluminosilicate, (6) and (C) X-ray respectively
maps of aluminium and silicon,
Interaction between
pethidine and selegiline
SIR,-Dr Zornberg and colleagues’ (Jan 26, p 246) report a serious drug interaction between pethidine (meperidine) and selegiline, a selective inhibitor of monoamine oxidase (MAO) type B. They state that the "Physician’s Desk Reference reports no known drug interactions" with selegiline. The PDR, which adds that clinical experience with the drug is limited, refers the reader to its warning section. There, it is pointed that fatal reactions have occurred when MAO inhibitors have been given in combination with pethidine. It is then quite clearly stated "because the mechanism of interaction between MAOIs and meperidine (pethidine) is unknown, it seems prudent, in general, to avoid this combination". I believe it is wise to read all pertinent drug information presented in a reference book before prescribing the drug.
(two) origin. They had normal renal function and had not received compounds in the preceding months. Synovial fluid was drawn into polypropylene syringes to avoid contamination with silicon. Synovial concentrations of aluminium and silicon, measured by argon plasma emission spectrometry (’Spectrospan V’, Beckman), were significantly higher in the haemodialysis patients: aluminium
out
Drug Topics Magazme, Oradeli, NJ 07649. USA
CYNTHIA STARR
The synovial fluid of six haemodialysis patients and ten controls filtered (Millipore, 0-45 and 5 )-uft). The filter was made conductive by a carbon film laid under a vacuum. It was then studied in a scanning electron microscope (Cambridge S250) with an energy dispersive X-ray microanalysis system (PGT III was
detector).
Amorphous aluminosilicates in synovial fluid in
dialysis-associated arthropathy
SIR,-Aluminium accumulates in the synovial tissue and articular cartilage of long-term haemodialysis patients, especially when there are &bgr;2-microglobulin amyloid deposits.’ This metal is toxic to bone and nervous tissue, and promotes inflammation in rats and rabbits.2 However, its role in the physiopathology of dialysisassociated arthropathy (DAA) is poorly understood. Silicon, which sometimes binds to aluminium, accumulates in the serum of haemodialysis patients.3 We have measured aluminium and silicon concentrations in the synovial fluid of long-term haemodialysis patients with joint complications. The six patients (four men, two women) had been on haemodialysis for 1 5-16 years (mean 10 25 years) and had joint effusions of the knee (five patients) or shoulder (one). Five had DAA, in three cases associated with histologically proven &bgr;2-microglobulin amyloidosis. The controls were fifteen patients with knee effusions of either inflammatory (thirteen) or mechanical
Aluminosilicates were observed on the filters with the synovial fluids of three haemodialysis patients, in one case accompanied by calcium phosphate crystals. The aluminosilicates looked like tiny plates up to 70 pm across (figure). The largest plates, which seemed crystalline, were collected with tweezers and studied with X-ray by the oscillating-crystal method. They turned out to be amorphous In some controls we saw sodium urate crystals or calcium
phosphate, in keeping with the joint disorders of these patients (eg, gout or articular chondrocalcinosis). An aluminosilicate compound was seen in one control, suggesting either contamination despite our precautions or aluminium silicates in a small number of nondialysed patients. The first explanation is the more likely-indeed, two aluminosilicate compounds were also found when distilled water was processed under the same conditions. The X-ray maps of the aluminosilicate compounds from the synovial fluids of the haemodialysis patients showed an apparently homogeneous distribution of silicon and aluminium in the preciptated compounds (figure). This may indicate a true aluminosilicate, though even at the pH of synovial fluid one cannot