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Fatal Degenerative Neurologic Disease in Patients Who Received Pituitary-Derived Human Growth Hormone

Reports of rapidly progressive and fatal degenerative neurologic disorders in three recipients of human growth hormone (hGH) have been received by the U.S. Food and Drug Administration (FDA) and the National Institutes of Health (NIH). In two cases, diagnoses of Creutzfeldt-Jakob disease (CJD) were made at autopsy.

All three patients had had growth failure secondary to growth hormone deficiency. They had been treated during childhood and adolescence with hGH extracted from pooled human cadaver pituitary glands. The hormone used to treat these patients was produced and distributed by the National Hormone and Pituitary Program (NHPP, formerly the National Pituitary Agency) under an investigational exemption for the use of a new drug (IND).

Case 1. A 20-year-old man with hypopituitarism and Type I diabetes mellitus developed dysarthria and a gait disturbance in May 1984. By September, his neurologic status had deteriorated so that he was no longer able to walk, could not care for himself, and required bladder catheterization. His mental status had deteriorated, and he was unable to carry on a meaningful conversation. He died in November 1984. Examination of the brain revealed spongiform encephalopathy consistent with CJD.

This patient had grown poorly during the first year of life. Hypothyroidism was diagnosed when he was 15 months old. In September 1966, a diagnosis of growth hormone deficiency was made. The patient was treated with daily injections of hGH from September 1966 to July 1980.

Case 2. A 22-year-old man developed weakness and gait disturbance in the fall of 1983. During the next 6 months, he developed severe ataxia involving extremities, trunk, and head. He also had speech impairment, difficulty swallowing, and dementia. He died in April 1985. Histologic examination of the brain at the Armed Forces Institute of Pathology revealed extensive changes of spongiform encephalopathy compatible with CJD.

This patient was evaluated for growth failure at 7 years of age and was found to be growth hormone deficient. He was treated with hGH from June 1969 through October 1977.

Case 3. A 34-year-old man with hypopituitarism developed a gait disturbance in December 1983. He had received hGH from 1963 to 1969. Examination in June 1984 showed bilateral horizontal end gaze nystagmus, mild intention tremor, and wide-based gait. The symptoms worsened over the next several months, with increasing somnolence, memory loss, and urinary incontinence.

The patient's symptoms progressed to include swallowing difficulties, diplopia, and finally, dementia. He died in February 1985. No autopsy was done. Reported by R Hintz, MD, Stanford University School of Medicine, Stanford, California; M MacGillivray MD, A Joy, MD, Children's Hospital of Buffalo, New York; R Tintner, MD, University of Texas Health Science Center, Dallas; Center for Drugs and Biologics, U.S. Food and Drug Administration; National Institute for Arthritis, Diabetes, and Digestive and Kidney Diseases.

Editorial Note

Editorial Note: CJD occurs with a frequency of approximately one case per million population per year in the United States and Europe (1). Most cases occur sporadically and involve patients over 50 years of age. Innoculation of chimpanzees with brain tissue from affected patients results in a similar neurodegenerative disease in the animals within 18-36 months (2). Iatrogenic CJD has been reported in a patient who received a corneal transplant from an affected donor (3) and in two patients exposed to intracranial electrodes that had previously been used in a patient with CJD (4).

The CJD pathogen is resistant to chemical and physical methods commonly used for decontamination or sterilization (5). There is evidence suggesting that procedures used recently to extract and purify hGH from cadaver pituitary glands may eliminate experimental contamination by scrapie, an agent similar to the CJD pathogen. The methods used by the NHPP were changed in 1977, but there is no assurance that current procedures eliminate the risk of transmitting the CJD pathogen.

From 1963 to early 1985, approximately 10,000 U.S. patients received hGH through the NHPP. The average duration of therapy was 4 years. Each patient received hormone from two or three batches per year. Each batch was derived from a pool of approximately 16,000 cadaver pituitary glands.

The three patients described here received hGH for 14, 8, and 6 years, respectively. Records of the NHPP indicate that patients 1 and 2 received several common lots. Patients 1 and 3 received one lot in common. No single lot was administered to all three patients; however, all three received hormone during 1969. The occurrence of fatal neurodegenerative disorders consistent with CJD in three of 10,000 patients exposed to hGH between 1963 and 1985 strongly suggests that the hormone, a product of pooled human tissue, may have been the vehicle for transmission of the CJD pathogen. It is not yet known how many other members of this cohort may have developed similar neurodegenerative disorders. Epidemiologic studies will be undertaken to determine the status of recipients of hGH.

Patients under 40 years of age with progressive dementing neurodegenerative disorders who may have received pituitary derived human growth hormone either through the NHPP or from commercial sources should be reported to: E Rappaport, MD, HFN-810, Center for Drugs and Biologics, U.S. Food and Drug Administration, 5600 Fishers Lane, Rockville, Maryland 20857; telephone (301)443-3520.


  1. Brown P. An epidemiologic critique of Creutzfeldt-Jakob disease. Epidemiol Rev 1980;2:113-35.

  2. Gibbs CJ Jr, Gajdusek DC, Asher DM, et al. Creutzfeldt-Jakob disease (spongiform encephalopathy): transmission to the chimpanzee. Science 1968;161:388-9.

  3. Duffy P, Wolf J, Collins G, et al. Possible person-to-person transmission of Creutzfeldt-Jakob disease. N Engl J Med (letter) 1974;290:692-3.

  4. Bernoulli C, Siegfried J, Baumgartner G, et al. Danger of accidental person-to-person transmission of Creutzfeldt-Jakob disease by surgery. Lancet (letter) 1977;I:478-9.

  5. Brown P, Gibbs CJ Jr, Amyx HL, et al. Chemical disinfection of Creutzfeldt-Jakob disease virus. N Engl J Med 1982;306:1279-82.

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