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DUPUYTREN'S DISEASE AND DIABETES MELLITUS
1420
abnormality cannot be considered to be a late complication, and its presence in a patient not known to be diabetic should alert the doctor to the possibility of carbohydrate intolerance. At present it is not known what proportion of people with Dupuytren’s disease will go on to develop diabetes. The aetiology and pathogenesis of Dupuytren’s disease remain obscure, although the proliferation of fibrobl’asts in the superficial compartment of the palm may reflect a lesion in the genetic material of the cells.7 Glucose intolerance might further disturb fibroblast function: cultured skin fibroblasts from diabetics display abnormal patterns of growth and protein biosynthesis.8Investigation of the
graphic analysis of the hexane extract of the plasma indicated that the canthaxanthine levels steadily increased over the first 16 days and then remained at ten times pretreatment levels for the rest of the study period. Trace amounts of retinol and retinol palmitate were also present. Since canthaxanthine interferes with carotene and vitamin A assays we could not measure vitamin A. Following cessation of treatment, return to baseline values was slow, requiring 10 days before pretreatment levels were attained. Thus, although toxic levels of vitamin A did not occur with one of the tanning compounds used, accumulation and persistence of canthaxanthine in the other volunteer would prompt us to recommend that blood donors taking such compounds should be excluded from blood or plasma donation. The effect of transfusion of these compounds or their breakdown products is not known. Attention to this detail is necessary since the compounds are sold as a cosmetic agent and therefore routine questioning of blood donors about drug use will not uncover these products. Orange plasma is apparently a sign of the times. Ottawa Centre, Canadian Red Cross Blood Transfusion Service, Ottawa, Ontario K1S 3E2, Canada; and Montreal Centre, Canadian Red Cross Blood Transfusion Service
effects of diabetes
We thank Sister L. Wadeson and the staff of the diabetic clinic
1977; 14: 170-74.
LP, Zorrilla E. Disorders of the skin in diabetes. In. Marble A, White P, Bradley RF, Krall LP, eds. Joslin’s diabetes mellitus. 11th edition. Philadelphia: Lea and
4 Krall
5. 6.
Febiger, 1971: 653-65 Boyes JH. Bunnell’s surgery of the hand. 5th edition. Philadelphia: J. B. Lippincott Co., 1970: 225-39. Spring M, Fleck H, Cohen BD. Dupuytren’s contracture. Warning of diabetes? New York State J Med 1970; 70: 1037-41.
under-
at
Salford
Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, U.S.A.
J. G. HEATHCOTE
Diabetic Clinic, Salford Royal Hospital, Salford
HAROLD COHEN
Department of Orthopaedic Surgery, University of Manchester, Hope Hospital, Salford M6 8HD
SIR,-An association between Dupuytren’s disease and diabetes mellitus has often been claimed 1-3although not all authorities accept its validity,4 partly because both conditions are common in the general population. The reported prevalence of Dupuytren’s
neuropathy. Hand lesions In: Pfeiffer EF, ed Handbook of diabetes mellitus. Munich J. F. Lehmann Verlag, 1971. 614-16. 2. Günther O, Miosga R Dupuytrensche Kontraktur als Diabetes—Spätkomplikation. Zschr Inn Med 1972; 27: 77-82. 3 Ravid M, Dinai Y, Sohar E. Dupuytren’s disease in diabetes mellitus. Acta Diabet Lat
our
Royal Hospital.
DUPUYTREN’S DISEASE AND DIABETES MELLITUS
1. Schneider T. Diabetic
fibroblast function may increase
disease.
