- Email: [email protected]
Fifty Years Ago in The Journal of Pediatrics
39. Heinemann L. Hypoglycemia and insulin analogues: is there a reduction in the incidence? J Diabetes Complications 1999;13:105-14. 40. Hogan P, Dall T, Nikolov P. Economic costs of diabetes in the US in 2002. Diabetes Care 2003;26:917-32. 41. Curtis JR, To T, Muirhead S, Cummings E, Daneman D. Recent trends in hospitalization for diabetic ketoacidosis in Ontario children. Diabetes Care 2002;25:1591-6. 42. The Diabetes Control and Complications Trial Research Group. Lifetime benefits and costs of intensive therapy as practiced in the Diabetes Control and Complications Trial. JAMA 1996;276:1409-15.
43. Eastman RC, Javitt JC, Herman WH, Dasbach EJ, Copley-Merriman C, Maier W, et al. Model of complications of NIDDM. II. Analysis of the health benefits and cost-effectiveness of treating NIDDM with the goal of normoglycemia. Diabetes Care 1997;20:735-44. 44. Stern Z, Levy R. Analysis of direct cost of standard compared with intensive insulin treatment of insulin-dependent diabetes mellitus and cost of complications. Acta Diabetol 1996;33:48-52. 45. Rewers A, Chase HP, Mackenzie T, Walravens P, Roback M, Rewers M, et al. Predictors of acute complications in children with type 1 diabetes. JAMA 2002; 287:2511-8.
Fifty Years Ago in The Journal of Pediatrics LOEFFLER’S
PNEUMONIA ASSOCIATED WITH HYPOGAMMAGLOBULINEMIA
Aziza C, Lapin JH. J Pediatr 1957;50:296-303
Aziza and Lapin describe an infant with recurrent pneumonia, which began when the patient was 7.5 months old. The gammaglobulin level was 5.43% (reference range for age, 8.8% ⫾ 1.2%) with the Tiselius method (electrophoresis assay). Specific antibodies were anti-B 1:64, but the Schick test for measuring neutralizing antibody titer to diphtheria was not performed because the patient was not fully immunized. Intramuscular gammaglobulin (5-15mL) was administered every 2 weeks (1.7-5 g monthly). The gamma globulin level rose to 6.22% when the patient was 2.5 years old, and the level was 10.4% when the patient was 3 years old. The authors concluded that the child had, per “. . . the recent review by Good and Zak (1956) . . . transient hypogammaglobulinemia of infancy.” What amazingly astute physicians! In the intervening years, the advances in understanding, examining, and treating immunodeficiencies of what Robert A. Good called in his report “Experiments of Nature” have exploded. Quantitative levels of immunoglobulin (Ig) G (and 4 IgG subclasses), IgA (and 2 IgA subclasses), IgM, IgE, and IgD have been identified. Immunological responses of T cell and B cell responses to protein, polysaccharide, and lipid antigens is appreciated. Identification and function of T cells, T cell subpopulations, B cells, B cell subpopulations, and natural killer studies is routine. The authors measured properdin of the complement pathway; 3 complement pathways have since been described (classical, alternate, and mannose binding lectin). Molecules of the innate immune system have been described and are routinely examined, so-called pathogen associated molecular pattern molecules. The World Health Organization–International Union of Immunologic Societies has categorized primary immunodeficiency diseases into 8 categories.1 Twenty separate B cell immunodeficiency disorders have been described, with the genetic defect identified in many. Transient hypogammaglobulinemia of infancy is still a recognized primary B cell immunodeficiency. The treatment of hypogammaglobulinemia has also evolved. Intramuscular gammaglobulin was the standard treatment until intravenous gamma globulin was licensed for use in the early 1980s.2 This allowed for the first time an increase in the dosage of gamma globulin used to control the infections. The current recommended dosage is 300 to 600 mg/kg/month, which is approximately what I estimate that this patient received at the high end. It is fascinating, however, that investigators led by Melvin Berger began administrating intramuscular gammaglobulin subcutaneously. In 2006, there is a licensed subcutaneous gammaglobulin preparation (Vivaglobulin) available for the treatment of patients with B-cell immunodeficiencies. Alan P. Knutsen, MD Pediatric Allergy and Immunology Saint Louis University St. Louis, Missouri 10.1016/j.jpeds.2006.09.036
REFERENCES 1. Notarangelo L, Casanova JL, Conley ME, Chapel H, Fischer A, Puck J, et al. International Union of Immunological Societies Primary Immunodeficiency Diseases Classifications Committee. Primary immunodeficiency diseases: an update from the International Union of Immunological Societies Primary Immunodeficiency Diseases Classification Committee Meeting in Budapest, 2005. J Allergy Clin Immunol 2006;117:883-96. 2. Durandy A, Wahn V, Petteway S, Gelfand EW. Immunoglobulin replacement therapy in primary antibody deficiency diseases—maximizing success. Int Arch Allergy Immunol 2005;136:217-29.
