Acta Pzdiatr Scand 67: 525-528, 1978
CASE REPORT
KAWASAKI DISEASE IN KUWAIT A Report of Two Cases H. A. MAJEED and I . A. OLSON From the Department of Paediatrics, the Chest Hospital and Kuwait University Medical School, Kuwait
ABSTRACT. Majeed, H. A. and Olson, I. A. (Department of Paediatrics, The Chest Hospital and Department of Human Morphology and Experimental Pathology, Kuwait University Medical School, Kuwait). Kawasaki disease in Kuwait. A report on two cases. Acta Paediatr Scand, 67: 525, 1978.-Kawasaki disease was first reported in Japan in 1967. Since then, it has been reported from the United States, South Korea, Greece, Canada, Australia, Scandinavia and Scotland. Two cases of Kawasaki disease are presented from Kuwait and believed to be the first report of the disease from the Arab world. KEY WORDS: Kawasaki disease, infantile polyarteritis nodosa, mucocutaneous lymph node syndrome
In 1967, Kawasaki described a febrile mucocutaneous disease, affecting infants and children, which he designated as mucocutaneous lymph node syndrome (MLNS) (8). The Japanese MLNS study group has recently adopted the name Kawasaki disease, thus accepting it as a nosological entity (9). Outside Japan, the disease has so far been reported from the United States, South Korea, Greece, Canada (17), Australia ( 11), Scandinavia (1) and Scotland (20). This report describes two cases of Kawasaki disease in Kuwait and is believed to be the first report of the disease from the Arab world.
CASE HISTORIES Case I . A. S., a ten-year-old Kuwaiti boy, presented on May 1975 with fever, headache, abdominal pain and arthralgia of both knees of three days duration which had not responded to oral penicillin. Examination showed an ill looking child who was unable to walk because of pain in both knees which were not red or swollen. Temperature was 39.2"C. The throat and oral cavity were congested with a post natal discharge; no vesicles were noted. The conjunctivae were mildly congested, lips dry and the neck
was stiff. There was bilateral anterior cervical lymphadenities. A discrete maculo-erythematous rash involved the trunk and extremities; the palms and soles showed diffuse erythema. Laboratory blood examination showed haemoglobin 8.6 mmol/l, leucocytosis (12X 109/1) with neutrophilia, platelets normal, and erythrocyte sedimentation rate of 30 mm/h and positive C-reactive protein. Throat culture grew no organisms, AS0 titre was 100 Todd units and rheumatoid factor negative. C.S.F. was normal and urine microscopy revealed no deposits. Blood, urine and C.S.F. cultures were sterile. Widal and Paul Bunnel tests were negative. Chest X-ray, E.C.G., blood urea, serum electrolytes and proteins were all normal. SGPT and alkaline phosphatase were normal, but SGOT was mildly elevated. Oral penicillin was continued. On the 4th day, reddening of the palms and soles were more obvious with no induration, and lips fissured. On the 7th day, temperature started settling down, conjunctivae were normal, the rash was fading, although the palms and soles were still mildly erythematous, and the child could walk with no joint pains. On the 9th day the temperature was normal and on the 17th day he was completely well apart from the characteristic desquamation of palms and soles near the finger tips and along the sides of the nails. Follow up for two years showed no recurrences and normal cardiovascular system. Case 2 . R. H., a 5-year-old English boy, who had arrived in Kuwait from England six weeks before, presented on April 1977 with fever and unilateral painful anterior cervical adenitis of two days duration. Examination showed an ill looking child; temperature was 40.3"C. The throat and oral cavity were severely congested with post Acta Paediatr Scand 67
526
H . A . Majeed and I . A . Olson
DISCUSSION
Fig. 1 . Erythema of the palms with the characteristic
desquamation in Case 2.
