Patients with retinitis pigmentosa and neurological abnormalities detected on screening Case Age No (years) Clinical findings Group 1 (with deafness) 26* 65 Deaf, diminished vibration sense in feet, diminished ankle jerks 37 70 Deaf, old right cerebrovasculkr accident 42* 40 Deaf, anosmia, ataxia, diminished tendon jerks 45* 34 Deaf, mild ataxia Group 2 (withozut deafness) 1 60 Vertebrobasilar ischaemia 5* 39 Small pupils, absent ankle jerks 12 65 Myasthenia gravis 16 36 Right hemiparesis (mitral valve prolapse) 21 62 Dementia, epilepsy, spinocerebellar degeneration, red ragged myopathy 30 62 Disc prolapse L4-5, ulnar nerve palsy 40* 31 Ataxia, mild sensory neuropathy 44* 59 Diminished peripheral sensation, diminished ankle jerks 46 11 Laurence-Moon-Biedl syndrome 55 16 Congenital sensory neuropathy *Clinical suspicion of heredopathia atactica polyneuritiformis. deteriorating retinitis pigmentosa, and deafness. She had suffered an acute episode of ataxia after a viral illness. Examination showed pes cavus, anosmia, retinitis pigmentosa, small reacting pupils, nerve deafness, wasting of the small muscles of the hands, diminished tendon reflexes, and reduced sensation in the feet. She was ataxic on heel and toe walking and coordination was poor in all limbs. Nerve conduction studies disclosed a mild sensory and motor polyneuropathy. The plasma phytanic acid concentration (1-1 mmol/l; 34 mg/100 ml) declined to 0-2 mmol/l (7 mg/100 ml) with a low phytanic acid diet.4 Comment I Wilson JK, Hammond JJ, Kirkendall WM. The captopril induced eruption.
SUMMARY Sixteen patients with corrosive acid ingestion were studied. The majority of patients (n= 10) had ingested sulphuric acid, and three other patients had ingested hydrochloric acid. The extent and severity of upper gastrointestinal tract injury was determined by fibreoptic endoscopy and necropsy. All the patients had oesophageal and gastric involvement but the duodenum was spared in the majority. The injury was not considered as mild (grade I) in any of these patients; five patients having moderate (grade II) and 10 patients having severe (grade III) injury. Complications and mortality occurred only in patients with grade III injury. Feeding jejunostomy for nutritional support was used in five patients (all grade III) with good results.
SUMMARY The effects on intraluminal pressure in the oesophagus, the cardiac sphincter, and the gastric fundus of intravenous prostaglandin F2a, E2, and of rectal indomethacin were studied in 41 subjects. Intravenous infusion of prostaglandin F2a (005 to 0-8 ,tg kg-' min-') produced marked, dose-related and sustained elevation of cardiac sphincter pressure without significantly affecting oesophageal peristalsis or gastric fundal motility. Sphincteric relaxation during swallowing was prolonged. Plasma gastrin levels were unchanged. Intravenous infusion of PGE2 (0-08 ,tg kg-' min-') inhibited sphincter contractions to serial bolus intravenous injections of pentagastrin (0.1 or 0-2 ,ug kg-'). Rectal indomethacin (200 mg) resulted in a rise of cardiac sphincter pressure, suggesting that endogenous synthesis of an inhibitory (E-type) prostaglandin was suppressed. The results indicate that prostaglandin E2 may be concerned in the regulation of cardiac sphincter tone in man, whilst prostaglandin F2a may be useful in the treatment of gastrooesophageal reflux.Pressure level in the cardiac sphincter plays a part in the prevention of gastrooesophageal reflux and depends upon the tone of circular oesophageal muscle in that area. The neural and humoral control of sphincteric tone is not completely understood. Human alimentary muscle is highly sensitive to prostaglandins (PGs): in vitro PGE2 produces relaxations and PGF2, contractions of the circular muscle layer (Bennett, Murray, and Wyllie, 1968;Bennett, Eley, and Scholes, 1968;Bennett and Posner, 1971). Prostaglandin E2 occurs naturally in the human gastric mucosa (Bennett, Stamford, and Unger, 1972). We have recorded motor responses of the human gastrooesophageal junction to intravenous PGF2a and PGE2. The effects on cardiac sphincteric pressure of rectally administered indomethacin have also been studied. Methods and SubjectsIntraluminal pressures were measured with a four-'Present address: The Middlesex Hospital, London 2Present address: Mount Sinai Hospital,
