1177
Effect of vegetarian diet
systemic lupus erythematosus on
SIR,-Kjeldsen-Kragh and colleagues’ have reported that subtotal fasting for 7-10 days plus a subsequent one-year vegetarian diet seems to be a useful supplement to conventional treatment of rheumatoid arthritis. In rheumatoid arthritis, similar benefits of fasting2 or "diet therapy"3 have been reported by others but we know of no reports of diet therapy in systemic lupus erythematosus (SLE). We describe here a patient with SLE whose urinary excretion of protein and antinuclear and anti-DNA antibody decreased after steroids were tapered off and a vegetarian diet was adopted. A 16-year-old girl presented with fever, arthralgia, facial erythema, and stomatitis, and was admitted to hospital in June, 1980. She had proteinuria (0-6-2-5 g in 24 h), a raised erythrocyte sedimentation rate (47 mm/h), anaemia, thrombocytopenia; a fluorescent antinuclear antibody test was positive (titre 320, shaggy and homogeneous pattern), as was her DNA antibody titre (150 U/rnl); and she was LE cell positive and had hypocomplementaemia. Needle biopsy revealed membranous proliferative glomerulonephritis and deposition of IgG, IgA, IgM, and C3 in glomeruli. These findings suggested SLE, and prednisolone 60 mg daily was initiated. However, the proteinuria worsened and complement values did not improve. Plasmapheresis and pulsed steroid therapy were tried later in 1980 but urinary protein excretion continued. Azathioprine was tried from January to June, 1981, with daily prednisolone. Her 24 h urinary protein fell below 1gand she was discharged in August, 1981. From the end of 1983 (20 mg prednisolone daily), urinary protein increased with frequent episodes of hypoalbuminaemia and oedema. still 1985-when she had In late proteinuria, hypocomplementaemia, and positive antinuclear and anti-DNA titres-she tapered off the steroids and started a vegetarian diet. This
was
done
on
the instructions of her parents and without
our
permission. The diet was: Nutruitional analysis* Before After
Nutritional analysis*
/nfae Daily intake Da/7/
*Before and after vegetarian diet.
After she started this vegetarian diet antibody titres fell to normal, urinary excretion of protein decreased, and serum albumin rose:
Daily predESR
Antibody titres Date
FANA Anti-DNA
*DNA test (U/ml), other figures tlnitiation of vegetanan diet.
Protein and calorie intake
Serum Urinary albumin protein
nisolone
(mm/h) (g/dl) (mg/dl) (mg)
are tltres
was
(RIA)
much reduced
by the diet, with
little reduction in fat. It has been suggested that food allergy or intolerance is involved in the pathogenesis of rheumatoid arthritis4 and beneficial effects of diet therapy have been reported. 1-3 However, food allergy was not evident in this patient’s history. Interest has also focused on dietary fatty acids and the inflammatory
process.sA change to a vegetarian diet might alter the fatty acid profile of phospholipids.6 On the other hand, malnutrition can suppress
immunity,7 and energy intake in patients with
SLE who
need steroid therapy has been reported to be higher than that in patients who are not steroid dependent. Furthermore, Nishimura et al8 have reported that foods containing reduced amounts of phenylalanine and tyrosine improve clinical and laboratory findings in discoid lupus erythematosus, rheumatoid arthritis, and progressive systemic sclerosis. A diet low in energy (especially animal fat and protein) may exert beneficial effects on disease activity in patients with SLE. First Department of Internal Medicine, Tottori University, School of Medicine,
Yonago 683, Japan
CHIAKI SHIGEMASA TAKASHI TANAKA HIROTO MASHIBA
Kjkeldsen-Kragh J, Haugen M, Brochgrevink CF, et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet 1991; 338: 899-904. 2. Uden A, Trang L, Venizelos N, Palmblod J, Harms-Ringdahl M. Neutrophil function and clinical performance after total fasting in patients with rheumatoid arthritis. 1.
