1341
Vancomycin and histamine release SiR,—Your April 28 editorial (p 1006) suggests that Hl receptor antagonists may provide protection from the anaphylactoid or pseudoallergic type of reaction in some patients receiving vancomycin. An alternative and perhaps simpler approach where anti-grampositive therapy is needed would be to use the glycopeptide antibiotic teicoplanin. Teicoplanin has antibacterial activity similar to that of vancomycin and is effective in the treatment of various gram-positive infections. Importantly the incidence of crossreactivity between vancomycin and teicoplanin seems low. Twelve patients who had anaphylactoid reactions to vancomycin were successfully treated with teicoplanin without evidence of crossreactivity.1-3 McElrath et al4 recorded cross-reactivity in an opiate abuser with staphylococcal endocarditis. There has been only one report of an anaphylactoid reaction in a patient receiving teicoplanin.5 This experience suggests that teicoplanin is well tolerated in patients with vancomycin sensitivity. It is noteworthy that anaphylactoid reactions occur even when the chromatographically purified form of vancomycin is used and when the drug is given as a slow 2-h intravenous infusion, as recommended by the manufacturers. Teicoplanin may therefore provide a safe alternative to vancomycin in the treatment of infection associated with sensitive gram-positive organisms. Magnetic Resonance Research Centre and Department of Haematology, Liverpool University, Liverpool L69 3BX, UK
STEPHEN R. SMITH
1. Smith
SR, Cheesbrough JS, Makris M, Davies JM. Teicoplanin administration in patients experiencing reactions to vancomycin. J Antimicrob Ther 1989; 23: 810-12. 2. Van Laethem Y, Goossens H, Cran S, Butzler JP, Clumesk N. Teichomycin in severe methicillin resistant gram positive septicaemia. (Twenty-fourth Interscience Conference on Antimicrobial Agents and Chemotherapy, Washington DC, 8-10 October.) Washington, DC: American Society for Microbiology, 1984, abstract 1219: 306. 3. Schlemmer B, Falkman H, Boudjada A, Jacob L, LeGall JR. Teicoplanin for patients allergic to vancomycin. N Engl J Med 1988; 318: 1127-28. 4. McElrath MJ, Goldberg D, Neu HC. Allergic cross-reactivity of teicoplanin and vancomycin. Lancet 1986; i: 47. 5. Lewis P, Garaud J, Parenti F. A multicentre open clinical trial of infections caused by Ther 1988; 21 (suppl A): 61-67. J gram-positive bacteria. Antimicrob
Diabetes
mortality in a tertiary referral hospital in India
SIR,-A cross-sectional analysis of hospital records of the All India Institute of Medical Sciences (AIIMS) from 1977 to 19871 led to the identification of 580 "diabetic deaths" (all ages). 11patients had childhood onset (under 20 years of age) and 20 had onset of diabetes at
age 21-30. Ketoacidosis accounted for 91 % and 25% of diabetes
deaths, respectively; most deaths were at or soon after the diagnosis of diabetes (table). In a cohort of patients with childhood onset diabetes being followed up at the AIIMS diabetic clinic diabetes duration was 1-3 months in 26%,4-12 months in 24%, 1-5 years in 27%, 6-10 years in 13%, and greater than 10 years in only 9%. To the best of our knowledge this is the first report of childhood diabetes mortality data from India: the prognosis remains alarmingly dismal. Ketoacidosis, a preventable and treatable condition, accounted for 91 % of deaths, usually at the time of or within a few months of the diabetes being diagnosed. PROFILE OF DIABETES DEATHS
Possibly, in the Indian health scene, only a very few children with diabetes survive long enough for the chronic complications to develop. In the United States deaths in childhood onset diabetes are usually caused by coronary heart disease (48%) or renal failure (31%), and 90% of children surviving 20 years of diabetes, 77% 30 years, and 46% 40 years.2 Departments of Paediatrics and Endocrinology, Metabolism, and Diabetes, All India Institute of Medical Sciences, Diabetes Foundation (India), New Delhi 110029, India
ANJU VIRMANI P. USHABALA P. V. RAO
A, Ushabala P, Rao PV. Mortality in IDDM observed in a tertiary referral hospital in India. Diabetes Bull 1989; 9 (suppl 1): 18-19. Christlieb AR, Warram JH, Krolewski AS, et al. Hypertension: the major risk factor in juvenile-onset insulin-dependent diabetes. Diabetes 1981; 30 (suppl 2): 90.
