Archives of Internal Medicine

MÖLLERSTRÖM, JAKOB

doi: 10.1001/archinte.1933.00160050002001pmid: N/A

Abstract If a diabetic patient is kept on a constant diet somewhat above his carbohydrate tolerance, with other conditions of life, particularly exercise, also constant, the amount of sugar excreted nevertheless will vary from day to day. If frequent samples of urine are examined, the excretion of sugar will be found to vary somewhat, independently of the meals. Some meals are followed by an immediate glycosuria, while others are followed by a slight increase or none. Closer investigation reveals these variations as expressions of a regular daily periodicity. Often in diabetic patients there is a minimum excretion of sugar around noon, even with a constant diet. In severe diabetes during starvation, Hatlehol1 found a continuous decrease in the sugar content during the day and an increase during the night, often with the greatest excretion in the early morning hours. When first encountered, these phenomena were puzzling and inexplicable. Now light References 1. Hatlehol: Acta med. Scandinav. ( (supp. 8) ), 1924, p. 1.. 2. Forsgren: Klin. Wchnschr. 8:1110, 1929Crossref 3. Acta med. Scandinav. 73:60, 1930. 4. Holmgren: Ztschr. f. mikr.-anat. Forsch. 24:632, 1931. 5. Ågren, Wilander and Jorpes: Biochem. J. 25:777, 1931. 6. Pfaff and Balch: J. Exper. Med. 2:49, 1897.Crossref 7. Mann, F. C., and Magath, T. B.: Studies on the Physiology of the Liver , Arch. Int. Med. 30:73 ( (July) ) 1922.Crossref 8. Helly: Ztschr. f. exper. Path. u. Therap. 15:464, 1914.Crossref 9. Paulesco: Compt. rend. Soc. de biol. 83:562, 1920. 10. Petrén: Diabetes Studier , Copenhagen, Gyldendalske Boghandel, 1923. 11. The Albert biscuit is a standard biscuit used in Sweden, with the following constant composition per hundred grams: protein, 11 Gm.; fat, 4.6 Gm., and carbohydrate, 73.30 Gm., corresponding to 388 calories. Each biscuit has a weight of about 9 Gm. 12. Möllerström, J.: Acta Soc. med. suecanae 56:211, 1930. 13. Seyderhelm and Oestreich: Ztschr. f. klin. Med. 109:35, 1928.

JORDAN, WILLIAM R.