nasal discharge; no vesicles were seen. The left tonsillar lymph gland was tender and enlarged (5x2 cm). He was treated with oral penicillin, but within twelve hours (two doses) developed discrete maculo erythematous rash over the trunk and extremities. Penicillin was stopped and oral clindamycin started. By the fifth day, while still pyrexial, he developed a severe conjunctival congestion, diffuse erythema over the nose and anterior malar facial area, marked impressive diffuse erythema and induration of palms and soles and reddening and fissuring of the lips. Laboratory blood examination showed haemoglobin 6.5 mmol/l leucocytosis (18.7X 109/1) with marked neutrophilia, platelets normal, erythrocyte sedimentation rate 110 mm/h and positive C-reactive protein. LE cell and Coombs tests were negative. Total serum protein 76 g/l (albumin 35 g/l and globulins 41 g/l). SGOT and alkaline phosphatase were normal but LDH was mildly elevated. Microscopical examination of urine showed leucocytes I2/H.P.F. and urine culture was sterile. Tuberculin test was negative. Throat culture grew no organisms and A S 0 titre was 50 Todd units. Chest X-ray and E.C.G. were normal. A diagnosis of Kawasaki disease was made. On the 7th day the rash started fading but the child continued to be pyrexial, developed neck stiffness, pain and swelling of both knees and ankles, and he looked more ill. Prednisone orally, 40 mgiday was started. In 48 hours (9th day of illness) there was a dramatic improvement; temperature settled down to normal, neck stiffness and arthritis disappeared and the child looked well. Prednisone was stopped gradually over two weeks. On the 13th day he started the characteristics desquamation from palms and soles near the finger tips and along sides of nails (Fig. 1). On the 25th day while still desquamating from finger tips and along sides of nails, transverse ridges appeared on the nails. Follow-up for six months showed no recurrences and normal cardiovascular system. Acta Paediatr Scand
67
Kawasaki disease has been differentiated from scarlet fever and Steven-Johnson syndrome (10) and its clinical pattern clearly outlined. The combination of marked impressive erythema of palms and soles, intense conjunctivitis, non-suppurative cervical adenitis, in the acute stage, with the characteristic membranous desquamation of fingers and toes in the convalescent stage, in the course of a febrile exanthematous childhood disease, should make a confident diagnosis of Kawasaki disease possible. Our patients fitted well with this characteristic clinical pattern which seems to be different from all other childhood exanthemata (5). They are, however, in the upper age group for the disease (10). They both developed transient neck stiffness and joint involvement, originally described by Kawasaki et al. as significant findings which are important for the diagnosis in combination with the principal symptoms (10); examination of the C.S.F. in one of our patients revealed normal findings. The second child was English who arrived from England six weeks before he became ill in Kuwait. The disease has recently been reported from Britain (20). Of current interest is the relationship between Kawasaki disease (KD) and infantile polyarteritis nodosa (IPN). Fetterman & Roberts in 1963 (18) reviewed 20 cases of IPN and outlined a clinical syndrome which showed clinical resemblance to KD (4, 10). The findings of widespread arteritis involving the brachial, iliac, mesenteric, renal, testicular and other arteries in cases of KD (21) suggests that this may be a “vasculitis syndrome” (7). Polyarteritis nodosa has been classified as a subtype of necrotising angiitis (12). The infantile form is characterised by the high incidence of coronary artery involvement (18). Recent studies on KD have shown similar findings. Tanaka et al. (21) carried out autopsy studies on 29 cases of fatal MLNS; the incidence of coronary artery involvement was 100 % and the vascular pathological findings
