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3. Kambova L. Psychological studies on patients with ESRD by regular dialysis. Ph.D . Thesis, Sofia: 1993: 36-112 4. Temple RM, Sarah J, Langan I, Deary J, Winney RJ. Recombinant erythropoietin improves cognitive function in chronic hemodialysis patients. Nephrol Dial Transplant 1992; 7: 240-245

Parenteral iron, yes but how? Sir, The main consequences of chronic iron overload are hepatic fibrosis, cirrhosis, hepatocellular cancer, cardiac disease, and diabetes. Besides the lesions due to overload, free iron related toxicity is mainly the product of the formation of free oxygen radicals [1]. On the other hand, supplementation with intravenous (i.v.) iron improves the response to treatment with erythropoietin [2]. The most widely used form of parenteral iron is ferric gluconate (Ferrlecit'"), because of good clinical tolerance and scarcity of allergic reactions . Lately, methods have been described for the administration of high doses of iron to haemodialysis patients [3,4]. Zan en et al. [5] have also studied the safest way to administer iron in order not to saturate transferrin over 100%, thus avoiding the risk of iron toxicity. We have analysed transferrin saturation after haemodialysis in nine patients in basal situation and after the administration ofi.v. ferric gluconate through five different methods: (i) 12.5 mg of iron in slow pulse; (ii) 31.25 mg in slow pulse; (iii) 31.25 mg in continuous infusion for 2 h; (iv) 31.25 mg of iron diluted with heparin in continuous infusion for 4 h through the heparin pump; (v) 62.5 mg of iron diluted with heparin infused for 4 h. Thc results obtained with these different protocols are depicted in Figure I. According to our results, to avoid 'oversaturation' and possible adverse effects, we believe that the best method for giving iron to haemodialysis patients is to administer ferric gluconate up to 12.5 mg in slow pulse, or, alternatively, the continuous infusion for 4 h of up to 31.25 mg of iron. B. Bayes J . Bonal J. Junca

Hospital Universitari Germans Trias i Pujol Badalona Spain

1. Britton RS, Tavill AS, Bacon BR. Mechan isms of iron toxicity. In: Brock JH , Halliday JW, Pippard MJ , Powell LW, eds. Iron metabolism in health and disease. W. B. Saunders & Company Ltd , London: 1994: 312-351

2. Fishbane S, Frei GL, Maesaka J . Reduction in recombinant human erythropoietin doses by the use of chronic intravenous iron supplemen tation. Am J Kidney Dis 1995; 26: 41-46 3. Calca r C, Mata D, Alonso C, Ramos B, Lopez de Novales E. J OO

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Intravenous administration of iron gluconate during haemodialysis. Nephrol Dial Transplant 1997; 12: 574-575 4. Granolleras C, Zein A, Oules R, Branger B, Fourcade J, Shaldon S. Continuous administration of intravenous iron during haemodialysis. Nephrol Dial Transplant 1997; 12: 1007-1008 5. Zanen AL , Adriaansen HJ, Van Bommel EFH, Posthuma R, de Jong GMTh. 'Oversaturation' of transferrin after intravenous ferric gluconate (Ferrlecitw) in haemodialysis patients. Nephrol Dial Transplant 1996; II : 820-824

More about watermelon stomach: a case report in a CAPD patient Sir, Gastric antral vascular ectasia is a rarely reported cause of occult upper gastrointestinal blood loss. Jabbari et 01. coined the term 'watermelon stomach' to describe the most common endoscopic presentation of this entity [1]. The difficulty and importance of this condition lies in the problems surrounding its recognition. We present a CAPD patient with watermelon stomach and confirm the therapeutic value of an oestrogenprogesterone treatment. A 72-year-old man on CAPD for I year for end-stage renal failure secondary to renal amyloidosis was admitted to our hospital for severe anaemia, hypotension, and haematemesis. Soon after the onset of dialysis he developed anaemia resistant to the prescription of iron supplements and erythropoietin. He had no previous history of gastrointestinal disease, liver disease, or valvular heart disease, and he had not taken steroid antiinflammatory drugs . On admission the following levels were recorded: haemoglobin 4.8 g/dl, haematocrit 13.5%, 335000/mm 3 platelets, normal coagulation study , TA 100/60 mmHg and cardiac frequency 110 bpm . Haemoccult stools were positive and upper gastrointestinal endoscopy revealed multiple, apparently submucosal, reddish spots that were interpreted as severe antral haemorragic gastritis. Other examinations such as total colonoscopy or medulla osea study failed to demonstrate a bleeding focus. Despite the administration of ranitidin and omeprazol he was admitted on another three occasions for blood transfusion due to major decrease in haematocrit. On each occasion a gastroendoscopy was performed and interpreted as 'severe antritis'. The diagnosis of gastric antral vascular ectasia was only made on the fourth endoscopy, and the lesion was histologically proved by biopsy specimen that showed dilatation of antral mucosal capillaries with fibromuscular hyperplasia of the lamina propia, accompanied by Helicobacter pylori epithelial colonization. There was no evidence of amyloid deposits (Figure 1). Anaemia could not be controlled using iron supplements, erythropoietin, oral antiulcerous drugs, treatment of Helicobacter pylori, and multiple blood transfusions were needed to maintain his haemoglobin concentration. Therefore , he was referred for endoscopic laser photocoagulation of the antral vascular ectasia. After three successive laser sessions his transfusion requirements were unchanged and he still required an average of 2 U of packed red blood cells weekly to maintain an haemoglobin level of 8.5 g/dl, Instead of surgical antrectomy, the patient agreed to a medical trial of ethinyl estradiol 0.05 mg plus norethindrone acetate 1 mg daily. After beginning medical therapy no additional units of packed red blood cells were required and haemoccult stools became negative. The patient died at home 6 weeks after beginning medical therapy. No necropsy was performed, but we suspected myocardial infarction as cause of death.