doi: 10.1001/archinte.1933.00160050017002pmid: N/A

Abstract INCIDENCE Extreme rarity of the coexistence of diabetes mellitus and epilepsy apparently has been accepted as a fact. According to Talbot (1930), "Study of the literature has so far failed to reveal a single report of the coincidence of idiopathic epilepsy and true diabetes mellitus." Trumper (1930) maintained that the theoretical incidence of epilepsy in persons with diabetes should be extremely small because of the ketosis and dehydration which are so constantly associated with diabetes and which are so antagonistic to epilepsy. Joslin (1928), writing about epilepsy, stated, "No clear cut case can be found among my 6,000 glycosurias of whom 5,086 are true diabetics." He did, however, mention several possible cases of epilepsy. Subsequent study of Joslin's diabetic patients furnishes the material for the present report.Bolduan (1932) stated that 2.5 per cent of all deaths in New York City in 1931 were due to diabetes; and Weeks and References 1. Lennox and Cobb (1928) 2. Weston (1916) 3. Heidema (1919) 4. Schwab (1922) 5. Kooy (1919) 6. Olmsted and Gay (1922) 7. Weeks and co-workers (1923) 8. Holmström (1924) 9. Nielson (1925) 10. Drury and Farren-Ridge (1925) 11. Lennox, O'Connor and Bellinger (1927) 12. Lennox and Bellinger (1927) 13. Osnato and co-workers (1927) 14. Munch-Petersen (1928) 15. Felsen (1930) 16. MacKay and Barbash (1930). 17. There is among our diabetic patients one (case 11252) with epilepsy which is attributed to a tumor of the brain by reason of headache, vomiting and papilledema. She has just been transferred to the neurosurgical service at the Boston City Hospital. This case is not included in the present series. Nor are two other cases, case 5367, which is one of definite epilepsy with glycosuria but without proved diabetes, and case 2364. The latter is that of a young man of 22 years, who had been subject to nocturnal convulsions, presumably of hypoglycemic origin; on one occasion he had a convulsion at 5:45 a. m., eleven and three-quarter hours after his previous dose of insulin, a time at which he usually excreted much sugar. 18. Hoeffel and Moriarty (1924) 19. Shaw and Moriarty (1924) 20. Talbot, Metcalf and Moriarty (1927) 21. Peterman (1927 and 1928) 22. Lennox and Cobb (1928) 23. Lennox (1928) 24. Geyelin (1929) 25. McQuarrie (1929) 26. McQuarrie and Husted (1929) 27. Higgins (1930) 28. Talbot (1930) 29. Helmholz and Keith (1930) 30. Barborka (1930) 31. Fay (1930) 32. Doolittle (1931) 33. Bridge and Iob (1931). 34. Weir, Larson and Rowntree (1922) 35. Gamble, Ross and Tisdall (1923) 36. Rowntree (1926) 37. Lennox (1928) 38. Lennox, Nelson and Beetham (1929) 39. Gamble (1929) 40. Bridge and Iob (1931) 41. Mcquarrie and Peeler (1931). 42. Peterman (1927) 43. Nelson (1928) 44. McQuarrie (1929) 45. Higgins (1930) 46. Barborka (1930) 47. Guthrie (1930) 48. Greer (1930) 49. Regan (1931). 50. Allan, F. N.: Survey of a Year's Work with Diabetic Patients , Proc. Staff Meet., Mayo Clin. 7:137, 1932. 51. Allen, F. M., and Wishart, M. B.: Experimental Studies in Diabetes , J. Metab. Research 4:613, 1923. 52. Anderson, B.: Insulin Poisoning and Babinski Toe Reflex , Ugesk. f. læger 93:5, 1931. 53. André and Baylac: Cited by Labbé. 54. Andrews, E., and Schlegel, K. W.: Water Metabolism: Effect of Varying Degrees of Hydration on Sugar Metabolism , Arch. Int. Med. 40:637 ( (Nov.) ) 1927.Crossref 55. Barborka, C. J.: Epilepsy in Adults: Results of Treatment by Ketogenic Diet in One Hundred Cases , Arch. Neurol. & Psychiat. 23:904 ( (May) ) 1930. 56. Behrendt, H., and Hopmann, R.: Ueber nichttetanoide Erregbarkeits-Veränderungen , Klin. Wchnschr. 3: 2233, 1924. 57. Block, E. B.: The Relation of Organic Brain Disease to Epilepsy , Ann. Int. Med. 2:531, 1928-1929. 58. Bloor, W. R.: Diet and the Blood Lipids , Proc. Soc. Exper. Biol. & Med. 28:701, 1931. 59. Blotner, H.: Coronary Disease in Diabetes Mellitus , New England J. Med. 203: 709, 1930. 60. Blum, L.: Dangers des injections intraveineuses alcalines; action toxique du sodium , Semaine méd. 31:433, 1911. 61. Symptomatologie und Therapie des Coma Diabeticum , Ergebn. d. inn. Med. u. Kinderh. 11:442, 1913. 62. Bolduan, C.: Diabetes an Important Health Problem , New England J. Med. 207:49, 1932. 63. Bridge, E. M., and Iob, L. V.: The Mechanism of the Ketogenic Diet in Epilepsy , Bull. Johns Hopkins Hosp. 48:373, 1931. 64. Carr, A. D.; Parker, R.; Grove, E.; Fisher, A. O., and Larimore, J. W.: Hyperinsulinism from B.-Cell Adenoma of the Pancreas , J. A. M. A. 96:1363 ( (April 25) ) 1931. 65. Chauffard, A., and Rendu, H.: Un cas d'éclampsie diabétique , Rev. de méd. 32:161, 1912. 66. Clark, A. L.: Bacilluria Under Ketogenic Treatment , Proc. Staff Meet., Mayo Clin. 7:257, 1932. 67. Claude, H., and Rafflin, R.: Vertiges épileptiques et acidose , Encéphale 23:239, 1928. 68. Collip, J. B.: The Parathyroid Glands , Medicine 5:1, 1926. 69. Doolittle, G. J.: Report of Results from Use of Ketogenic Diet and Ketogenic Diet with Water Restriction in a Series of Epileptics , Psychiat. Quart. 5:135 and 225, 1931. 70. Drabkin, D. L., and Shilkret, H.: Insulin Anhydremia, Importance of Water Reservoir in Physiological Crisis , Am. J. Physiol. 83:141, 1927. 71. Drury, K. K., and Farren-Ridge, C.: Observations on Types of Blood Sugar Curves Found in Insanity , J. Ment. Sc. 71:8, 1925. 72. Dufourt, E.: La question des convulsions dans le coma diabétique , Province méd. , 22: 211, 1911. 73. Fay, T.: Therapeutic Effect of Dehydration on Epileptic Patients , Arch. Neurol. & Psychiat. 23:920 ( (May) ) 1930. 74. Felsen, J.: Laboratory Studies in Epilepsy , Arch. Int. Med. 46:180 ( (Aug.) ) 1930. 