Kawasaki disease in Kuwait were identical with IPN. Kato et al. (7) studied the non-fatal clinical form of MLNS; they performed coronary angiography on 20 patients who survived the illness and found abnormal angiograms in 12 (60%). Recently, the Japanese research committee on KD (11) found that of 321 cases given coronary angiography, 63 % showed abnormal angiograms. Asai et al. ( 2 ) reported E.C.G. abnormalities and/or cardiac enlargement in 70% in the acute stage. Physical examination of our patients showed no abnormal clinical cardiac findings, and their plain chest X-rays and E.C.G. tracings were normal. The clinical and pathological close similarities between KD and IPN have not escaped the attention of Kawasaki et al. (lo), Fetterman & Roberts (4)and Tanaka et al. (21), and have rightly tempted Ahlstrom et al. (1) and Smith (20) to suggest that the two diseases may in fact represent one entity. Similar, though possibly less striking, clinico-pathological overlaps are known to occur amongst certain subtype$ of necrotising angiitis (polyarteritis nodosa, allergic angiitis and collagen disease angiitis) (3). A familiar example is the problem of differentiating the most severe forms of Henoch-Schonlein’s purpura (H.S.) from poiyarteritis nodosa (PA) where there is considerable clinical overlap and pathological distinction may not be possible (16), and suggestions were in fact made to consider H.S. and PA as presentations of the same disease (16). Yet, we are impressed by the close clinico-pathological similarities between IPN and the fatal form of KD (21), and the high incidence of coronary arteritis in the non-fatal clinical form of KD (7, 11). It may be that the fatal form of KD and IPN are probably one entity representing one end of a disease process, that tends to occur in young babies, while the more common non-fatal clinical form of KD, which tends to occur in older children represents the other end. The aetiology of KD is still obscure. The Group A-Beta haemolytic streptococcus was ruled out as the causative agent (lo); this fitted
527
with our observations in Kuwait, where though rheumatic fever has been fairly common (15), our two patients are the first and only report of KD from the country. The finding of rickettsia-like bodies in patients with KD (6) was not supported by other reports (19) and the unresponsiveness of the disease to antibiotics failed to confirm the rickettsia1 aetiology . Hypersensitivity mechanism is implicated in the adult form of PA (20) and recently elevated serum levels of IgE have been reported in both KD and IPN (13, 14). The results of a comparative study of adult polyarteritis nodosa and IPN that does not show the MLNS manifestations (21) will be awaited with interest. ACKNOWLEDGEMENTS We are grateful to Dr T. Kawasaki for his help and to Mrs G. U. Greenshields for typing the manuscript.
REFERENCES 1. Ahlstrom, H . , Lundstrom, N., Mortensson, W . , Ostberg, G. & Lantorp, K.: Infantile periarteritis nodosa or mucocutaneous lymph node syndrome. Acta Paediatr Scand, 66: 193, 1977. 2. Asai, T., Kiguchi, H., Nagai, Y. & Kusakawa, S.: Analysis of cardiac involvement in 29 cases with MLNS (in Japanese). J a p J Pediarr, 26: 824, 1973. 3. Benyo, R. B. & Perrin, E. V.: Periarteritis nodosa in infancy. Am J Dis Child, 116:539, 1968. 4. Fetterman, G. H. & Hashida, Y.: Mucocutaneous lymph node syndrome: A disease widespread in Japan which demands our attention. Pediatrics, 54: 268, 1974. 5. Goldsmith, R. W., Gribetz, D. & Strauss, L.: Mucocutaneous lymph node syndrome (MLNS) in the continental United States. Pediatrics, 57: 431, 1976. 6. Hamashima, Y., Kishi, K. & Tasaka, K.: Rickettsialike bodies in infantile acute febrile mucocutaneous lymph node syndrome. Lancet, 11: 42, 1973. 7. Kato, H., Hoike, S., Yamamoto, M., Ito, Y. & Yano, E.: Coronary aneurysms in infants and young children with acute febrile MLNS. J Pediarr, 86: 892, 1975. 8. Kawasaki, T.: MCLS: Clinical observation of 50 cases. Jap J Allergy, 16: 178, 1967 (in Japanese). 9. Kawasaki, T., Kusakawa, S. & Shigematsu, I. (eds.): Progress of research on Kawasaki disease ( M . C . L . S . ) . Tokyo 1976 (in Japanese). 10. Kawasaki, T., Kosaki, T., Okawa, S., Shigematsu, I . & Yanangawa, H.: A new infantile acute febrile mucocutaneous lymph node syndrome (MLNS) prevailing in Japan. Pediatrics, 54: 271, 1974.