1. Virmani 2.
Diabetes in Asian children SiR,—Two medicolegal reports on death due to undiagnosed diabetes in children (March 10, p 595; March 17, p 652) call to mind two fatalities in children whose referral to hospital was delayed because diabetes had not been recognised as the cause for their symptoms. Both came from Asian families. On contacting the general practitioners concerned we found a widely held belief that true insulin-dependent diabetes is rare in Asians.’ We have studied in detail the prevalence of insulin-dependent diabetes in 20 267 Asian and 44 268 white children below the age of 15 in Leicestershire. The prevalence (per 1000) for Asians is 0-54 and for whites 0-99 (relative risk 055, 95% confidence interval 0-3-11). This rate for Asians is higher than that recorded in other Far and Middle Eastern populations in which methodologically stringent prevalence studies have been done. In Japan and Israel the prevalence rates of insulin-dependent diabetes in children are 0-06 and 0 16, respectively.2 Insulin-treated diabetes was rare in the young adult Asian indirectly suggesting an increased prevalence of insulin-dependent diabetes in Asian children after migration to the UK.4 A. SAMANTA A. C. BURDEN Diabetes Research, J. R. HEARNSHAW Leicester General Hospital, Leicester LE5 4PW, UK P. G. F. SWIFT 1. Samanta A, Burden AC, Jones GR, et al. Prevalence of insulin-dependent diabetes in
Asian children. Diabetic Med 1987; 4: 65-67. AS, Warram JH. Epidemiology of diabetes mellitus. In: Marble A, Krall LP, Bradley RF, Christlieb AR, Soeldner JS, eds. Joslin’s diabetes mellitus. Philadelphia: Lea & Febiger, 1985. 3. Chaudhuri KR, Samanta A, Burden AC. Prevalence of insulin-treated diabetes mellitus: differences between whites and (Indian) Asians in the UK. Diabetic Med 1989; 6 (suppl 2): 21A. 4. Burden AC, Hearnshaw JR, Swift PGF. Childhood diabetes: an increasing incidence. Diabetic Med 1989; 6: 334-36. 2. Knowleski
Nutrition and
hip fracture
SIR,-Dr Delmi and colleagues (April 28, p 1013) suggest that malnutrition may be an important determinant of the incidence of and complications from hip fractures in the elderly, and they provide evidence for a more favourable clinical outcome in patients given nutritional supplements. However, the only evidence for an improvement in nutritional status is an increase in serum albumin, but this responded in the normal manner of a negative acute-phase protein and I question the evidence for malnutrition in these patients. The biochemical evidence given for malnutrition is based on concentrations of retinol binding protein (RBP), vitamin A, carotene, and 25-hydroxycholecalciferol (250HD) for which the means were reported to be below normal. Many 250HD values were indeed low but this probably reflects the lifestyle of these patients before their injury since most vitamin D is obtained from endogenous synthesis in response to sunlight. For the other indices the means were not below normal. The normal range for RBP is 20-2-5 pmol/1 (40-50 mg/1) and for retinol it is above 0-7 umol/1 serum
Figures m Italic type show diabetes duration in years at time of death. Frequency of hypertension 0% and 40% in the childhood and youth onset group, respectively. CAD=coronary artery disease; CRF = chronic renal disease; other includes chronic vascular disease and infection.