75. Fincher, E. F., and Dowman, C. E.: Epileptiform Seizures of Jacksonian Character , J. A. M. A. 97:1375 ( (Nov. 7) ) 1931. 76. Gamble, J. L.: Dehydration , New England J. Med. 201:909, 1929. 77. Gamble Ross, G. S., and Tisdall, F. F.: The Metabolism of Fixed Base During Fasting , J. Biol. Chem. 57:633, 1923. 78. Geyelin, H. R.: Fasting as a Method for Treating Epilepsy , M. Rec. 99:1037, 1921. 79. Fasting and Ketogenic Diet in Epilepsy , Ann. Int. Med. 2:678, 1929. 80. Goodall, E.: Blood Cholesterol During the Menstrual and Epileptic Cycles , Lancet 1:384, 1929. 81. Gosden, M.; Fox, J. T., and Brain, W. R.: The Cholesterol of the Blood Plasma in Epilepsy , Lancet 2:12, 1929. 82. Gouget, A.: Comp. rend. Soc. de biol. , (July 8) , 1830. 83. Greer, A. E.: Pellagra-Like Lesions Due to the Ketogenic Diet , J. A. M. A. 95:863 ( (Sept. 20) ) 1930. 84. Guelpa, G., and Marie, A.: La lutte contre l'épilepsie par la désintoxication et par la rééducation alimentaire , Bull. gén. de thérap. 160:616, 1910. 85. Guthrie, R. H.: Pellagra-Like Lesions Appearing in Course of Ketogenic Diet , J. A. M. A. 95:1912 ( (Dec. 20) ) 1930. 86. Harrop, G. A.: The Production of Tetany by the Intravenous Infusion of Sodium Bicarbonate , Bull. Johns Hopkins Hosp. 30:62, 1919. 87. Healey, F. H.: Menstruation in Relation to Mental Disorders , J. Ment. Sc. 74: 488, 1928. 88. Heidema, S. T.: Blutzuckerbestimmungen bei psychiatrischen und neurologischen Patienten , Ztschr. f. d. ges. Neurol. u. Psychiat. 48:111, 1919. 89. Helmholz, H. F.: The Bactericidal Effect of Ketonurine , Proc. Staff Meet., Mayo Clin. 7:260, 1932. 90. Helmholz and Keith, H. M.: Eight Years' Experience with the Ketogenic Diet in the Treatment of Epilepsy , J. A. M. A. 95:707 ( (Sept. 6) ) 1930. 91. Hetényi, G.: Angina pectoris während Insulinbehandlung , Wien. Arch. f. inn. Med. 13:95, 1927. 92. Higgins, H. L.: Some Physiological and Clinical Effects of High Fat Feeding , New England J. Med. 203:145, 1930.Crossref 93. Hoeffel, G., and Moriarty, M.: The Effect of Fasting on the Metabolism of Epileptic Children , Am. J. Dis. Child. 28:16 ( (Jan.) ) 1924. 94. Holmström, R.: Blutzuckerbestimmungen bei Epileptikern , Upsala läkaref. förh. 29:17, 1924 95. abstr., Brit. M. J. 1:506, 1924.Crossref 96. Howland, G.; Campbell, W. R.; Maltby, E. J., and Robinson, W. L.: Dysinsulinism, Convulsions and Coma Due to Islet Cell Tumor of the Pancreas with Operation and Cure , J. A. M. A. 93:674 ( (Aug. 31) ) 1929.Crossref 97. von Jaksch, R.: Epilepsie acetonica , Ztschr. f. klin. Med. 10:362, 1886. 98. Joslin, E. P.: Treatment of Diabetes Mellitus , Philadelphia, Lea & Febiger, 1928. 99. Joslin Root, H. F., and White, P.: Diabetic Coma , M. Clin. North America 10: 1281, 1927. 100. Joslin Root, H. F.; White, P.; Jordan, W. R., and Hunt, H. M.: Diabetic Coma , M. Clin. North America 15:829, 1932. 101. Kersten, H.: Ergebnisse zur Frage des elementaren Krampfes , Ztschr. f. d. ges. Neurol. & Psychiat. 63:48, 1921. 102. Kooy, F. H.: Hyperglycemia in Mental Disorders , Brain 42:214, 1919. 103. Kussmaul: Zur Lehre vom Diabetes Mellitus , Deutsches Arch. f. klin. med. 14:1, 1874. 104. Labbé, M.: Epilepsie et diabète , Paris méd. 35:354 ( (May 1) ) 1920 105. L'épilepsie acidosique , Bull. et mém. Soc. méd. d. hôp. de Paris 44:810 ( (June 11) ) 1920. 106. Lawrence, R. D., and Hollins, A. S.: Two Cases of Hematuria Caused by Insulin Treatment , Brit. M. J. 1:977, 1928. 107. Lennox, W. G.: Ketogenic Diet in the Treatment of Epilepsy , New England J. Med. 199:74, 1928. 108. Studies of the Metabolism in Epilepsy: The Bicarbonate Content of the Blood , Arch. Neurol. & Psychiat. 20:155 ( (July) ) 1928. 109. —and Allen, Margaret B.: Studies in Epilepsy: IX. The Sugar Content of the Spinal Fluid , Arch. Neurol. & Psychiat. 23:521 ( (March) ) 1930. 110. —and Bellinger, Margaret: Repeated Blood Sugar Curves in Non-Diabetic Subjects , J. Clin. Investigation 4:331, 1927. 111. — Studies of Metabolism in Epilepsy: III. The Blood Sugar Curve , Arch. Neurol. & Psychiat. 18:395 ( (Sept.) ) 1927. 112. —and Cobb, S.: Epilepsy , Medicine 7:105, 1928. 113. Studies in Epilepsy: VIII. The Clinical Effect of Fasting , Arch. Neurol. & Psychiat. 20:771 ( (Oct.) ) 1928. 114. —and Wright, L. H.: Studies in Epilepsy: VII. The Basal Metabolism , Arch. Neurol. & Psychiat. 20:764 ( (Oct.) ) 1928. 115. —Nelson, R., and Beetham, W.: Factors Affecting Convulsions Induced in Rabbits , Arch. Neurol. & Psychiat. 21:625 ( (March) ) 1929. 116. —O'Connor, Marie, and Bellinger, Margaret: Studies of Metabolism in Epilepsy: II. The Sugar Content of the Blood , Arch. Neurol. & Psychiat. 18:383 ( (Sept.) ) 1927. 117. Lepine, R.: Diabète: Accidents attribuables à une intoxication par les acides formique et oxybutyrique , Rev. de méd. , Paris 8:1004, 1888. 118. Le diabète sucré , Paris, F. Alcan, 1909. 119. Traitement de l'acétonémie diabètique , Progrès méd. 18:217, 1911. 120. Lossen, J.: Ueber das Vorkommen epileptischer Krämpfe beim Coma der Diabetiker , Ztschr. f. klin. Med. 56:31, 1905. 121. Lyons, C.: Emotional Hypercholesterolemia , Am. J. Physiol. 98:156, 1931. 122. MacKay, G. W. J., and Barbash, H.: The Glucose Tolerance Curve in Epilepsy , J. Ment. Sc. 77:83, 1931. 123. MacLeod, J. J. R.: Carbohydrate Metabolism and Insulin , London, Longmans, Green & Co., 1926. 124. The Fuel of Life , Princeton, N. J., Princeton University Press, 1928. 125. McQuarrie, I.: Protein Metabolism of Children on Diets Extremely Low in Carbohydrate , J. Nutrition 2:31, 1929. 126. McQuarrie and Husted, C.: Epilepsy in Children: Relation of Water Balance to Occurrence of Seizures , Am. J. Dis. Child. 38:451 ( (Sept.) ) 1929. 127. McQuarrie and Peeler, D. B.: The Effect of Sustained Pituitary Antidiuresis and Forced Water Drinking in Epileptic Children , J. Clin. Investigation 10:915, 1931. 