Ann Rheum Dis 1983; 42: 45-51. 3. Panush RS, Carter RL, Katz P, Kowsan B, Longley S, Finnie S. Diet therapy for rheumatoid arthritis. Arthritis Rheum 1983; 26: 462-71. 4. Panush RS. Food induced ("allergic") arthritis: clinical and serologic studies. J Rheumatol 1990; 17: 291-94. 5. Kremer JM, Lawrence DA, Jubiz N, et al. Dietary fish oil and olive oil supplementation in patients with rheumatoid arthritis. clinical and immunological effects. Arthritis Rheum 1990; 33: 810-20. 6. Phinney SO, Odin RS, Johnson SB, Holman RT. Reduced arachidonate in serum phospholipids and cholesterol esters associated with vegetarian diets in humans. Am J Clin Nutr 1990; 51: 585-95. 7. Good RA. Nutrition and immunity. J Clin Immunol 1981; 1: 3-11. 8. Nishimura N, Okamoto H, Yasui M, Maeda K, Ogura K. Intermediary metabolism of phenylalanine and tyrosine in diffuse collagen disease. AMA Archs Dermatol 1959; 80: 466-77.
Dermatan
sulphate in acute leukaemia
SIR,-Consumption coagulopathy in acute leukaemia is due mainly to the release of procoagulant activity from blast cells and intravascular production of thrombin.1 Heparin, which rapidly inhibits thrombin formation, has been widely used to control this coagulopathy, but not universally because of the risk of excessive bleeding.2,3 Dermatan sulphate enhances thrombin inhibition by heparin cofactor II with far less activated partial thromboplastin time (aPTT) prolongation than heparin, and without appreciable interference with platelet function.4 It has been shown to be an effective antithrombotic agent in experimental thrombosis, with a better haemorrhagic to antithrombotic ratio than heparin.S Professor Lane and colleagues (Feb 8, p 334) report it to be effective as an anticoagulant in patients on maintenance haemodialysis, and it has also proved useful in the prevention of deep-vein thrombosis in hip fracture 6 We have evaluated the efficacy and safety of dermatan sulphate compared with heparin in quenching the intravascular thrombin generation triggered by blast cells in acute leukaemia. Dermatan sulphate (MF 701, Mediolanum Farmaceutica, Milan: 0-3 mg/kg per h) or heparin (8-5 U/kg per h) was randomly administered by continuous intravenous infusion to ten patients under 70 years of age with acute leukaemia (treated with intensive antiblastic chemotherapy) and consumption coagulopathy was diagnosed by two or all three of the following: prothrombin activity < 70%, fibrinogen < 150 mg/dl, cross-linked fibrin degradation products (XDP) > 500 ng/ml. It was calculated that these anticoagulant doses would be safe and result in a moderate prolongation of standard coagulation indices. Supportive treatment with packed red cells, platelet concentrates, fresh frozen plasma, and fibrinogen cryoprecipitate was given if needed. The two treatment groups were similar with respect to major baseline characteristics. All had presented with minor haemorrhagic diatheses (petechiae, ecchymoses, gingival bleeding). The mean duration of treatment was 11 days (range 4-15) in the heparin group and 13 days (7-18 days) in the dermatan group. Laboratory tests were daily (aPTT, thrombin time [TT], fibrinogen [Clauss]) or thrice weekly (thrombin-antithrombin complexes [ATM] by Boehringer Mannheim Asserachrom; D-dimer by kit Ortho Diagnostic Systems Immertest) for about 20 days from the start of antiblastic chemotherapy.