G. A. ROCK F. DECARY R. S. COLE
disease among diabetics varies from 1.6 6 to 32% but a number of genuine cases may have been missed since some surveys have concentrated on the presence of the contracture, i.e., the thickened band of palmar fascia and the flexion deformity, and have ignored milder lesions such as tethering of the skin and knuckle pads. As part of a larger investigation into the natural history of Dupuytren’s disease (report in preparation) we have re-examined the association between these two conditions. When an unselected series of 273 adults over the age of sixteen attending a diabetic clinic were examined by a physician, signs of Dupuytren’s disease were detected in 51 (19%). This figure was increased to 42% when hand examination was carried out in consultation with an orthopaedic surgeon. Since Dupuytren’s disease was found in only 13% of a group of age and sex-matched non-diabetics it would appear to be much commoner in diabetics, although this will only be appreciated if an experienced doctor examines the hands. The milder features of the abnormality predominate in diabetics and are easily missed; this is particularly true for women. Most patients were unaware of any change in the appearance of their hands and few had symptoms. In diabetics the lesions were principally located in the middle and ring finger rays, whereas in the general populatioq the little and ring finger rays are commonly involved.5Diabetics with Dupuytren’s disease were significantly older and had longer histories of diabetes than those with no disease, but there were no major differences in treatment or quality of diabetic control. disease has been considered as both an early Dupuytren’s 1,6 and a late warning-sign complication2of diabetes. Of our patients with Dupuytren’s disease 57% had had overt diabetes for less than ten years and characteristic lesions could be found in 16% of newly diagnosed diabetics. These results indicate that the fascial
on
standing of the cellular mechanisms which operate in the development of the more important angiopathic complications of this
JONATHAN NOBLE
MARBURG AND EBOLA VIRUS ANTIBODIES IN KENYAN PRIMATES
SIR,-Although Marburg and Ebola virus diseases, both of which human haemorrhagic fevers, have been referred to as "green monkey disease", the true role of primates in the ecology of these viruses is unknown. Marburg virus was first described after being recovered from patients who had been working with African green monkeys (Cercopithecus aethiops) and from the tissues of the monkeys during a European outbreak in 1967.’ Serological examination of a large number of primate sera after that outbreak showed all species to be negative and, in fact, the 100% mortality rate observed in experimentally infected monkeys indicated that they were incidental hosts and played no part in the ecology of the virus. 11,12, " Ebola virus, which is morphologically identical but serologically unrelated to Marburg virus, has not been recovered from primates, but when monkeys are experimentally inoculated they develop an illness indistinguishable from Marburg disease. 14 After two human cases of Marburg virus disease in Kenya in 1980,15 epidemiological investigatiions were undertaken which included the testing of sera from primates in captivity at the cause severe
.
Institute of Primate Research and the Wellcome Trust Research Laboratories in Kenya, for evidence of exposure to Marburg and Ebola viruses. 98 vervet monkeys (C. aethiops johns tom), 183 baboons (Papio anubis), and 80 blue and Sykes monkeys (C. mitis spp.) were tested for antibodies by indrect immunofluorescence.16 7.
8.
Bowser-Riley S, Bain AD, Nobel J, Lamb DW. Chromosome abnormalities in Dupuytren’s disease. Lancet 1975; 1i: 1282-83. Rowe DW, Starman BJ, Fujimoto WY, Williams RH. Abnormalities in proliferation and protein synthesis in skin fibroblast cultures from patients with diabetes
mellitus. Diabetes 1977; 26: 284-90. 9. Smith CEG, Simpson DIH, Bowen ETW, Zlotnik I. Fatal human disease from vervet monkeys. Lancet 1967; 1i: 1119. 10. Robin Y, Bres P, Camain R. Passage of Marburg virus in guinea pigs. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971: 136-43. 11. Simpson DIH, Bowen ETW, Bright WF. Vervet monkey disease: experimental infection in monkeys with the causative agent and antibody studies in wild caught monkeys. Laboratory Animals 1968; 2: 75-81. 12. Haas R, Maas G. Experimental infection of monkeys with the Marburg virus. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971. 136-43. 13. Strickland-Chomley M, Malherbe H. Examination of South African primates for the presence of Marburg virus. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971: 195-202. 14. Bowen ETW, Platt GS, Simpson DIH, McArdell LB, Raymond RT Ebola haemorrhagic fever: experimental infection in monkeys. Trans Roy Soc Trop Med Hyg 1978; 72: 188-91. 15. Marburg virus disease-Kenya. Weekly Epidemiol Record 1980; 52: 59-60 16. Wulff H, Lange JV. Indirect immunofluorescence for the diagnosis of Lassa fever infection. Bull WHO 1975; 52: 429-36.