128. Munch-Petersen, C. J.: Recherches sur le métabolisme des hydrates de carbone chez les épileptiques , Compt. rend. Soc. de biol. 98:891, 1928. 129. Munch-Petersen Boyd, J. D., and Nelson, M. V.: Calcium and Phosphorus Metabolism of Epileptic Children Receiving a Ketogenic Diet , Am. J. Dis. Child. 36:716 ( (May) ) 1928. 130. Nielson, J. M.: Etiology of Epileptiform Convulsions , M. J. & Rec. ( (Supp.) ) 122:338, 1925. 131. Okey, R., and Robb, E. J.: Studies in the Metabolism of Women: Variations in the Fasting Blood Sugar Level and Sugar Tolerance in Relation to the Menstrual Cycle , J. Biol. Chem. 65:165, 1925. 132. Olkon, D. M.: "Genuine Epilepsy": Studies of the Microscopic Changes in the Capillary System as a Probable Etiologic Factor , J. Nerv. & Ment. Dis. 72:538, 1930. 133. Olmstead, J. M. D., and Taylor, A. C.: The Effect of Insulin on the Blood , Am. J. Physiol. 69:142, 1924. 134. Olmsted, W. H., and Gay, L. P.: Study of Blood Sugar Curves Following a Standardized Glucose Meal , Arch. Int. Med. 29:384 ( (March) ) 1922. 135. Osnato, M.; Killian, J. A.; Garcia, T., and Mattice, M. R.: Comparative Chemical Studies of the Blood and Spinal Fluid in Epilepsy , Brain 50:581, 1927. 136. Parsonnet, A. E., and Hyman, A. S.: Insulin Angina , Ann. Int. Med. 4:1247, 1931.Crossref 137. Partridge, J. C.: Epilepsy and the Endocrines , Am. J. Psychiat. 8:137, 1928. 138. Patterson, H. A.: Some Laboratory Findings in Epilepsy , New York State J. Med. 29:138, 1929. 139. Peterman, M. G.: Epilepsy in Childhood , J. A. M. A. 88:1868 ( (June 11) ) 1927.Crossref 140. The Ketogenic Diet , Peterman J. A. M. A. 90:1427 ( (May 5) ) 1928.Crossref 141. Convulsions in Childhood , Peterman J. A. M. A. 99:546 ( (Aug. 13) ) 1932.Crossref 142. Pezzali, G.: Ricerche sul contenuto del sangue in azoto (residuo), cloruri, colesterina, grassi, glucosi, indicano e calcio nell'epilessia , Riforma med. 39:433, 1923. 143. Rabinowitch, I. M.: Clinical and Laboratory Experiences with High Carbohydrate-Low Calorie Diets in Treatment of Diabetes Mellitus , New England J. Med. 204:799, 1931.Crossref 144. Regan, J. R.: Pellagra-Like Syndrome Occurring in Course of Ketogenic Diet Deficient in Protein , Wisconsin M. J. 30:554, 1931. 145. Riesman, D., and Fitz-Hugh, T.: Epilepsia Tarda , Ann. Int. Med. 1:273, 1927.Crossref 146. Robinson, S. H. G.; Brain, W. R., and Kay, H. D.: Association of Low Blood Cholesterol with Occurrence of Fits in Epileptics , Lancet 2:325, 1927.Crossref 147. Rome, R.: Existe-t-il une épilepsie Jacksonienne essentielle? Rev. de méd. , Paris (spec. no.) 31:741, 1911. 148. Root, H. F., and Graybiel, A.: Angina Pectoris and Diabetes Mellitus , J. A. M. A. 96:925 ( (March 21) ) 1931.Crossref 149. Rowntree, L. G.: Effects on Mammals of Administration of Excessive Quantities of Water , J. Pharmacol. & Exper. Therap. 29:135, 1926. 150. Scheube: Ztschr. f. Heilk. , 1878. 151. Labbé. Clin. 2: 307, 1921. 152. Schwab, S. I.: Diagnostic Values of Blood Sugar Curves in Neurology , Arch. Neurol. & Psychiat. 8:401 ( (Oct.) ) 1922. 153. Shaw, E. B., and Moriarty, M.: Hypoglycemia and Acidosis in Fasting Children with Idiopathic Epilepsy , Am. J. Dis. Child. 28:553 ( (Nov.) ) 1924. 154. Shera, G.: Investigation of the Acid-Base Balance in Mental Cases, with Special Reference to Epilepsy , J. Ment. Sc. 74:454, 1928. 155. Souques, A.: Epilepsie et menstruation , Presse méd. 39:185, 1931. 156. Spielmeyer, W.: Anatomic Substratum of the Convulsive State , Arch. Neurol. & Psychiat. 23:869 ( (May) ) 1930. 157. Stadelmann, E.: Weitere Beiträge zur Behandlung des Diabetes mellitus und des Coma diabeticum , Deutsches Arch. f. klin. Chir. 37:580, 1885. 158. Klinisches und Experimentelles über Coma diabeticum und seine Behandlung , Deutsche med. Wchnschr. 15:938, 1889.Crossref 159. Stauder, A.: Epileptiforme Krämpfe bei Diabetes mellitus , München. med. Wchnschr. 53:1719, 1906. 160. Talbot, F. B.: Treatment of Epilepsy , New York, The Macmillan Company, 1930. 161. Talbot Metcalf, K. M., and Moriarty, M.: Epilepsy: Chemical Investigations of Rational Treatment by Production of Ketosis , Am. J. Dis. Child. 33:218 ( (Feb.) ) 1927.Crossref 162. Tileston, W., quoted by Palmer, W. W., and Van Slyke, D. D.: J. Biol. Chem. 32:499, 1917. 163. Tracy, E. A.: The White Spots of Epilepsy , Boston, Richard T. Howard, 1926. 164. Trumper, M.: Epilepsy vs. Diabetes , Pennsylvania M. J. 34:18, 1930. 165. Wahl, E. F.: The Significance of Cerebrospinal Fluid Sugar , Arch. Int. Med. 48:446 ( (Sept.) ) 1931.Crossref 166. Waltner, K.: Insulin und galvanische Erregbarkeit , Klin. Wchnschr. 4:168, 1925.Crossref 167. Weeks, D. F.; Allen, F. M.; Renner, D. S., and Wishart, M. B.: Fasting and Diets in Epilepsy , J. Metab. Research 3:317, 1923. 168. Weir, J. F.; Larson, E. E., and Rowntree, L. G.: Studies in Diabetes Insipidus, Water Balance, and Water Intoxication , Arch. Int. Med. 29:306 ( (March) ) 1922.Crossref 169. Weston, P. G.: Sugar Content of the Blood and Spinal Fluid of Insane Subjects , J. M. Research 35:199, 1916. 170. White, P.: Diabetes in Childhood and Adolescence , Philadelphia, Lea & Febiger, 1932. 171. Wilbur, L. L.: Acidosis: Experimental Evidence That Its Nervous Symptoms Are Not Wholly Due to Lack of Alkali , J. A. M. A. 43:1228 ( (Oct. 22) ) 1904.Crossref 172. Wilder, R. M.: The Effect of Ketonemia on the Course of Epilepsy , Bull. Mayo Clin. 2:307, 1921. 173. Wladyczko, S.: La cure sucrée dans l'épilepsie , Presse méd. 33:1475 ( (Nov. 7) ) 1925. 174. Wohlwill, F.: Ueber Hirnbefunde bei Insulin-Ueberdosierung , Klin. Wchnschr. 7:344, 1928.Crossref 175. Woodyatt, R. T.: The Clinical Use of Insulin , J. Metab. Research 2:793, 1922.