1178
HEPARIN
DERMATAN SULPHATE
Fibrinogen, ATM, and D-dimer values during treatment with heparin Dotted
areas
indicate normal range, 0 basal values, and 1 day of
Fibrinogen, ATM, and D-dimer values are shown in the figure. Mean TT values fluctuated between 18-8and 27 8sin the dermatan group and between 47.6and 66 4 in the heparin group (normal range 17-26 s), and aPTT fluctuated between 262and 31 ’8 s and between 32-5 and 62-4 s, respectively (normal range 24-34 s) during anticoagulant treatment. Blood product support was higher in the heparin than in the dermatan group. The sole serious cutaneous bleeding complication during chemotherapy occurred in the heparin group. In line with Lane and colleagues’ findings, this pilot study confirms that it is possible to control intravascular thrombin production through the heparin cofactor II pathway of thrombin inhibition rather than through action on antithrombin III. The availability of glycosaminoglycans with reduced charge density, reduced effect upon TT and aPTT, and without interference with platelet function may represent a safer alternative to heparin in the management of consumption coagulopathy in acute leukaemia. Department of Infectious Diseases and Immunopathology, Institute of Internal Medicine, University of Milan, 20122 Milan, Italy
ELISABETTA COFRANCESCO CARLA BOSCHETTI PATRIZIA LEONARDI MICHELE CORTELLARO
KA, Rosenberg RD. Thrombin generation m acute promyelocytic leukemia. Blood 1984; 64: 791-96. 2. Cunningham I, Gee TS, Reich LM, Kempin SJ, Naval AN, Clarkson BD. Acute promyelocytic leukemia: treatment results during a decade at Memorial Hospital. Blood 1989; 73: 1116-22. 3. Rodeghiero F, Avvisati G, Castaman G, Barbui T, Mandelli F. Early deaths and anti-hemorrhagic treatments in acute promyelocytic leukemia: a GIMEMA retrospective study in 268 consecutive patients. Blood 1990; 75: 2112-17. 4. Cofrancesco E, Colombi M, Gianese F, Cortellaro M. The effect of dermatan sulfate on in vitro human plasma coagulation platelet aggregation and &bgr;TG and PF4 release. Thromb Res 1990; 57: 405-14. 5. Femandez FA, Van Ryn J, Ofosu FA, Hirsh J, Buchanan MR. The haemorrhagic and antithrombotic effects of dermatan sulphate. BrJ Haematol 1986; 64: 309-17. 6. Agnelli G, Cosmi B, Di Filippo P, et al. A randomized, double blind, placebocontrolled trial of dermatan sulfate for prevention of deep vein thrombosis in hip fracture. Thromb Haemost 1992; 67: 203-08. 1. Bauer
River blindness SIR,- Your note about river blindness (Mar 28, p 803) provides excellent summary of the outstanding achievements of the Onchocerciasis Control Programme in West Africa (OCP). Unfortunately, the title you have chosen is distinctly misleading. The OCP is starting its final attack on river blindness in most parts of the 11West African countries covered by its remit. Nevertheless, there are still more than 16 million persons infected with Onchocerca volvulus in the remaining 23 endemic countries an
or
dermatan
starting antiblastic
sulphate.
chemotherapy.
outside the OCP area, most ot which are m Atnca. At least /3U UUU of these dwellers in remote rural areas are blind as a result; and a
similar number have severe visual impairment. For them, the attack on river blindness has scarcely begun. Their only hope lies in regular annual dosing with ivermectin. The World Health Organisation, several non-governmental organisations (especially the recently-founded River Blindness Foundation), UN agencies, USAID, and the Mectizan (ivermectin) Expert Committee are now just beginning to assist the Ministries of Health in other affected countries that are untouched by OCP. The task of delivering ivermectin in a cost-effective manner is even greater than that which faced the OCP at its outset; and the struggle will take just as long. Success may well depend on the world bank and OCP donors being prepared to help fmance the scheme. The OCP’s final attack may signal the end of one campaign, but it is far from being the end of the war against river blindness. River Blindness Foundation, 1 Sugar Creek Place, Sugar Land, Texas 77478, USA
W. R. BALDWIN B.O.L. DUKE