Temporal Trends in the Treatment of Pediatric Type 1 Diabetes and Impact on Acute Outcomes
285
43. Eastman RC, Javitt JC, Herman WH, Dasbach EJ, Copley-Merriman C, Maier W, et al. Model of complications of NIDDM. II. Analysis of the health benefits and cost-effectiveness of treating NIDDM with the goal of normoglycemia. Diabetes Care 1997;20:735-44. 44. Stern Z, Levy R. Analysis of direct cost of standard compared with intensive insulin treatment of insulin-dependent diabetes mellitus and cost of complications. Acta Diabetol 1996;33:48-52. 45. Rewers A, Chase HP, Mackenzie T, Walravens P, Roback M, Rewers M, et al. Predictors of acute complications in children with type 1 diabetes. JAMA 2002; 287:2511-8.
Fifty Years Ago in The Journal of Pediatrics LOEFFLER’S
PNEUMONIA ASSOCIATED WITH HYPOGAMMAGLOBULINEMIA
Aziza C, Lapin JH. J Pediatr 1957;50:296-303
Aziza and Lapin describe an infant with recurrent pneumonia, which began when the patient was 7.5 months old. The gammaglobulin level was 5.43% (reference range for age, 8.8% ⫾ 1.2%) with the Tiselius method (electrophoresis assay). Specific antibodies were anti-B 1:64, but the Schick test for measuring neutralizing antibody titer to diphtheria was not performed because the patient was not fully immunized. Intramuscular gammaglobulin (5-15mL) was administered every 2 weeks (1.7-5 g monthly). The gamma globulin level rose to 6.22% when the patient was 2.5 years old, and the level was 10.4% when the patient was 3 years old. The authors concluded that the child had, per “. . . the recent review by Good and Zak (1956) . . . transient hypogammaglobulinemia of infancy.” What amazingly astute physicians! In the intervening years, the advances in understanding, examining, and treating immunodeficiencies of what Robert A. Good called in his report “Experiments of Nature” have exploded. Quantitative levels of immunoglobulin (Ig) G (and 4 IgG subclasses), IgA (and 2 IgA subclasses), IgM, IgE, and IgD have been identified. Immunological responses of T cell and B cell responses to protein, polysaccharide, and lipid antigens is appreciated. Identification and function of T cells, T cell subpopulations, B cells, B cell subpopulations, and natural killer studies is routine. The authors measured properdin of the complement pathway; 3 complement pathways have since been described (classical, alternate, and mannose binding lectin). Molecules of the innate immune system have been described and are routinely examined, so-called pathogen associated molecular pattern molecules. The World Health Organization–International Union of Immunologic Societies has categorized primary immunodeficiency diseases into 8 categories.1 Twenty separate B cell immunodeficiency disorders have been described, with the genetic defect identified in many. Transient hypogammaglobulinemia of infancy is still a recognized primary B cell immunodeficiency. The treatment of hypogammaglobulinemia has also evolved. Intramuscular gammaglobulin was the standard treatment until intravenous gamma globulin was licensed for use in the early 1980s.2 This allowed for the first time an increase in the dosage of gamma globulin used to control the infections. The current recommended dosage is 300 to 600 mg/kg/month, which is approximately what I estimate that this patient received at the high end. It is fascinating, however, that investigators led by Melvin Berger began administrating intramuscular gammaglobulin subcutaneously. In 2006, there is a licensed subcutaneous gammaglobulin preparation (Vivaglobulin) available for the treatment of patients with B-cell immunodeficiencies. Alan P. Knutsen, MD Pediatric Allergy and Immunology Saint Louis University St. Louis, Missouri 10.1016/j.jpeds.2006.09.036
REFERENCES 1. Notarangelo L, Casanova JL, Conley ME, Chapel H, Fischer A, Puck J, et al. International Union of Immunological Societies Primary Immunodeficiency Diseases Classifications Committee. Primary immunodeficiency diseases: an update from the International Union of Immunological Societies Primary Immunodeficiency Diseases Classification Committee Meeting in Budapest, 2005. J Allergy Clin Immunol 2006;117:883-96. 2. Durandy A, Wahn V, Petteway S, Gelfand EW. Immunoglobulin replacement therapy in primary antibody deficiency diseases—maximizing success. Int Arch Allergy Immunol 2005;136:217-29.
Temporal Trends in the Treatment of Pediatric Type 1 Diabetes and Impact on Acute Outcomes
285