abnormality cannot be considered to be a late complication, and its presence in a patient not known to be diabetic should alert the doctor to the possibility of carbohydrate intolerance. At present it is not known what proportion of people with Dupuytren’s disease will go on to develop diabetes. The aetiology and pathogenesis of Dupuytren’s disease remain obscure, although the proliferation of fibrobl’asts in the superficial compartment of the palm may reflect a lesion in the genetic material of the cells.7 Glucose intolerance might further disturb fibroblast function: cultured skin fibroblasts from diabetics display abnormal patterns of growth and protein biosynthesis.8Investigation of the
graphic analysis of the hexane extract of the plasma indicated that the canthaxanthine levels steadily increased over the first 16 days and then remained at ten times pretreatment levels for the rest of the study period. Trace amounts of retinol and retinol palmitate were also present. Since canthaxanthine interferes with carotene and vitamin A assays we could not measure vitamin A. Following cessation of treatment, return to baseline values was slow, requiring 10 days before pretreatment levels were attained. Thus, although toxic levels of vitamin A did not occur with one of the tanning compounds used, accumulation and persistence of canthaxanthine in the other volunteer would prompt us to recommend that blood donors taking such compounds should be excluded from blood or plasma donation. The effect of transfusion of these compounds or their breakdown products is not known. Attention to this detail is necessary since the compounds are sold as a cosmetic agent and therefore routine questioning of blood donors about drug use will not uncover these products. Orange plasma is apparently a sign of the times. Ottawa Centre, Canadian Red Cross Blood Transfusion Service, Ottawa, Ontario K1S 3E2, Canada; and Montreal Centre, Canadian Red Cross Blood Transfusion Service
effects of diabetes
We thank Sister L. Wadeson and the staff of the diabetic clinic
1977; 14: 170-74.
LP, Zorrilla E. Disorders of the skin in diabetes. In. Marble A, White P, Bradley RF, Krall LP, eds. Joslin’s diabetes mellitus. 11th edition. Philadelphia: Lea and
4 Krall
5. 6.
Febiger, 1971: 653-65 Boyes JH. Bunnell’s surgery of the hand. 5th edition. Philadelphia: J. B. Lippincott Co., 1970: 225-39. Spring M, Fleck H, Cohen BD. Dupuytren’s contracture. Warning of diabetes? New York State J Med 1970; 70: 1037-41.
under-
at
Salford
Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, U.S.A.
J. G. HEATHCOTE
Diabetic Clinic, Salford Royal Hospital, Salford
HAROLD COHEN
Department of Orthopaedic Surgery, University of Manchester, Hope Hospital, Salford M6 8HD
SIR,-An association between Dupuytren’s disease and diabetes mellitus has often been claimed 1-3although not all authorities accept its validity,4 partly because both conditions are common in the general population. The reported prevalence of Dupuytren’s
neuropathy. Hand lesions In: Pfeiffer EF, ed Handbook of diabetes mellitus. Munich J. F. Lehmann Verlag, 1971. 614-16. 2. Günther O, Miosga R Dupuytrensche Kontraktur als Diabetes—Spätkomplikation. Zschr Inn Med 1972; 27: 77-82. 3 Ravid M, Dinai Y, Sohar E. Dupuytren’s disease in diabetes mellitus. Acta Diabet Lat
our
Royal Hospital.
DUPUYTREN’S DISEASE AND DIABETES MELLITUS
1. Schneider T. Diabetic
fibroblast function may increase
disease.