Inadequate information on needlestick accidents SIR,- The article by Klein and colleagues1 reinforces the need for health-care workers to regard patients as potentially infected with a communicable blood-borne agent. The agents potentially transmissible by accidental needlestick inoculation and for which routine screening assays are available include hepatitis B virus (HBV), hepatitis C virus (HCV), human T-cell leukaemia virus (types I and II), and human immunodeficiency virus types 1 and 2. While analysing the risk of infection in two London hospitals to health-care personnel who had been exposed parenterally to blood via accidental inoculation, we reviewed data and serum samples received from donors in needlestick accidents from mid-1986 to the end of 1990. For 1990 we analysed the type of accident and looked at how often paired sera (donor and recipient) were available, at what proportion of accidents were reported to our division of virology, and at identification of donor and/or recipient. Sera were randomised and tested for antibodies to HIV-1, HTLV-I, and HCV.1All had previously been tested for HBV infection (HBsAg ELISA). Between mid-1986 and the end of 1990, sera from 528 donors in needlestick accidents (parenteral exposure to blood) were identified. 135 related to accidents in 1990. On 85 (63%) of donor request forms it was possible to identify the recipient. During the same year the division received 211 sera from the injured recipients; 84 (40%)
Effect of vegetarian diet
systemic lupus erythematosus on
SIR,-Kjeldsen-Kragh and colleagues’ have reported that subtotal fasting for 7-10 days plus a subsequent one-year vegetarian diet seems to be a useful supplement to conventional treatment of rheumatoid arthritis. In rheumatoid arthritis, similar benefits of fasting2 or "diet therapy"3 have been reported by others but we know of no reports of diet therapy in systemic lupus erythematosus (SLE). We describe here a patient with SLE whose urinary excretion of protein and antinuclear and anti-DNA antibody decreased after steroids were tapered off and a vegetarian diet was adopted. A 16-year-old girl presented with fever, arthralgia, facial erythema, and stomatitis, and was admitted to hospital in June, 1980. She had proteinuria (0-6-2-5 g in 24 h), a raised erythrocyte sedimentation rate (47 mm/h), anaemia, thrombocytopenia; a fluorescent antinuclear antibody test was positive (titre 320, shaggy and homogeneous pattern), as was her DNA antibody titre (150 U/rnl); and she was LE cell positive and had hypocomplementaemia. Needle biopsy revealed membranous proliferative glomerulonephritis and deposition of IgG, IgA, IgM, and C3 in glomeruli. These findings suggested SLE, and prednisolone 60 mg daily was initiated. However, the proteinuria worsened and complement values did not improve. Plasmapheresis and pulsed steroid therapy were tried later in 1980 but urinary protein excretion continued. Azathioprine was tried from January to June, 1981, with daily prednisolone. Her 24 h urinary protein fell below 1gand she was discharged in August, 1981. From the end of 1983 (20 mg prednisolone daily), urinary protein increased with frequent episodes of hypoalbuminaemia and oedema. still 1985-when she had In late proteinuria, hypocomplementaemia, and positive antinuclear and anti-DNA titres-she tapered off the steroids and started a vegetarian diet. This
was
done
on
the instructions of her parents and without
our
permission. The diet was: Nutruitional analysis* Before After
Nutritional analysis*
/nfae Daily intake Da/7/
*Before and after vegetarian diet.
After she started this vegetarian diet antibody titres fell to normal, urinary excretion of protein decreased, and serum albumin rose:
Daily predESR
Antibody titres Date
FANA Anti-DNA
*DNA test (U/ml), other figures tlnitiation of vegetanan diet.
Protein and calorie intake
Serum Urinary albumin protein
nisolone
(mm/h) (g/dl) (mg/dl) (mg)
are tltres
was
(RIA)
much reduced
by the diet, with
little reduction in fat. It has been suggested that food allergy or intolerance is involved in the pathogenesis of rheumatoid arthritis4 and beneficial effects of diet therapy have been reported. 1-3 However, food allergy was not evident in this patient’s history. Interest has also focused on dietary fatty acids and the inflammatory
process.sA change to a vegetarian diet might alter the fatty acid profile of phospholipids.6 On the other hand, malnutrition can suppress
immunity,7 and energy intake in patients with
SLE who
need steroid therapy has been reported to be higher than that in patients who are not steroid dependent. Furthermore, Nishimura et al8 have reported that foods containing reduced amounts of phenylalanine and tyrosine improve clinical and laboratory findings in discoid lupus erythematosus, rheumatoid arthritis, and progressive systemic sclerosis. A diet low in energy (especially animal fat and protein) may exert beneficial effects on disease activity in patients with SLE. First Department of Internal Medicine, Tottori University, School of Medicine,
Yonago 683, Japan
CHIAKI SHIGEMASA TAKASHI TANAKA HIROTO MASHIBA
Kjkeldsen-Kragh J, Haugen M, Brochgrevink CF, et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet 1991; 338: 899-904. 2. Uden A, Trang L, Venizelos N, Palmblod J, Harms-Ringdahl M. Neutrophil function and clinical performance after total fasting in patients with rheumatoid arthritis. 1.
