- Email: [email protected]
Diabetes insipidus as a presenting manifestation of acute myelogenous leukemia
LETTERS
TO T H E E D I T O R
Clinical notes
"Clinical notes" represent clinical a n d / o r laboratory experiences which can be presented in 200 to 400 words, 3 or 4 references, and, if contributory, one illustration or short table. "Clinical notes" are subject to the same critical peer review and editing as papers published in other sections o f TIa~ JOURNAL.
Diabetes insipidus as a presenting manifestation of acute myelogenous leukemia
intestine. The hypothalamus and posterior pituitary contained areas of gliosis and hemosiderin pigment similar to that described in previously reported cases.' No leukemic infiltration was seen in any organ. DISCUSSION
To the Editor: Diabetes insipidus is an unusual complication of childhood leukemia; it has been reported to develop during the course of treatment in only three children. ~-~ This report describes a child in whom diabetes insipidus of central origin was present at the time of diagnosis. CASE REPORT Patient D. B. (65-05-962), an eight-year-old white girl, was admitted to St. Christopher's Hospital for Children following one week of fever, vomiting, and a ten-pound weight loss. The patient was moderately dehydrated and pale. There were bilateral retinal hemorrhages and gingival bleeding. Liver and spleen were not enlarged. Initial hemoglobin level was 8.1 gm/dl, platelet count was 16,000/mm :', and white blood cell count was 88,000/mm ~ with 80% blast forms. The urine showed low specific gravity and low osmolality on repeated testing despite serum hypernatremia and hyperosmolality. Marrow aspirate examination showed acute myelogenous leukemia; chemotherapy initially effected a good response. Lumbar puncture revealed "a few" blast cells, so cytosine arabinoside was given intrathecally. Pitressin was given intravenously rather than intramuscularly because of thrombocytopenia. Severe pressor effects of hypertension and tachycardia precluded the further use of pitressin intravenously, either by rapid infusion or by slower constant infusion. Intranasal pitressin did not correct diuresis, but intramuscular pitressin tannate in oil brought rapid control. No complications of intramuscular injections occurred. When the patient's clinical condition stabilized and pitressin effects had worn off, a water deprivation test demonstrated diabetes insipidus. Pitressin injections were required every two to three days. Therapeutic irradiation of 2,200 rads to the whole cranium and and additional 2,200 rads to the pituitary were given without change in pitressin requirement. After three months of treatment the patient suffered a hematologic relapse and died from septicemia. Autopsy revealed disseminated fungal micro-abscesses in the lungs, liver, and small
In our patient, destruction of the hypothalamic nuclei in which antidiuretic hormone is synthesized was likely caused by anoxia, hemorrhage, and necrosis due to vascular compromise and hypoperfusion as a consequence of either stasis infarction ~ (white blood cell thrombi) or arachnoid infiltration by leukemic cells ~ at diagnosis. This CNS complication o f acute leukemia, diabetes insipidus, was recognized and treated vigorously with intrathecal drugs and irradiation, That no improvement occurred is not surprising in view of the probable pathogenesis.
Garrett E. Bergman, M.D. Department of Pediatrics Medical College of Pennsylvania 3300 Henry Ave. Philadelphia, Pa. 19129 H. Jorge Baluarte, M.D. J. Lawrence Naiman, M.D. St. Christopher's Hospital for Children Department of Pediatrics Temple University School of Medicine Philadelphia, Pa. REFERENCES 1. Joseph M, and Levin S: Leukemia and diabetes insipidus, Br Med J 1:1328, 1956. 2. Malter IJ, Gross S, and Teree TM: Diabetes insipidus complicating acute lymphocytic leukemia, Am J Dis Child 117:228, 1969. 3. Reussi C, Arditi J, Rigoli MH, and Izquierdo J: Hodgkins disease and diabetes insipidus, leukemia and diabetes insipidus, Rev Assoc Med Argent 75:401, 1961. 4. Miller VI, and Campbell WG: Diabetes insipidus as a complication of leukemia, Cancer 28:666, 197l 5. Price RA, and Johnson WW: The central nervous system in childhood leukemia: I. The arachnoid, Cancer 31:520, 1973.