Acra Paediatr Scand 67
528
H . A . Majeed and I . A . Olson
1 1 . Kawasaki, T.: Personal communication. 12. Knowles, H. C., Zeek, P. M. & Blankenhorn, M. A,: Studies on necrotising angiitis. IV. Periartritis nodosa and hypersensitivity angiitis. Arch Intern Med, 82: 789,1953. 13. Krous, H. F., Clansen, C. R. & Ray, C. G.: Elevated levels of immunoglobulin E in infantile polyarteritis nodosa. J Pediatr, 84: 841, 1974. 14. Kusakawa, S. & Heiner, D. C.: Elevated levels of immunoglobulin E in acute febrile mucocutaneous lymph node syndrome. Pediatr Res, 10: 108, 1976. IS. Majeed, H. A,: Unpublished observation. 16. Reimold, E. W., Weinberg, A. G., Finle, W. C. & Battles, N. D.: Polyarteritis in children. A m J Dis Child, 130: 534, 1976. 17. Riley, H . D . , Jr: Mucocutaneous lymph node syndrome (Kawasaki disease). Editorial. J Infect Dis, 134: 302, 1976.
Acta Paediatr Scand 67
18. Roberts, F. B. & Fetterman, G. H . : Polyarteritis nodosa in infancy. J Pediatr, 63: 519, 1963. 19. Shishido, A. & Adachi, Y.: In T. Kawasaki, S. Kusakawa & I. Shigematsu (eds.). Progress on research on Kawasaki disease (MLNS). Tokyo 1976. 20. Smith, A. D.: Infantile polyarteritis and Kawasaki disease. Acta Paediatr Scand, 66: 381, 1977. 21. Tanaka, N., Sekimoto, K. & Naoe, S.: Kawasaki disease, relationship with infantile periarteritis nodosa. Arch PatholLab Med, 100:81, 1976.
Submitted Oct. 21, 1977 Accepted Dec. 21, 1977 (H. A . M.) Department of Paediatrics The Chest Hospital P.O. Box 4082 Safat Kuwait
CASE REPORT
KAWASAKI DISEASE IN KUWAIT A Report of Two Cases H. A. MAJEED and I . A. OLSON From the Department of Paediatrics, the Chest Hospital and Kuwait University Medical School, Kuwait
ABSTRACT. Majeed, H. A. and Olson, I. A. (Department of Paediatrics, The Chest Hospital and Department of Human Morphology and Experimental Pathology, Kuwait University Medical School, Kuwait). Kawasaki disease in Kuwait. A report on two cases. Acta Paediatr Scand, 67: 525, 1978.-Kawasaki disease was first reported in Japan in 1967. Since then, it has been reported from the United States, South Korea, Greece, Canada, Australia, Scandinavia and Scotland. Two cases of Kawasaki disease are presented from Kuwait and believed to be the first report of the disease from the Arab world. KEY WORDS: Kawasaki disease, infantile polyarteritis nodosa, mucocutaneous lymph node syndrome
In 1967, Kawasaki described a febrile mucocutaneous disease, affecting infants and children, which he designated as mucocutaneous lymph node syndrome (MLNS) (8). The Japanese MLNS study group has recently adopted the name Kawasaki disease, thus accepting it as a nosological entity (9). Outside Japan, the disease has so far been reported from the United States, South Korea, Greece, Canada (17), Australia ( 11), Scandinavia (1) and Scotland (20). This report describes two cases of Kawasaki disease in Kuwait and is believed to be the first report of the disease from the Arab world.