Ann Rheum Dis 1983; 42: 45-51. 3. Panush RS, Carter RL, Katz P, Kowsan B, Longley S, Finnie S. Diet therapy for rheumatoid arthritis. Arthritis Rheum 1983; 26: 462-71. 4. Panush RS. Food induced ("allergic") arthritis: clinical and serologic studies. J Rheumatol 1990; 17: 291-94. 5. Kremer JM, Lawrence DA, Jubiz N, et al. Dietary fish oil and olive oil supplementation in patients with rheumatoid arthritis. clinical and immunological effects. Arthritis Rheum 1990; 33: 810-20. 6. Phinney SO, Odin RS, Johnson SB, Holman RT. Reduced arachidonate in serum phospholipids and cholesterol esters associated with vegetarian diets in humans. Am J Clin Nutr 1990; 51: 585-95. 7. Good RA. Nutrition and immunity. J Clin Immunol 1981; 1: 3-11. 8. Nishimura N, Okamoto H, Yasui M, Maeda K, Ogura K. Intermediary metabolism of phenylalanine and tyrosine in diffuse collagen disease. AMA Archs Dermatol 1959; 80: 466-77.
Dermatan
sulphate in acute leukaemia
SIR,-Consumption coagulopathy in acute leukaemia is due mainly to the release of procoagulant activity from blast cells and intravascular production of thrombin.1 Heparin, which rapidly inhibits thrombin formation, has been widely used to control this coagulopathy, but not universally because of the risk of excessive bleeding.2,3 Dermatan sulphate enhances thrombin inhibition by heparin cofactor II with far less activated partial thromboplastin time (aPTT) prolongation than heparin, and without appreciable interference with platelet function.4 It has been shown to be an effective antithrombotic agent in experimental thrombosis, with a better haemorrhagic to antithrombotic ratio than heparin.S Professor Lane and colleagues (Feb 8, p 334) report it to be effective as an anticoagulant in patients on maintenance haemodialysis, and it has also proved useful in the prevention of deep-vein thrombosis in hip fracture 6 We have evaluated the efficacy and safety of dermatan sulphate compared with heparin in quenching the intravascular thrombin generation triggered by blast cells in acute leukaemia. Dermatan sulphate (MF 701, Mediolanum Farmaceutica, Milan: 0-3 mg/kg per h) or heparin (8-5 U/kg per h) was randomly administered by continuous intravenous infusion to ten patients under 70 years of age with acute leukaemia (treated with intensive antiblastic chemotherapy) and consumption coagulopathy was diagnosed by two or all three of the following: prothrombin activity < 70%, fibrinogen < 150 mg/dl, cross-linked fibrin degradation products (XDP) > 500 ng/ml. It was calculated that these anticoagulant doses would be safe and result in a moderate prolongation of standard coagulation indices. Supportive treatment with packed red cells, platelet concentrates, fresh frozen plasma, and fibrinogen cryoprecipitate was given if needed. The two treatment groups were similar with respect to major baseline characteristics. All had presented with minor haemorrhagic diatheses (petechiae, ecchymoses, gingival bleeding). The mean duration of treatment was 11 days (range 4-15) in the heparin group and 13 days (7-18 days) in the dermatan group. Laboratory tests were daily (aPTT, thrombin time [TT], fibrinogen [Clauss]) or thrice weekly (thrombin-antithrombin complexes [ATM] by Boehringer Mannheim Asserachrom; D-dimer by kit Ortho Diagnostic Systems Immertest) for about 20 days from the start of antiblastic chemotherapy.