WEIR, JAMES F.;COMFORT, MANDRED W.

doi: 10.1001/archinte.1933.00160050038003pmid: N/A

Abstract Shortly after the introduction of cinchophen into the therapeutic armamentarium, patients revealing toxic effects were observed, and their cases were reported in the literature. In 1922, Schroeder1 reported a series of cases, and urged caution in the use of the drug. In 1923, Worster-Drought2 first reported the occurrence of jaundice as a toxic manifestation. The toxic symptoms are of various types: cutaneous, anaphylactoid, gastro-intestinal, cardiac, renal and hepatic. An extensive review of the question of the toxicity of cinchophen is being prepared by our colleague, Dr. Hench.3 In this paper we are concerned only with cases in which there were hepatic manifestations. We have been able to find 98 cases reported in the literature, exclusive of those previously reported from the Mayo Clinic. The latter cases, together with others reported now for the first time, total 19, in 5 of which the results were fatal. This gives References 1. Schroeder, K.: Cases of Cinchophen Poisoning , Ugesk. f. laeger 84:1141 ( (Sept. 7) ) 1922. 2. Worster-Drought, Cecil: Atophan Poisoning , Brit. M. J. 1:148 ( (Jan. 27) ) 1923.Crossref 3. Hench, P. S.: Derivatives of Cinchophen and Their Toxicity , Proc. Staff Meet., Mayo Clin. 7:427 ( (July 20) ) 1932. 4. Nicolaier, Arthur, and Dohrn, Max: Ueber die Wirkung von Chinolincarbonsäuren und ihrer Derivate auf die Ausscheidung der Harnsäure , Deutsches Arch. f. klin. Med. 93:331, 1908. 5. Brugsch, Theodor, and Horsters, Hans: Cholerese und Choleretica, ein Beitrag zur Physiologie der Galle , Ztschr. f. d. ges. exper. Med. 38:367, 1923.Crossref 6. Davis.12 7. Dassen, Rodolfo: Sobre la acción hepatotóxica de los derivados de la fenilquinoleina , Semana méd. 36:368 ( (Feb. 14) ) 1929. 8. Nathorf and Willert, quoted by Adler, A.: Therap. d. Gegenw. 67:174 ( (April) ) 1926. 9. Weiss, Samuel: Acute Yellow Atrophy of the Liver: Acute Necrosis of the Liver , M. J. & Rec. 135:316 ( (April 6) ) 1932. 10. Pribram, quoted by Einhorn, Stewart and Ryan.9b 11. Einhorn, Max, and Stewart, W. H.: On Hepatography , M. J. & Rec. 126:430 ( (Oct. 5) ) 1927. 12. Einhorn, Max; Stewart, W. H., and Ryan, E. J.: Experiences with Biloptin (Diiodoatophan) for Cholecystography by Oral or Duodenal Method , M. J. & Rec. 125:457 ( (April 6) ) 1927. 13. Spurling, R. G., and Hartman, E. E.: Serum-Colorimetry and Other Evidence of the Choleretic Action of Tolysin (Ethyl Ester of ParamethylPhenylcinchoninic Acid) in Man , J. Lab. & Clin. Med. 13:854 ( (June) ) 1928. 14. Lichtman, S. S.: Cinchophen Oxidation Test of the Function of the Hepatic Cells , Arch. Int. Med. 48:98 ( (July) ) 1931. 15. Davis, J. S., Jr.: The Relation of Neocinchophen to the Question of Cinchophen Toxicity , Am. J. M. Sc. 184:555 ( (Oct.) ) 1932. 16. Biberfeld, J.: Zur Wirkungsweise des Atophans , Ztschr. f. exper. Path. u. Therap. 13:301, 1913. 17. Cabot, R. C., and Cabot, Hugh: Case Records of Massachusetts General Hospital: Case 11231; Acute Yellow Atrophy , Boston M. & S. J. 192:1122 ( (June 4) ) 1925. 18. Brown, W. L.: Atophan Derivatives in Rheumatism: A Caution , Brit. M. J. 2:37 ( (July 3) ) 1926. 19. Graham, George: The Treatment of Gout , Proc. Roy. Soc. Med. (Sect. Therap. & Pharmacol.) 20:1 ( (Jan.) ) 1927. 20. Evans, Geoffrey: Atophan Derivatives in Rheumatism , Brit. M. J. 2:93 ( (July 10) ) 1926. 21. Glover, L. G.: Atophan-Derivatives in Rheumatism , Brit. M. J. 2:136 ( (July 17) ) 1926. 22. Willcox, W. H.: Atophan Derivatives in Rheumatism , Brit. M. J. 2:273 ( (Aug. 7) ) 1926. 23. Wells, C. J. L.: Atophan Derivatives in Rheumatism , Brit. M. J. 2:759 ( (Oct. 23) ) 1926.Crossref 24. Klinkert, D.: Gelbsucht als Folge längeren Gebrauchs von Atophan , Therap. d. Gegenw. 67:334, 1926. 25. Kinkert, D.: Gelbsucht als Folge längeren Gebrauches von Atophan , Klin. Wchnschr. 6:24 ( (Jan. 1) ) 1927.Crossref 26. Kingreen, Otto: Vorsicht bei der Verabreichung von Dijodatophan (Biloptin) , Deutsche med. Wchnschr. 1:971 ( (June 3) ) 1927.Crossref 27. Hitzenberger, K.: Acute Leberatrophie nach Biloptin , Wien. klin. Wchnschr. 40:205 ( (Feb. 17) ) 1927. 28. Schwartz, G.: Schweren Ikterus nach "Biloptin," Wien. klin. Wchnschr. 40:238 ( (Feb. 17) ) 1927. 29. In discussion on Schwartz.25 30. Rake, G. W.: A Case of Subacute Yellow Atrophy Following the Taking of Atophan , Guy's Hosp. Rep. 77:229 ( (April) ) 1927. 31. de Rezende, Cassio: Rheumatismo atophan e ictericia , Brasil-med. 41:1005 ( (Sept. 24) ) 1927. 32. Rabinowitz, M. A.: Toxic Hepatitis and Hepatolysis Following the Use of Atophan , M. Clin. North America 11:1025 ( (Jan.) ) 1928. 33. Weil, Paul: Leberatrophie nach Atophanbehandlung? Ein Obergutachten , Med. Welt 2:257 ( (Feb. 18) ) 1928. 34. Klinkert, D.: Atophantherapie und Leber , Therap. d. Gegenw. 69:140, 1928. 35. Lowenthal, L. J. A.; Mackay, W. A., and Lowe, E. C.: Two Cases of Acute Yellow Atrophy of the Liver Following Administration of Atophan , Brit. M. J. 1:592 ( (April 7) ) 1928.Crossref 36. London Letter: The Danger of Atophan , J. A. M. A. 90:1229 ( (April 14) ) 1928. 37. Sutton, D. C.: Acute Yellow Atrophy of the Liver Following the Taking of Cinchophen: Report of a Case , J. A. M. A. 91:310 ( (Aug. 4) ) 1928.Crossref 38. Motzfeldt, K.: Cinchophen and Jaundice , Norsk mag. f. laegevidensk. 90:283 ( (March) ) 1929. 39. Braun, L. I.: Jaundice with Ascites, Due to Intravenous Atophanyl Injections , J. M. A. South Africa 3:157 ( (March 23) ) 1929. 40. Frenzel, W. C.: Liver: Subacute Yellow Atrophy Due to Cinchophen Poisoning: Report of a Case , Wisconsin M. J. 28:264 ( (June) ) 1929. 41. Anderson, S. D., and Teter, D. P.: Acute Yellow Atrophy of the Liver Following Administration of Oxyl Iodide , J. A. M. A. 93:93 ( (July 13) ) 1929.Crossref 42. Reichle, H. S.: Toxic Cirrhosis of Liver Due to Cinchophen , Arch. Int. Med. 44:281 ( (Aug.) ) 1929.Crossref 43. Liedberg, Nils: Atophan Icterus , Hygiea 91:801 ( (Dec. 15) ) 1929. 44. Fink, A. I.: Cinchophen Poisoning in Allergic Individuals: Report of Two Cases , J. Allergy 1:280 ( (March) ) 1930.Crossref 45. Tak, P.: Dangers of Atophan , Nederl. tijdschr. v. geneesk. 74:1744 ( (April 5) ) 1930. 46. Rabinowitz, M. A.: Atrophy of the Liver Due to Cinchophen Preparations , J. A. M. A. 95:1228 ( (Oct. 25) ) 1930.Crossref 47. Grolnick, Max: Toxic Hepatitis Due to Cinchophen Containing Patent Medicine , M. J. & Rec. 132:240 ( (Sept. 3) ) 1930. 48. Lambert, Alexander, in discussion on Rabinowitz.43 49. Parsons, Lawrence, and Harding, W. G., Jr.: Cinchophen (Atophan) Poisoning: Report of Four Cases , Am. J. M. Sc. 181:115 ( (Jan.) ) 1931. 50. Walker, W. G.: Cinchophen and Acute Yellow Atrophy of the Liver: Report of Two Cases , New England J. Med. 204:253 ( (Feb. 5) ) 1931. 51. Ross, J. B.: Liver Damage Following Cinchophen Preparations, with a Report of Five Cases , Canad. M. A. J. 24:632 ( (May) ) 1931. 52. Sherwood, K. K., and Sherwood, H. H.: Acute Toxic Hepatitis (Acute Yellow Atrophy) Due to Cinchophen: Report of a Case , Arch. Int. Med. 48:82 ( (July) ) 1931. 53. Willcox, William: Toxic Jaundice , Lancet 2:57 ( (July 11) ) 1931. 54. Cabot, R. C.: Case Records of Massachusetts General Hospital: Case 17291; Four Months' Pain in the Legs and Five Days' Edema Below the Waist , New England J. Med. 205:153 ( (July 16) ) 1931. 55. Eimer, Karl: Atophanvergiftung und ihre Behandlung , Deutsche med. Wchnschr. 57:1663 ( (Sept. 25) ) 1931. 56. Bogen, Emil: Cinchophen Poisoning: Report of Case , California & West. Med. 35:269 ( (Oct.) ) 1931. 57. Elliot, A. H.: Toxic Cirrhosis of the Liver from "Oxyl-Iodide": Report of Case , J. A. M. A. 97:1384 ( (Nov. 7) ) 1931. 58. Gargill, S. L.: Cinchophen Poisoning: A Report of Three Cases , New England J. Med. 206:183 ( (Jan. 28) ) 1932. 59. Lind, S. C.: Report of a Case of Acute Yellow Atrophy of the Liver Due to the Use of a Small Amount of Cinchophen , Ohio State M. J. 28:28 ( (Jan.) ) 1932. 60. Weis, C. R.: Toxic Cirrhosis of the Liver Due to Cinchophen Compounds: Report of Three Fatal Cases , J. A. M. A. 99:21 ( (July 2) ) 1932. 61. Berger, S. S., and Schweid, H. H.: Cinchophen Poisoning in a Diabetic with Induction of Hypoglycemia , M. J. & Rec. 136:50 ( (July 20) ) 1932. 62. Reah, T. J.: Cinchophen Poisoning , Lancet 2:504 ( (Sept. 3) ) 1932. 63. Parsons, Lawrence, and Harding, W. G., Jr.: Fatal Cinchophen Poisoning: Report of Six Cases , Ann. Int. Med. 6:514 ( (Oct.) ) 1932. 64. MacGregor, D. A.: Cinchophen Poisoning, Proc. Staff Conf. , Wheeling Clin. 3:46 ( (Sept. 1) ) 1932. 65. Jones, Chester, in discussion on Cabot.51 66. Snell, A. M., and Jordan, F. M.: Intrahepatic Jaundice , Northwest Med. 29:295 ( (July) ) 1930. 67. Comfort, M. W.: Toxic Cirrhosis Due to Derivatives of Cinchophen: Report of Four Nonfatal Cases , Proc. Staff Meet., Mayo Clin. 7:419 ( (July 20) ) 1932. 68. Weir, J. F.: The Association of Jaundice and Ascites in Diseases of the Liver , J. A. M. A. 91:1888 ( (Dec. 15) ) 1928.Crossref 69. Beaver, D. C., and Robertson, H. E.: The Specific Character of Toxic Cirrhosis as Observed in Cinchophen Poisoning: A Review of Five Fatal Cases , Am. J. Path. 7:237 ( (May) ) 1931. 70. Stacy, Leda J., and Vanzant, Frances R.: Poisoning from Cinchophen , Minnesota Med. 13:327 ( (May) ) 1930. 71. Weir, J. F., and Jordan, F. M.: Clinical Consideration of Some Types of Intrahepatic Jaundice , M. Clin. North America 13:1439 ( (May) ) 1930. 72. McVicar, C. S., and Weir, J. F.: Acute Yellow Atrophy, Possibly Due to Poisoning by Atophan , M. Clin. North America 12:1526 ( (May) ) 1929. 73. Bassler, Anthony: Toxic Hepatitis due to Cinchophen , J. A. M. A. 99:495 ( (Aug. 6) ) 1932.Crossref 74. Fink.41 Eimer.52