The Journal of P E D l A T R I C S Vol. 88, No. 2, pp. 355-366
355
TO T H E E D I T O R
Clinical notes
"Clinical notes" represent clinical a n d / o r laboratory experiences which can be presented in 200 to 400 words, 3 or 4 references, and, if contributory, one illustration or short table. "Clinical notes" are subject to the same critical peer review and editing as papers published in other sections o f TIa~ JOURNAL.
Diabetes insipidus as a presenting manifestation of acute myelogenous leukemia
intestine. The hypothalamus and posterior pituitary contained areas of gliosis and hemosiderin pigment similar to that described in previously reported cases.' No leukemic infiltration was seen in any organ. DISCUSSION
To the Editor: Diabetes insipidus is an unusual complication of childhood leukemia; it has been reported to develop during the course of treatment in only three children. ~-~ This report describes a child in whom diabetes insipidus of central origin was present at the time of diagnosis. CASE REPORT Patient D. B. (65-05-962), an eight-year-old white girl, was admitted to St. Christopher's Hospital for Children following one week of fever, vomiting, and a ten-pound weight loss. The patient was moderately dehydrated and pale. There were bilateral retinal hemorrhages and gingival bleeding. Liver and spleen were not enlarged. Initial hemoglobin level was 8.1 gm/dl, platelet count was 16,000/mm :', and white blood cell count was 88,000/mm ~ with 80% blast forms. The urine showed low specific gravity and low osmolality on repeated testing despite serum hypernatremia and hyperosmolality. Marrow aspirate examination showed acute myelogenous leukemia; chemotherapy initially effected a good response. Lumbar puncture revealed "a few" blast cells, so cytosine arabinoside was given intrathecally. Pitressin was given intravenously rather than intramuscularly because of thrombocytopenia. Severe pressor effects of hypertension and tachycardia precluded the further use of pitressin intravenously, either by rapid infusion or by slower constant infusion. Intranasal pitressin did not correct diuresis, but intramuscular pitressin tannate in oil brought rapid control. No complications of intramuscular injections occurred. When the patient's clinical condition stabilized and pitressin effects had worn off, a water deprivation test demonstrated diabetes insipidus. Pitressin injections were required every two to three days. Therapeutic irradiation of 2,200 rads to the whole cranium and and additional 2,200 rads to the pituitary were given without change in pitressin requirement. After three months of treatment the patient suffered a hematologic relapse and died from septicemia. Autopsy revealed disseminated fungal micro-abscesses in the lungs, liver, and small
In our patient, destruction of the hypothalamic nuclei in which antidiuretic hormone is synthesized was likely caused by anoxia, hemorrhage, and necrosis due to vascular compromise and hypoperfusion as a consequence of either stasis infarction ~ (white blood cell thrombi) or arachnoid infiltration by leukemic cells ~ at diagnosis. This CNS complication o f acute leukemia, diabetes insipidus, was recognized and treated vigorously with intrathecal drugs and irradiation, That no improvement occurred is not surprising in view of the probable pathogenesis.
Garrett E. Bergman, M.D. Department of Pediatrics Medical College of Pennsylvania 3300 Henry Ave. Philadelphia, Pa. 19129 H. Jorge Baluarte, M.D. J. Lawrence Naiman, M.D. St. Christopher's Hospital for Children Department of Pediatrics Temple University School of Medicine Philadelphia, Pa. REFERENCES 1. Joseph M, and Levin S: Leukemia and diabetes insipidus, Br Med J 1:1328, 1956. 2. Malter IJ, Gross S, and Teree TM: Diabetes insipidus complicating acute lymphocytic leukemia, Am J Dis Child 117:228, 1969. 3. Reussi C, Arditi J, Rigoli MH, and Izquierdo J: Hodgkins disease and diabetes insipidus, leukemia and diabetes insipidus, Rev Assoc Med Argent 75:401, 1961. 4. Miller VI, and Campbell WG: Diabetes insipidus as a complication of leukemia, Cancer 28:666, 197l 5. Price RA, and Johnson WW: The central nervous system in childhood leukemia: I. The arachnoid, Cancer 31:520, 1973.
The Journal of P E D l A T R I C S Vol. 88, No. 2, pp. 355-366
355