CASE HISTORIES Case I . A. S., a ten-year-old Kuwaiti boy, presented on May 1975 with fever, headache, abdominal pain and arthralgia of both knees of three days duration which had not responded to oral penicillin. Examination showed an ill looking child who was unable to walk because of pain in both knees which were not red or swollen. Temperature was 39.2"C. The throat and oral cavity were congested with a post natal discharge; no vesicles were noted. The conjunctivae were mildly congested, lips dry and the neck
was stiff. There was bilateral anterior cervical lymphadenities. A discrete maculo-erythematous rash involved the trunk and extremities; the palms and soles showed diffuse erythema. Laboratory blood examination showed haemoglobin 8.6 mmol/l, leucocytosis (12X 109/1) with neutrophilia, platelets normal, and erythrocyte sedimentation rate of 30 mm/h and positive C-reactive protein. Throat culture grew no organisms, AS0 titre was 100 Todd units and rheumatoid factor negative. C.S.F. was normal and urine microscopy revealed no deposits. Blood, urine and C.S.F. cultures were sterile. Widal and Paul Bunnel tests were negative. Chest X-ray, E.C.G., blood urea, serum electrolytes and proteins were all normal. SGPT and alkaline phosphatase were normal, but SGOT was mildly elevated. Oral penicillin was continued. On the 4th day, reddening of the palms and soles were more obvious with no induration, and lips fissured. On the 7th day, temperature started settling down, conjunctivae were normal, the rash was fading, although the palms and soles were still mildly erythematous, and the child could walk with no joint pains. On the 9th day the temperature was normal and on the 17th day he was completely well apart from the characteristic desquamation of palms and soles near the finger tips and along the sides of the nails. Follow up for two years showed no recurrences and normal cardiovascular system. Case 2 . R. H., a 5-year-old English boy, who had arrived in Kuwait from England six weeks before, presented on April 1977 with fever and unilateral painful anterior cervical adenitis of two days duration. Examination showed an ill looking child; temperature was 40.3"C. The throat and oral cavity were severely congested with post Acta Paediatr Scand 67
526
H . A . Majeed and I . A . Olson
DISCUSSION
Fig. 1 . Erythema of the palms with the characteristic
desquamation in Case 2.
nasal discharge; no vesicles were seen. The left tonsillar lymph gland was tender and enlarged (5x2 cm). He was treated with oral penicillin, but within twelve hours (two doses) developed discrete maculo erythematous rash over the trunk and extremities. Penicillin was stopped and oral clindamycin started. By the fifth day, while still pyrexial, he developed a severe conjunctival congestion, diffuse erythema over the nose and anterior malar facial area, marked impressive diffuse erythema and induration of palms and soles and reddening and fissuring of the lips. Laboratory blood examination showed haemoglobin 6.5 mmol/l leucocytosis (18.7X 109/1) with marked neutrophilia, platelets normal, erythrocyte sedimentation rate 110 mm/h and positive C-reactive protein. LE cell and Coombs tests were negative. Total serum protein 76 g/l (albumin 35 g/l and globulins 41 g/l). SGOT and alkaline phosphatase were normal but LDH was mildly elevated. Microscopical examination of urine showed leucocytes I2/H.P.F. and urine culture was sterile. Tuberculin test was negative. Throat culture grew no organisms and A S 0 titre was 50 Todd units. Chest X-ray and E.C.G. were normal. A diagnosis of Kawasaki disease was made. On the 7th day the rash started fading but the child continued to be pyrexial, developed neck stiffness, pain and swelling of both knees and ankles, and he looked more ill. Prednisone orally, 40 mgiday was started. In 48 hours (9th day of illness) there was a dramatic improvement; temperature settled down to normal, neck stiffness and arthritis disappeared and the child looked well. Prednisone was stopped gradually over two weeks. On the 13th day he started the characteristics desquamation from palms and soles near the finger tips and along sides of nails (Fig. 1). On the 25th day while still desquamating from finger tips and along sides of nails, transverse ridges appeared on the nails. Follow-up for six months showed no recurrences and normal cardiovascular system. Acta Paediatr Scand
67