An elderly woman with chronic ulcerative colitis who developed proximal muscle weakness, increased serum creatine phosphokinase activity, and histological and electromyographic abnormalities characteristic of polymyositis is described. Treatment with corticosteroids and 5-acetylsalicylic acid was followed by a remission in bowel symptoms, improvement in muscle power, and reversal of electromyographic changes. An autoimmune link between the two disorders seems likely. (Gut 1993; 34: 567-569) Case report A 78 year old woman was admitted to hospital for investigation and management of diarrhoea and muscle weakness. She had been having recurrent episodes of diarrhoea associated with the passage of blood and mucus, low grade fever, and a feeling of exhaustion for the past 15 years. Each episode lasted for 7 to 10 days, followed by a symptom free period of 2-3 months. She had never visited hospital and was treated symptomatically by general practitioners with antidiarrhoeal drugs. During the past 15 days, she had started having arthralgias that affected multiple joints and appreciable proximal muscle weakness of both lower and upper limbs. The patient was prescribed indomethacin (25 mg thrice daily) for arthralgia by her treating physician. She had lost about 4 kg of weight over the previous 2 weeks.Physical examination at the time of hospital admission showed moderate pallor and mild dehydration. The patient's pulse rate was 96 bpm and the volume was slightly decreased. Her blood pressure was 100/60 mm Hg. The small joints of the hands were tender to pressure and movement. Abdominal examination showed mild tenderness in the hypogastrium, and the patient's spleen was palpable 2 cm below the left costal margin and was firm in consistency. Neurological examination showed weakness of the proximal muscles of the lower and upper Laboratory investigations showed a haemoglobin concentration of 78 g/l and a haematocrit of 23%. The patient's total leukocyte count was 8600/mm3 (8-6x 109/l), with neutrophils 85%, lymphocytes 13%, and eosinophils 2%. The erythrocyte sedimentation rate was 67 mm in the first hour (Westergren) and reticulocyte count 5%. A coagulogram was normal. Platelets were 110000/mm3 (110x109/l). Serum Na was 135 mmol/l and K 3-3 mmol/l. Blood urea was 28 mg/dl (9 9 mmol/l) and serum creatinine 1-0 mg/dl (88-4 mmol/l). Serum bilirubin was 0-8 mg/dl (13-6 mmol/l); SGOT was 13 U/1, SGPT was 7 U/l and alkaline phosphatase was 10 KAU. The total serum protein was 74 g/l with an albumin concentration of 36 g/l, globulin 38 g/l, and an albumin/globulin ratio of 0 95. The patient's urine was negative for protein and sugar, and microscopy showed 10-12 pus cells/ high power field. Urine culture showed growth of Pseudomonas aeruginosa. Stools showed the presence of red cells (+++++) but no ova or cysts, and culture grew Candida albicans. Upper gastrointestinal endoscopy showed features of oesophagitis and erosive gastritis. A barium enema showed extensive ulceration in the entire large bowel (Figs 1 and 2) and...
SUMMARY The effect of oral metoclopramide, 10 mg, was studied with intraluminal manometry in 20 patients suffering from symptoms of gastrooesophageal reflux. The drug increased cardiac sphincter pressure and the amplitude of oesophageal peristaltic waves, but gastric motility was stimulated in only half of the patients. The clinical value of these pharmacological effects should be confirmed in therapeutic trials.Metoclopramide (Maxolon, Primperan) is frequently prescribed for heartburn or regurgitation, the symptoms of gastrooesophageal reflux. Although metoclopramide increases cardiac sphincter pressure in normal people when given intravenously (Heitmann and Moller, 1970), it is not known whether it has a similar effect when given to patients by mouth. We have therefore measured the effect of oral metoclopramide on the pressures in the oesophagus, cardiac sphincter, and the stomach in patients with symptoms of reflux. Patients and MethodsTwenty-five patients, all with symptoms of reflux, were studied: brief clinical details are in Intraluminal pressures were measured with an assembly of four polyvinyl tubes (internal diameter 1.2 mm) with side-opening tips 5 cm apart; the tubes were perfused with water at the rate of 7 gl sec-'. Pressures were recorded on a multichannel pen writer. Swallowing was monitored with a pneumograph placed over the larynx. The patients were intubated following an overnight fast. With the patient supine, the tube assembly was positioned so that the two proximal tips were in the oesophagus, the third in the cardiac sphincter, and the fourth in the stomach. The cardiac sphincter was identified as a zone of high pressure which relaxed on swallowing. Pressures were continuously recorded for a basal 30 minutes. The patient then swallowed a tablet of metoclopramide 10 mg (20 patients) or a placebo (lactose 100 mg, five patients) with 100 ml of water.The pressures were then recorded for a further 90 minutes.The pressure tracings were analysed in consecutive 10-min periods. The average cardiac sphincter pressure was calculated in each period as the difference between end expiratory fundal and sphincteric pressures. In each 10-min period the mean amplitude of oesophageal peristaltic contractions and the duration and amplitude of gastric pressure waves were also measured.The action of metoclopramide on the cardiac sphincter was analysed in three different ways, with each patient acting as his own control. First, the mean sphincteric pressures in the group of patients given the placebo or metoclopramide were compared before and after the drug for each 10-min period, and the differences examined with Student's t test.
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