Vancomycin and histamine release SiR,—Your April 28 editorial (p 1006) suggests that Hl receptor antagonists may provide protection from the anaphylactoid or pseudoallergic type of reaction in some patients receiving vancomycin. An alternative and perhaps simpler approach where anti-grampositive therapy is needed would be to use the glycopeptide antibiotic teicoplanin. Teicoplanin has antibacterial activity similar to that of vancomycin and is effective in the treatment of various gram-positive infections. Importantly the incidence of crossreactivity between vancomycin and teicoplanin seems low. Twelve patients who had anaphylactoid reactions to vancomycin were successfully treated with teicoplanin without evidence of crossreactivity.1-3 McElrath et al4 recorded cross-reactivity in an opiate abuser with staphylococcal endocarditis. There has been only one report of an anaphylactoid reaction in a patient receiving teicoplanin.5 This experience suggests that teicoplanin is well tolerated in patients with vancomycin sensitivity. It is noteworthy that anaphylactoid reactions occur even when the chromatographically purified form of vancomycin is used and when the drug is given as a slow 2-h intravenous infusion, as recommended by the manufacturers. Teicoplanin may therefore provide a safe alternative to vancomycin in the treatment of infection associated with sensitive gram-positive organisms. Magnetic Resonance Research Centre and Department of Haematology, Liverpool University, Liverpool L69 3BX, UK
STEPHEN R. SMITH
1. Smith
SR, Cheesbrough JS, Makris M, Davies JM. Teicoplanin administration in patients experiencing reactions to vancomycin. J Antimicrob Ther 1989; 23: 810-12. 2. Van Laethem Y, Goossens H, Cran S, Butzler JP, Clumesk N. Teichomycin in severe methicillin resistant gram positive septicaemia. (Twenty-fourth Interscience Conference on Antimicrobial Agents and Chemotherapy, Washington DC, 8-10 October.) Washington, DC: American Society for Microbiology, 1984, abstract 1219: 306. 3. Schlemmer B, Falkman H, Boudjada A, Jacob L, LeGall JR. Teicoplanin for patients allergic to vancomycin. N Engl J Med 1988; 318: 1127-28. 4. McElrath MJ, Goldberg D, Neu HC. Allergic cross-reactivity of teicoplanin and vancomycin. Lancet 1986; i: 47. 5. Lewis P, Garaud J, Parenti F. A multicentre open clinical trial of infections caused by Ther 1988; 21 (suppl A): 61-67. J gram-positive bacteria. Antimicrob
Diabetes
mortality in a tertiary referral hospital in India
SIR,-A cross-sectional analysis of hospital records of the All India Institute of Medical Sciences (AIIMS) from 1977 to 19871 led to the identification of 580 "diabetic deaths" (all ages). 11patients had childhood onset (under 20 years of age) and 20 had onset of diabetes at
age 21-30. Ketoacidosis accounted for 91 % and 25% of diabetes
deaths, respectively; most deaths were at or soon after the diagnosis of diabetes (table). In a cohort of patients with childhood onset diabetes being followed up at the AIIMS diabetic clinic diabetes duration was 1-3 months in 26%,4-12 months in 24%, 1-5 years in 27%, 6-10 years in 13%, and greater than 10 years in only 9%. To the best of our knowledge this is the first report of childhood diabetes mortality data from India: the prognosis remains alarmingly dismal. Ketoacidosis, a preventable and treatable condition, accounted for 91 % of deaths, usually at the time of or within a few months of the diabetes being diagnosed. PROFILE OF DIABETES DEATHS
Possibly, in the Indian health scene, only a very few children with diabetes survive long enough for the chronic complications to develop. In the United States deaths in childhood onset diabetes are usually caused by coronary heart disease (48%) or renal failure (31%), and 90% of children surviving 20 years of diabetes, 77% 30 years, and 46% 40 years.2 Departments of Paediatrics and Endocrinology, Metabolism, and Diabetes, All India Institute of Medical Sciences, Diabetes Foundation (India), New Delhi 110029, India
ANJU VIRMANI P. USHABALA P. V. RAO
A, Ushabala P, Rao PV. Mortality in IDDM observed in a tertiary referral hospital in India. Diabetes Bull 1989; 9 (suppl 1): 18-19. Christlieb AR, Warram JH, Krolewski AS, et al. Hypertension: the major risk factor in juvenile-onset insulin-dependent diabetes. Diabetes 1981; 30 (suppl 2): 90.