Kawasaki disease has been differentiated from scarlet fever and Steven-Johnson syndrome (10) and its clinical pattern clearly outlined. The combination of marked impressive erythema of palms and soles, intense conjunctivitis, non-suppurative cervical adenitis, in the acute stage, with the characteristic membranous desquamation of fingers and toes in the convalescent stage, in the course of a febrile exanthematous childhood disease, should make a confident diagnosis of Kawasaki disease possible. Our patients fitted well with this characteristic clinical pattern which seems to be different from all other childhood exanthemata (5). They are, however, in the upper age group for the disease (10). They both developed transient neck stiffness and joint involvement, originally described by Kawasaki et al. as significant findings which are important for the diagnosis in combination with the principal symptoms (10); examination of the C.S.F. in one of our patients revealed normal findings. The second child was English who arrived from England six weeks before he became ill in Kuwait. The disease has recently been reported from Britain (20). Of current interest is the relationship between Kawasaki disease (KD) and infantile polyarteritis nodosa (IPN). Fetterman & Roberts in 1963 (18) reviewed 20 cases of IPN and outlined a clinical syndrome which showed clinical resemblance to KD (4, 10). The findings of widespread arteritis involving the brachial, iliac, mesenteric, renal, testicular and other arteries in cases of KD (21) suggests that this may be a “vasculitis syndrome” (7). Polyarteritis nodosa has been classified as a subtype of necrotising angiitis (12). The infantile form is characterised by the high incidence of coronary artery involvement (18). Recent studies on KD have shown similar findings. Tanaka et al. (21) carried out autopsy studies on 29 cases of fatal MLNS; the incidence of coronary artery involvement was 100 % and the vascular pathological findings
Kawasaki disease in Kuwait were identical with IPN. Kato et al. (7) studied the non-fatal clinical form of MLNS; they performed coronary angiography on 20 patients who survived the illness and found abnormal angiograms in 12 (60%). Recently, the Japanese research committee on KD (11) found that of 321 cases given coronary angiography, 63 % showed abnormal angiograms. Asai et al. ( 2 ) reported E.C.G. abnormalities and/or cardiac enlargement in 70% in the acute stage. Physical examination of our patients showed no abnormal clinical cardiac findings, and their plain chest X-rays and E.C.G. tracings were normal. The clinical and pathological close similarities between KD and IPN have not escaped the attention of Kawasaki et al. (lo), Fetterman & Roberts (4)and Tanaka et al. (21), and have rightly tempted Ahlstrom et al. (1) and Smith (20) to suggest that the two diseases may in fact represent one entity. Similar, though possibly less striking, clinico-pathological overlaps are known to occur amongst certain subtype$ of necrotising angiitis (polyarteritis nodosa, allergic angiitis and collagen disease angiitis) (3). A familiar example is the problem of differentiating the most severe forms of Henoch-Schonlein’s purpura (H.S.) from poiyarteritis nodosa (PA) where there is considerable clinical overlap and pathological distinction may not be possible (16), and suggestions were in fact made to consider H.S. and PA as presentations of the same disease (16). Yet, we are impressed by the close clinico-pathological similarities between IPN and the fatal form of KD (21), and the high incidence of coronary arteritis in the non-fatal clinical form of KD (7, 11). It may be that the fatal form of KD and IPN are probably one entity representing one end of a disease process, that tends to occur in young babies, while the more common non-fatal clinical form of KD, which tends to occur in older children represents the other end. The aetiology of KD is still obscure. The Group A-Beta haemolytic streptococcus was ruled out as the causative agent (lo); this fitted
527
with our observations in Kuwait, where though rheumatic fever has been fairly common (15), our two patients are the first and only report of KD from the country. The finding of rickettsia-like bodies in patients with KD (6) was not supported by other reports (19) and the unresponsiveness of the disease to antibiotics failed to confirm the rickettsia1 aetiology . Hypersensitivity mechanism is implicated in the adult form of PA (20) and recently elevated serum levels of IgE have been reported in both KD and IPN (13, 14). The results of a comparative study of adult polyarteritis nodosa and IPN that does not show the MLNS manifestations (21) will be awaited with interest. ACKNOWLEDGEMENTS We are grateful to Dr T. Kawasaki for his help and to Mrs G. U. Greenshields for typing the manuscript.