G. A. ROCK F. DECARY R. S. COLE
disease among diabetics varies from 1.6 6 to 32% but a number of genuine cases may have been missed since some surveys have concentrated on the presence of the contracture, i.e., the thickened band of palmar fascia and the flexion deformity, and have ignored milder lesions such as tethering of the skin and knuckle pads. As part of a larger investigation into the natural history of Dupuytren’s disease (report in preparation) we have re-examined the association between these two conditions. When an unselected series of 273 adults over the age of sixteen attending a diabetic clinic were examined by a physician, signs of Dupuytren’s disease were detected in 51 (19%). This figure was increased to 42% when hand examination was carried out in consultation with an orthopaedic surgeon. Since Dupuytren’s disease was found in only 13% of a group of age and sex-matched non-diabetics it would appear to be much commoner in diabetics, although this will only be appreciated if an experienced doctor examines the hands. The milder features of the abnormality predominate in diabetics and are easily missed; this is particularly true for women. Most patients were unaware of any change in the appearance of their hands and few had symptoms. In diabetics the lesions were principally located in the middle and ring finger rays, whereas in the general populatioq the little and ring finger rays are commonly involved.5Diabetics with Dupuytren’s disease were significantly older and had longer histories of diabetes than those with no disease, but there were no major differences in treatment or quality of diabetic control. disease has been considered as both an early Dupuytren’s 1,6 and a late warning-sign complication2of diabetes. Of our patients with Dupuytren’s disease 57% had had overt diabetes for less than ten years and characteristic lesions could be found in 16% of newly diagnosed diabetics. These results indicate that the fascial
on
standing of the cellular mechanisms which operate in the development of the more important angiopathic complications of this
JONATHAN NOBLE
MARBURG AND EBOLA VIRUS ANTIBODIES IN KENYAN PRIMATES
SIR,-Although Marburg and Ebola virus diseases, both of which human haemorrhagic fevers, have been referred to as "green monkey disease", the true role of primates in the ecology of these viruses is unknown. Marburg virus was first described after being recovered from patients who had been working with African green monkeys (Cercopithecus aethiops) and from the tissues of the monkeys during a European outbreak in 1967.’ Serological examination of a large number of primate sera after that outbreak showed all species to be negative and, in fact, the 100% mortality rate observed in experimentally infected monkeys indicated that they were incidental hosts and played no part in the ecology of the virus. 11,12, " Ebola virus, which is morphologically identical but serologically unrelated to Marburg virus, has not been recovered from primates, but when monkeys are experimentally inoculated they develop an illness indistinguishable from Marburg disease. 14 After two human cases of Marburg virus disease in Kenya in 1980,15 epidemiological investigatiions were undertaken which included the testing of sera from primates in captivity at the cause severe
.
Institute of Primate Research and the Wellcome Trust Research Laboratories in Kenya, for evidence of exposure to Marburg and Ebola viruses. 98 vervet monkeys (C. aethiops johns tom), 183 baboons (Papio anubis), and 80 blue and Sykes monkeys (C. mitis spp.) were tested for antibodies by indrect immunofluorescence.16 7.
8.
Bowser-Riley S, Bain AD, Nobel J, Lamb DW. Chromosome abnormalities in Dupuytren’s disease. Lancet 1975; 1i: 1282-83. Rowe DW, Starman BJ, Fujimoto WY, Williams RH. Abnormalities in proliferation and protein synthesis in skin fibroblast cultures from patients with diabetes
mellitus. Diabetes 1977; 26: 284-90. 9. Smith CEG, Simpson DIH, Bowen ETW, Zlotnik I. Fatal human disease from vervet monkeys. Lancet 1967; 1i: 1119. 10. Robin Y, Bres P, Camain R. Passage of Marburg virus in guinea pigs. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971: 136-43. 11. Simpson DIH, Bowen ETW, Bright WF. Vervet monkey disease: experimental infection in monkeys with the causative agent and antibody studies in wild caught monkeys. Laboratory Animals 1968; 2: 75-81. 12. Haas R, Maas G. Experimental infection of monkeys with the Marburg virus. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971. 136-43. 13. Strickland-Chomley M, Malherbe H. Examination of South African primates for the presence of Marburg virus. In: Martini GA, Siegert R, eds. Marburg virus disease. Berlin: Springer Verlag, 1971: 195-202. 14. Bowen ETW, Platt GS, Simpson DIH, McArdell LB, Raymond RT Ebola haemorrhagic fever: experimental infection in monkeys. Trans Roy Soc Trop Med Hyg 1978; 72: 188-91. 15. Marburg virus disease-Kenya. Weekly Epidemiol Record 1980; 52: 59-60 16. Wulff H, Lange JV. Indirect immunofluorescence for the diagnosis of Lassa fever infection. Bull WHO 1975; 52: 429-36.