OTTO, HAROLD L.;GOLD, HARRY;MESSELOFF, CHARLES R.

doi: 10.1001/archinte.1933.00160050078004pmid: N/A

Abstract A study of the elimination of digitalis in man was published in 1929 by Gold and DeGraff.1 The subjects were ambulatory patients with auricular fibrillation and moderate congestive heart failure. Slowing of the ventricular rate (depression of the auriculoventricular conduction) and the relief of the circulatory failure served as the criteria of the action of digitalis. It was found that during the first few weeks a fixed daily dose of digitalis produced progressive slowing of the ventricular rate, but that after this period the rate remained constant, although the same daily dose was continued without interruption for many weeks. A typical record obtained in the study is reproduced in chart 1. The facts were interpreted in the following manner: The progressive slowing of the ventricular rate in the first period was understood to indicate that the patient was not excreting completely each daily dose of 3 grains (0.2 Gm.), References 1. Gold, H., and DeGraff, A. C.: Studies on Digitalis in Ambulatory Cardiac Patients: II. The Elimination of Digitalis in Man , J. Clin. Investigation 6:613 ( (Feb.) ) 1929.Crossref 2. In the twenty-sixth week five doses were omitted because the patient failed to return in time to obtain an adequate supply. 3. Hatcher, R. A.: The Persistence of Action of the Digitalins , Arch. Int. Med. 10:268 ( (Sept.) ) 1912.Crossref 4. Gold, H.: Digitalis Elimination , Arch. Int. Med. 32:779 ( (Nov.) ) 1923.Crossref 5. Bromer, A. W., and Blumgart, H. L.: The Maintenance Dose of Digitalis , J. A. M. A. 92:204 ( (Jan. 19) ) 1929.Crossref 6. Pardee, H. E. B.: The Continued Use of Digitalis , New York State J. Med. 22: 131 ( (March) ) 1922. 7. Gold, H., and DeGraff, A. C.: Studies on Digitalis in Ambulatory Cardiac Patients. IV. Newer Principles of Digitalis Dosage , J. A. M. A. 95: 1237 ( (Oct. 25) ) 1930.Crossref

CHANUTIN, ALFRED;BARKSDALE, EDWIN E.

doi: 10.1001/archinte.1933.00160050092005pmid: N/A

Abstract It has long been recognized that hypertension is commonly accompanied by enlargement of the left ventricle. The cause for cardiac hypertrophy has been studied in recent years and the condition appears to be due solely to hypertrophy of the individual fibers rather than to hyperplasia. If this is correct, it would seem that some direct relationship between the height of the blood pressure, the degree of left ventricular enlargement and the width of the muscle fiber should exist. However, there has been surprisingly little study to establish such a relationship. To date the number of observations is insufficient to permit the application of statistical methods to this problem. Pässler and Heinecke,1 in their classic study of the relationship between cardiac hypertrophy and hypertension in partially nephrectomized dogs, employed the ratio of the weight of the left ventricle to the weight of the right ventricle as an index of hypertrophy References 1. Pässler and Heinecke: Versuche zur Pathologie des Morbus brightii , Verhandl. d. deutsch. path. Gesellsch. 9:99, 1905. 2. Karsner, H. T.; Saphir, Otto, and Todd, T. W.: Cardiac Muscle in Hypertrophy and Atrophy , Am. J. Path. 1:351 ( (July) ) 1925. 3. Mark, R. E., and Geisendörfer, H.: Untersuchungen über die Nierenfunktion: Zur Frage des Zusammenhanges von Nierenmasse, Herzhypertrophie and Blutdrucksteigerung , Ztschr. f. d. ges. exper. Med. 74:350, 1930.Crossref 4. Harrison, T. R.; Ashman, R., and Larson, R. M.: Congestive Heart Failure: XII. The Relation Between the Thickness of the Cardiac Muscle Fiber and the Optimum Rate of the Heart , Arch. Int. Med. 49:151 ( (Jan.) ) 1932.Crossref 5. Chanutin, Alfred, and Ferris, E. B., Jr.: Experimental Renal Insufficiency Produced by Partial Nephrectomy: I. Control Diet , Arch. Int. Med. 49:767 ( (May) ) 1932.Crossref 6. Frequency distribution refers to the total frequency of the fibers included in each step-interval (0.05 cm.). For example, for the left ventricle of rat 535, twelve fibers are included in the step-interval from 0.95 to 1 cm., or from 12.84 to 13.51 microns.