REFERENCES 1. Ahlstrom, H . , Lundstrom, N., Mortensson, W . , Ostberg, G. & Lantorp, K.: Infantile periarteritis nodosa or mucocutaneous lymph node syndrome. Acta Paediatr Scand, 66: 193, 1977. 2. Asai, T., Kiguchi, H., Nagai, Y. & Kusakawa, S.: Analysis of cardiac involvement in 29 cases with MLNS (in Japanese). J a p J Pediarr, 26: 824, 1973. 3. Benyo, R. B. & Perrin, E. V.: Periarteritis nodosa in infancy. Am J Dis Child, 116:539, 1968. 4. Fetterman, G. H. & Hashida, Y.: Mucocutaneous lymph node syndrome: A disease widespread in Japan which demands our attention. Pediatrics, 54: 268, 1974. 5. Goldsmith, R. W., Gribetz, D. & Strauss, L.: Mucocutaneous lymph node syndrome (MLNS) in the continental United States. Pediatrics, 57: 431, 1976. 6. Hamashima, Y., Kishi, K. & Tasaka, K.: Rickettsialike bodies in infantile acute febrile mucocutaneous lymph node syndrome. Lancet, 11: 42, 1973. 7. Kato, H., Hoike, S., Yamamoto, M., Ito, Y. & Yano, E.: Coronary aneurysms in infants and young children with acute febrile MLNS. J Pediarr, 86: 892, 1975. 8. Kawasaki, T.: MCLS: Clinical observation of 50 cases. Jap J Allergy, 16: 178, 1967 (in Japanese). 9. Kawasaki, T., Kusakawa, S. & Shigematsu, I. (eds.): Progress of research on Kawasaki disease ( M . C . L . S . ) . Tokyo 1976 (in Japanese). 10. Kawasaki, T., Kosaki, T., Okawa, S., Shigematsu, I . & Yanangawa, H.: A new infantile acute febrile mucocutaneous lymph node syndrome (MLNS) prevailing in Japan. Pediatrics, 54: 271, 1974.
Acra Paediatr Scand 67
528
H . A . Majeed and I . A . Olson
1 1 . Kawasaki, T.: Personal communication. 12. Knowles, H. C., Zeek, P. M. & Blankenhorn, M. A,: Studies on necrotising angiitis. IV. Periartritis nodosa and hypersensitivity angiitis. Arch Intern Med, 82: 789,1953. 13. Krous, H. F., Clansen, C. R. & Ray, C. G.: Elevated levels of immunoglobulin E in infantile polyarteritis nodosa. J Pediatr, 84: 841, 1974. 14. Kusakawa, S. & Heiner, D. C.: Elevated levels of immunoglobulin E in acute febrile mucocutaneous lymph node syndrome. Pediatr Res, 10: 108, 1976. IS. Majeed, H. A,: Unpublished observation. 16. Reimold, E. W., Weinberg, A. G., Finle, W. C. & Battles, N. D.: Polyarteritis in children. A m J Dis Child, 130: 534, 1976. 17. Riley, H . D . , Jr: Mucocutaneous lymph node syndrome (Kawasaki disease). Editorial. J Infect Dis, 134: 302, 1976.
Acta Paediatr Scand 67
18. Roberts, F. B. & Fetterman, G. H . : Polyarteritis nodosa in infancy. J Pediatr, 63: 519, 1963. 19. Shishido, A. & Adachi, Y.: In T. Kawasaki, S. Kusakawa & I. Shigematsu (eds.). Progress on research on Kawasaki disease (MLNS). Tokyo 1976. 20. Smith, A. D.: Infantile polyarteritis and Kawasaki disease. Acta Paediatr Scand, 66: 381, 1977. 21. Tanaka, N., Sekimoto, K. & Naoe, S.: Kawasaki disease, relationship with infantile periarteritis nodosa. Arch PatholLab Med, 100:81, 1976.
Submitted Oct. 21, 1977 Accepted Dec. 21, 1977 (H. A . M.) Department of Paediatrics The Chest Hospital P.O. Box 4082 Safat Kuwait