1. Virmani 2.
Diabetes in Asian children SiR,—Two medicolegal reports on death due to undiagnosed diabetes in children (March 10, p 595; March 17, p 652) call to mind two fatalities in children whose referral to hospital was delayed because diabetes had not been recognised as the cause for their symptoms. Both came from Asian families. On contacting the general practitioners concerned we found a widely held belief that true insulin-dependent diabetes is rare in Asians.’ We have studied in detail the prevalence of insulin-dependent diabetes in 20 267 Asian and 44 268 white children below the age of 15 in Leicestershire. The prevalence (per 1000) for Asians is 0-54 and for whites 0-99 (relative risk 055, 95% confidence interval 0-3-11). This rate for Asians is higher than that recorded in other Far and Middle Eastern populations in which methodologically stringent prevalence studies have been done. In Japan and Israel the prevalence rates of insulin-dependent diabetes in children are 0-06 and 0 16, respectively.2 Insulin-treated diabetes was rare in the young adult Asian indirectly suggesting an increased prevalence of insulin-dependent diabetes in Asian children after migration to the UK.4 A. SAMANTA A. C. BURDEN Diabetes Research, J. R. HEARNSHAW Leicester General Hospital, Leicester LE5 4PW, UK P. G. F. SWIFT 1. Samanta A, Burden AC, Jones GR, et al. Prevalence of insulin-dependent diabetes in
Asian children. Diabetic Med 1987; 4: 65-67. AS, Warram JH. Epidemiology of diabetes mellitus. In: Marble A, Krall LP, Bradley RF, Christlieb AR, Soeldner JS, eds. Joslin’s diabetes mellitus. Philadelphia: Lea & Febiger, 1985. 3. Chaudhuri KR, Samanta A, Burden AC. Prevalence of insulin-treated diabetes mellitus: differences between whites and (Indian) Asians in the UK. Diabetic Med 1989; 6 (suppl 2): 21A. 4. Burden AC, Hearnshaw JR, Swift PGF. Childhood diabetes: an increasing incidence. Diabetic Med 1989; 6: 334-36. 2. Knowleski
Nutrition and
hip fracture
SIR,-Dr Delmi and colleagues (April 28, p 1013) suggest that malnutrition may be an important determinant of the incidence of and complications from hip fractures in the elderly, and they provide evidence for a more favourable clinical outcome in patients given nutritional supplements. However, the only evidence for an improvement in nutritional status is an increase in serum albumin, but this responded in the normal manner of a negative acute-phase protein and I question the evidence for malnutrition in these patients. The biochemical evidence given for malnutrition is based on concentrations of retinol binding protein (RBP), vitamin A, carotene, and 25-hydroxycholecalciferol (250HD) for which the means were reported to be below normal. Many 250HD values were indeed low but this probably reflects the lifestyle of these patients before their injury since most vitamin D is obtained from endogenous synthesis in response to sunlight. For the other indices the means were not below normal. The normal range for RBP is 20-2-5 pmol/1 (40-50 mg/1) and for retinol it is above 0-7 umol/1 serum
Figures m Italic type show diabetes duration in years at time of death. Frequency of hypertension 0% and 40% in the childhood and youth onset group, respectively. CAD=coronary artery disease; CRF = chronic renal disease; other includes chronic vascular disease and infection.