1178
HEPARIN
DERMATAN SULPHATE
Fibrinogen, ATM, and D-dimer values during treatment with heparin Dotted
areas
indicate normal range, 0 basal values, and 1 day of
Fibrinogen, ATM, and D-dimer values are shown in the figure. Mean TT values fluctuated between 18-8and 27 8sin the dermatan group and between 47.6and 66 4 in the heparin group (normal range 17-26 s), and aPTT fluctuated between 262and 31 ’8 s and between 32-5 and 62-4 s, respectively (normal range 24-34 s) during anticoagulant treatment. Blood product support was higher in the heparin than in the dermatan group. The sole serious cutaneous bleeding complication during chemotherapy occurred in the heparin group. In line with Lane and colleagues’ findings, this pilot study confirms that it is possible to control intravascular thrombin production through the heparin cofactor II pathway of thrombin inhibition rather than through action on antithrombin III. The availability of glycosaminoglycans with reduced charge density, reduced effect upon TT and aPTT, and without interference with platelet function may represent a safer alternative to heparin in the management of consumption coagulopathy in acute leukaemia. Department of Infectious Diseases and Immunopathology, Institute of Internal Medicine, University of Milan, 20122 Milan, Italy
ELISABETTA COFRANCESCO CARLA BOSCHETTI PATRIZIA LEONARDI MICHELE CORTELLARO
KA, Rosenberg RD. Thrombin generation m acute promyelocytic leukemia. Blood 1984; 64: 791-96. 2. Cunningham I, Gee TS, Reich LM, Kempin SJ, Naval AN, Clarkson BD. Acute promyelocytic leukemia: treatment results during a decade at Memorial Hospital. Blood 1989; 73: 1116-22. 3. Rodeghiero F, Avvisati G, Castaman G, Barbui T, Mandelli F. Early deaths and anti-hemorrhagic treatments in acute promyelocytic leukemia: a GIMEMA retrospective study in 268 consecutive patients. Blood 1990; 75: 2112-17. 4. Cofrancesco E, Colombi M, Gianese F, Cortellaro M. The effect of dermatan sulfate on in vitro human plasma coagulation platelet aggregation and &bgr;TG and PF4 release. Thromb Res 1990; 57: 405-14. 5. Femandez FA, Van Ryn J, Ofosu FA, Hirsh J, Buchanan MR. The haemorrhagic and antithrombotic effects of dermatan sulphate. BrJ Haematol 1986; 64: 309-17. 6. Agnelli G, Cosmi B, Di Filippo P, et al. A randomized, double blind, placebocontrolled trial of dermatan sulfate for prevention of deep vein thrombosis in hip fracture. Thromb Haemost 1992; 67: 203-08. 1. Bauer
River blindness SIR,- Your note about river blindness (Mar 28, p 803) provides excellent summary of the outstanding achievements of the Onchocerciasis Control Programme in West Africa (OCP). Unfortunately, the title you have chosen is distinctly misleading. The OCP is starting its final attack on river blindness in most parts of the 11West African countries covered by its remit. Nevertheless, there are still more than 16 million persons infected with Onchocerca volvulus in the remaining 23 endemic countries an
or
dermatan
starting antiblastic
sulphate.
chemotherapy.
outside the OCP area, most ot which are m Atnca. At least /3U UUU of these dwellers in remote rural areas are blind as a result; and a
similar number have severe visual impairment. For them, the attack on river blindness has scarcely begun. Their only hope lies in regular annual dosing with ivermectin. The World Health Organisation, several non-governmental organisations (especially the recently-founded River Blindness Foundation), UN agencies, USAID, and the Mectizan (ivermectin) Expert Committee are now just beginning to assist the Ministries of Health in other affected countries that are untouched by OCP. The task of delivering ivermectin in a cost-effective manner is even greater than that which faced the OCP at its outset; and the struggle will take just as long. Success may well depend on the world bank and OCP donors being prepared to help fmance the scheme. The OCP’s final attack may signal the end of one campaign, but it is far from being the end of the war against river blindness. River Blindness Foundation, 1 Sugar Creek Place, Sugar Land, Texas 77478, USA
W. R. BALDWIN B.O.L. DUKE
Inadequate information on needlestick accidents SIR,- The article by Klein and colleagues1 reinforces the need for health-care workers to regard patients as potentially infected with a communicable blood-borne agent. The agents potentially transmissible by accidental needlestick inoculation and for which routine screening assays are available include hepatitis B virus (HBV), hepatitis C virus (HCV), human T-cell leukaemia virus (types I and II), and human immunodeficiency virus types 1 and 2. While analysing the risk of infection in two London hospitals to health-care personnel who had been exposed parenterally to blood via accidental inoculation, we reviewed data and serum samples received from donors in needlestick accidents from mid-1986 to the end of 1990. For 1990 we analysed the type of accident and looked at how often paired sera (donor and recipient) were available, at what proportion of accidents were reported to our division of virology, and at identification of donor and/or recipient. Sera were randomised and tested for antibodies to HIV-1, HTLV-I, and HCV.1All had previously been tested for HBV infection (HBsAg ELISA). Between mid-1986 and the end of 1990, sera from 528 donors in needlestick accidents (parenteral exposure to blood) were identified. 135 related to accidents in 1990. On 85 (63%) of donor request forms it was possible to identify the recipient. During the same year the division received 211 sera from the injured recipients; 84 (40%)