WOOD, FRANCIS CLARK;BELLET, SAMUEL;McMILLAN, THOMAS M.;WOLFERTH, CHARLES C.

doi: 10.1001/archinte.1933.00160050105006pmid: N/A

Abstract When acute coronary occlusion is produced in the dog, the conventional limb leads often yield an inadequate record of the change which takes place in the action current of the heart. However, when electrodes are applied in certain positions on the wall of the chest, clearly significant electrical disturbances can be recorded which may be partly or completely missed in the tracings of the limb leads.1 The electrocardiograms obtained from limb leads and chest leads supplement one another. If both are used together, a much more complete electrocardiographic picture of the effects of experimental coronary occlusion can be obtained. These results in the dog suggested the use of chest leads in the study of acute coronary occlusion in man.2 It was found that a similar situation presented itself: Chest leads yielded information that could not be obtained from limb leads. Moreover, it became evident that in certain cases References 1. Wood, F. C., and Wolferth, C. C.: An Electrocardiographic Study of Coronary Occlusion: The Inadequacy of the Three Conventional Leads in Recording Certain Characteristic Changes in Action Currents , J. Clin. Investigation 11:815 ( (July) ) 1932 2. Experimental Coronary Occlusion: Inadequacy of the Three Conventional Leads for Recording Characteristic Action Current Changes in Certain Sections of the Myocardium; an Electrocardiographic Study , Arch Int. Med. 51:771 ( (May) ) 1933.Crossref 3. Wolferth, C. C., and Wood, F. C.: The Electrocardiographic Diagnosis of Coronary Occlusion by the Use of Chest Leads , Am. J. M. Sc. 183:30 ( (Jan.) ) 1932Crossref 4. Further Observations upon the Use of Chest Leads in the Electrocardiographic Study of Coronary Occlusion , M. Clin. North America 16:161 ( (July) ) 1932. 5. These cases were obtained from the wards of the University of Pennsylvania Hospital, the Philadelphia General Hospital, the Mount Sinai Hospital and the Pennsylvania Hospital and from private practice. 6. This point has not been tested in a series of pathologic cases. It is possible that a large heart or a posterior infarct might give different results. However, in one case of probable posterior infarct, moving the posterior electrode produced no definite effect except to cause minor variations in lead VI. 7. Wolferth, C. C.: Diseases of the Heart and Blood Vessels, in Progressive Medicine , Philadelphia, Lea & Febiger, 1931, vol. 3, p. 169. 8. Bellet and McMillan: Unpublished observations. 9. The deviations of the RS-T interval and other deflections are probably magnified by the proximity of the anterior electrode to the heart. 10. Barnes, A. R., and Whitten, M. B.: Study of the R-T Interval in Myocardial Infarction , Am. Heart J. 5:142 ( (Dec.) ) 1929.Crossref 11. Wilson, F. N.; Barker, P. S.; MacLeod, A. G., and Klostermyer, L. L.: The Electrocardiogram in Coronary Thrombosis , Proc. Soc. Exper. Biol. & Med. 29:1006, 1932. 12. Fenichel, N. M., and Kugell, V. H.: The Large Q-Wave of the Electrocardiogram: A Correlation with Pathological Observations , Am. Heart J. 7:235, 1931. 13. Feil, H. S.; Katz, L. N.; Moore, R. A., and Scott, R. W.: The Electrocardiographic Changes in Myocardial Ischaemia , Am. Heart J. 6:522 ( (April) ) 1931. 14. This suggestion is based on the fact that when the experimental animal is placed in certain positions, the heart seems to twist on its pedicle of great vessels, and deviations of the RS-T interval appear. We have suspected that this was due to an angulation of one of the coronary arteries and a consequent impediment to the flow of blood through that vessel. It has seemed to us possible that this might occasionally occur in man. In fact, in certain patients with anginal pain, the assumption of the left lateral position seems to be a factor in the production of an attack. 15. Gilchrist, A. R., and Ritchie, W. T.: Ventricular Complexes in Myocardial Infarction and Fibrosis , Quart. J. Med. 23:273, 1930. 16. Unpublished observations. 17. Crawford, J. H.; Roberts, G. H.; Abramson, D. I., and Cardwell, G. C.: Localization of Experimental Ventricular Myocardial Lesions by the Electrocardiogram , Am. Heart J. 7:627 ( (June) ) 1932. 18. Barnes, A. R., and Ball, R. G.: The Incidence and Situation of Myocardial Infarction in One Thousand Consecutive Postmortem Examinations , Am. J. M. Sc. 183:215 ( (Feb.) ) 1932.

LANDIS, EUGENE M.;GIBBON, JOHN H.