Nephrol Dial Transplant (1998) 13: 231

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Fig. 1. Gastric antral mucosa with foveolar hyperplasia and dilated capillaries (H & E 10 x).

Upper gastrointestinal (GI) disease occurred with an increased frequency in chronic renal failure, and GI bleeding as a complication is frequently reported. Among the many causes of bleeding, angiodysplastic lesions are encountered frequently in uraemic and haemodialysed patients [2-4] . To the best of our knowledge, this is the first reported case concerning a CAPD patient. Angiodysplasia is a vascular lesion of GI tract affecting mucosal and submucosal veins [3]. The localized form of angiodysplasia confined to the gastric antrum was termed 'watermelon stomach' [I] . Two characteristic patterns of endoscopic presentation have been described in gastric antral vascular ectasia: the presence of tortuous dilated vascular ectasies radiating outward from the pylorus and resembling dark stripes on the surface of a watermelon, and diffuse involvement of the gastric antrum with circumferentially distributed speckled reddish spots that can appear coalescent [5]. By definition, the conclusive diagnosis would require histological confirmation. Jabbari described an hypertrophied antral mucosa, the presence of dilated and thrombosed capillaries with a concomitant fibromuscular hyperplasia in the lamina propia, and thickening of the submucosa with dilated tortuous venous channels and hypertrophied muscularis external muscularis hypertrophied. The cause of gastric antral vascular ectasia is unknown. It was suggested that lesions are a result of a degenerative process associated with ageing and they are frequently associated with aortic estenosis, hereditary haemorragic telangectasias, and chronic renal failure [2,3]. The control of chronic or recurrent bleeding constitutes the major clinical problem in patients affected by this disease. Surgical antrectomy was usually required before the advent of endoscopic haemostatic therapy. However endoscopy therapy is only effective in stopping the acute bleeding episode when the lesions are accessible and localized. A recent controlled clinical trial showed that an oestrogenprogesterone combination was effective in controlling bleeding from angiodysplasias in the upper and lower GI tract [4-6]. Despite the short course of hormonal treatment in our patient, the decreased blood transfusion requirements

after beginning the hormonal therapy seems to confirm the therapeutic value of oestrogen-progesterone combination. Departments of Nephrology and lpathology Xeral-Cies Hospital Vigo Spain

M. Moreiras G. Rguez Goyanes L. Cuifia A. Glez Pineiro! A. J. Perez

I. Jabbari M, Cherry R, Lough JO, Daly DS , Kinnear DG, Goresky CA. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterol 1984; 87: 1165-1170 2. Zuckerman GR, Cornette GL, Clouse RE, Harter HR. Upper gastrointestinal bleeding in patients with chronic renal failure . Ann Intern Med 1985; 102: 588-592 3. Foutch PG . Angiodysplasia of the gastrointestinal tract. Am J Gastroenterol1993; 88: 807-818 4. Hermans C, Goffin E, Horsmans Y, Laterre E, Van Ypersele de Strihou Ch. Watermelon stomach. An unusual cause of recurrent upper GI tract bleeding in the uraemic patient: efficient treatment with oestrogen-progesterone therapy. Nephrol Dial Transplant 1996; II: 871-874 5. Manning RJ . Estrogen-progesterone treatment of diffuse antral vascular ectasia . Am J Gastroenterol1995; 90: 154-156 6. van Cutsem E, Rutgeerts P, Vantrappen G. Treatment of bleeding gastrointestinal vascular malformations with oestrogenprogesterone. Lancet 1990; 335: 953-955

Uraemic pruritus is not related to p-endorphin serum levels in haemodialysis patients Sir, Uremic pruritus (UP) is still one of the most vexing and disabling symptoms in chronic renal failure afflicting up to 85% of patients on dialysis [I] . The pathogenesis of UP is obscure and effective therapeutic strategies are elusive [2]. Recently Peer and co-workers reported on the fl-receptor antagonist Naltrexone as an effective treatment modality in UP in patients on haemodialysis [3]. The way by which Naltrexone works in UP is not clear at the moment. It can be speculated that the fl-receptor antagonist acts either