doi: 10.1001/archinte.1933.00160050138007pmid: N/A

Abstract Recent advances in the surgery of the sympathetic nervous system have made it increasingly necessary to develop a simple method for determining early in the course of peripheral vascular disease whether the diminished flow of blood to an extremity is due to simple arterial spasm or to obliterative structural disease of the blood vessels. The several tests now in use, though different in method, are similar in principle. The surface temperature of the distal portion of the cool, exposed extremity is measured thermo-electrically. Dilatation of the peripheral vessels is then produced, and the rise in surface temperature is recorded. The level to which the temperature rises with complete vasodilatation has been determined in persons with normal peripheral circulation. If the surface temperature fails to reach this normal level in a room at suitable temperature, the arteries supplying the part are regarded as being unable to dilate owing to organic changes References 1. Gibbon, J. H., Jr., and Landis, E. M.: Vasodilatation in the Lower Extremlities in Response to Immersing the Forearms in Warm Water , J. Clin. Investigation 11:1019, 1932.Crossref 2. Morton, J. J., and Scott, W. J. M.: (a) Methods for Estimating the Degree of Sympathetic Vasoconstriction in Peripheral Vascular Diseases , New England J. Med. 204:955, 1931Crossref 3. The Differentiation of Peripheral Arterial Spasm and Occlusion in Ambulatory Patients , J. A. M. A. 97:1212 ( (Oct. 24) ) 1931 4. Sympathetic Activity in Certain Diseases, Especially Those of the Peripheral Circulation , Arch. Int. Med. 48:1065 ( (Dec.) ) 1931Crossref 5. Some Angiospastic Syndromes in the Extremities , Ann. Surg. 94:839, 1931Crossref 6. Lewis, T.: (a) Standard Colours for Use in the Study of Vascular Reactions of Human Skin , Heart 15:1, 1929 7. Experiments Relating to Peripheral Mechanism Involved in Spasmodic Arrest of Circulation in the Fingers, a Variety of Raynaud's Disease , Lewis Heart 15:7, 1929. 8. Krogh, A.; Turner, A. H., and Landis, E. M.: A Celluloid Capsule for Measuring Venous Pressures , J. Clin. Investigation 11:357, 1932.Crossref 9. Dr. Alfred Stengel permitted us to report this case and Dr. Lee Rademaker supplied determinations of the vasomotor index. 10. Brown, G. E.: The Treatment of Peripheral Vascular Disturbances of the Extremities , J. A. M. A. 87:379 ( (Aug. 7) ) 1926.Crossref 11. Lewis, T., and Landis, E. M.: Observations upon the Vascular Mechanism in Acrocyanosis , Heart 15:229, 1930. 12. Adson, A. W., and Brown, G. E.: Thrombo-Angiitis Obliterans: Results of Sympathectomy , J. A. M. A. 99:529 ( (Aug. 13) ) 1932.Crossref 13. Lewis, T., and Pickering, G. W.: Vasodilatation in the Limbs in Response to Warming the Body, with Evidence for Sympathetic Vasodilator Nerves in Man , Heart 16:33, 1931. 14. de Takats, G.: The Differentiation of Organic and Spastic Vascular Occlusions , Ann. Surg. 94:321, 1931.Crossref 15. Simpson, S. L.; Brown, G. E., and Adson, A. W.: Raynaud's Disease; Evidence That It Is a Type of Vasomotor Neurosis , Arch. Neurol. & Psychiat. 26:687 ( (Oct.) ) 1931.

THOMPSON, WILLARD O.;THOMPSON, PHEBE K.;DICKIE, LOIS F. N.;ALPER, JOSEPH M.

doi: 10.1001/archinte.1933.00160050162008pmid: N/A

Abstract We have just reported observations which show that when thyroxine is administered by mouth in the form of its monosodium salt to patients with myxedema it has only about from one-third to one-fifth as much effect as when it is administered intravenously in alkaline solution (sodium hydroxide).1 This conclusion was based on the amounts of the two substances which had to be administered every day in order to hold the basal metabolism at the normal level. Pure thyroxine had much less effect than its monosodium salt. Since when thyroxine is dissolved in an excess of sodium hydroxide the disodium salt is presumably formed, it seemed logical to try the effect of administering the hormone by mouth in an alkaline solution. Klein2 reported that Hoffmann-La Roche thyroxine solution for oral use, Schering thyroxine in alkaline solution with the same ph as the Hoffmann-La Roche solution and Schering's Trinktabletten References 1. Thompson, W. O.; Thompson, P. K., and Dickie, L. F. N.: Monosodium Thyroxine, Desiccated Thyroid and an Impure Sodium Salt of Thyroxine: Comparison of Their Effects When Administered Orally with the Effect of Thyroxine Injected Intravenously in an Alkaline Solution , Arch. Int. Med. 52:576 ( (Oct.) ) 1933.Crossref 2. Klein, B.: Ueber die hohe Wirksamkeit peroral verabreichten Thyroxinnatriums bei normalen und hypothyreotischen Individuen , Ztschr. f. klin. Med. 119:477, 1932. 3. Baur, H., and Loewe, G.: Ueber die Wirkung des synthetischen Thyroxins beim Menschen mit normaler Schilddrüse , Deutsches Arch f. klin. Med. 159:275, 1928. 4. One gram of sodium ethylmercuri-thiosalicylate in 1,000 cc. of water buffered with 1.4 Gm. of sodium borate in 1,000 cc. and containing sodium chloride to make the solution approximately isotonic. This preparation was supplied by the manufacturers, Eli Lilly and Company, Indianapolis. 5. Thompson, W. O.; Alper, J. M.; Thompson, P. K., and Dickie, L. F. N.: The Effect of Diiodotyrosine on the Basal Metabolism in Myxedema , to be published in the Journal of Clinical Investigation , (January) , 1934. 6. Thompson, W. O.; Thompson, P. K.; Brailey, A. G., and Cohen, A. C.: The Calorigenetic Action of Thyroxin at Different Levels of Basal Metabolism in Myxedema , J. Clin. Investigation 7:437, 1929.Crossref 7. Møller, E.; Gram, C. N. J., and Schou, S. A.: Quantitative Clinical and Spectrophotometrical Comparison Between Natural and Synthetic Thyroxine , Acta med. Scandinav. 74:85, 1930.Crossref 8. Thompson, W. O.; Taylor, S. G., III; Thompson, P. K., and Dickie, L. F. N.: Upublished data, 1933. 9. Thompson, W. O.; McLellan, L. L.; Thompson, P. K., and Dickie, L. F. N.: The Rates of Utilization of Thyroxine and of Desiccated Thyroid in Man: The Relation Between the Iodine in Desiccated Thyroid and in Thyroxine , J. Clin. Investigation 12:235, 1933.Crossref 10. Kendall, E. C.: Thyroxine , New York, The Chemical Catalog Company, Inc., 1929. 11. Harington, C. R., and Salter, W. T.: The Isolation of 1-Thyroxine from the Thyroid Gland by the Action of Proteolytic Enzymes , Biochem. J. 24:456, 1930. 12. Salter, W. T.; Lerman, J., and Means, J. H.: The Calorigenic Action of Thyroxine Polypeptide , J. Clin. Investigation 12:327, 1933.Crossref

doi: 10.1001/archinte.1933.00160050174009pmid: N/A

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This handbook is so extensive that it will be impossible to discuss the details of any of its chapters within the limits allowed for a book review. A general survey of its contents is about all that can be attempted. Volume I has been completed, and the first half of volume II has also been published. The present discussion is concerned with the former, which is made up of a series of twenty-four monographs, five of which have been written by the editors and the remainder by other contributors, among whom there are many well known names. As indicated by the title, this book deals with the general phases of hematology and not with the diseases of the blood as such. Many of the chapters, however, will be of great value to those whose interest is primarily in the diseases of the blood and their clinical aspects. Among these may

doi: 10.1001/archinte.1933.00160050179010pmid: N/A

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract There has long been a demand for a practical clinical hematologic text in English. This book fills a definite need and contains sufficiently complete discussions of the various aspects of hematology to be of value to the general practitioner. It was not intended to be, and does not serve as, an encyclopedia of hematology. The book is conveniently divided into three parts. The first part is devoted to the various components of the blood and methods of studying them; the second, to diagnosis of diseases primarily of the blood, and the third, to diseases not primarily of the blood. The laboratory findings in the various diseases are briefly and clearly stated, and the procedures that are most valuable in the differential diagnosis are discussed. The placing of references to key articles at the bottoms of the pages is of advantage. Theoretical discussion has been limited as much as possible, and