title: A case of acquired deficiency of pituitary GH, PRL and TSH, associated with type 1 diabetes mellitus.
abstract: A 75-year-old male showed combined anterior pituitary hormone deficiency (CPHD). Basal and TRH-stimulated PRL levels were undetectable. Basal and GRH-stimulated GH levels were very low, and could barely be measured by means of an ultrasensitive enzyme immunoassay. In addition, basal TSH levels were under the normal limit, and TRH-stimulated TSH secretions were impaired. On the other hand, the secretions of ACTH, LH and FSH remained intact. There was no mutation of Pit-1 gene in this patient, and immunohistochemical studies using human pituitary and the patient's serum showed no positive staining. The HLA types frequently detected in lymphocytic hypophysitis were recognized, supporting the view that the CPHD in this case may be caused by lymphocytic hypophysitis, although magnetic resonance imaging of the pituitary gland showed no specific findings. Interestingly, a high titer of anti-glutamic acid decarboxylase antibody, suggested that the patient suffered from type 1 diabetes mellitus (DM). Five years ago, his thyroid function was normal and the treatment of DM with oral hypoglycemic agent was effective, indicating that the onset of both diseases at least occurred within the last half decade. We report here a rare case of SPIDDM with CPHD which might be caused by lymphocytic hypophysitis.
authors.affiliation: Division of Diabetes and Endocrinology, Department of Internal Medicine, Jikei University School of Medicine, Minato-ku, Tokyo 105-8461, Japan.
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Saito
authors.forename: Katsuyoshi
authors.initials: K
authors.lastname: Tojo
authors.forename: Genshin
authors.initials: G
authors.lastname: Kuriyama
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Murakawa
authors.forename: Kei
authors.initials: K
authors.lastname: Fujimoto
authors.forename: Kanta
authors.initials: K
authors.lastname: Taniguchi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tanii
authors.forename: Hideki
authors.initials: H
authors.lastname: Katakami
authors.forename: Kozo
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Naoko
authors.initials: N
authors.lastname: Tajima
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000368:Aged; D001323:Autoantibodies / Q000097:blood; D004268:DNA-Binding Proteins / Q000235:genetics; D003922:Diabetes Mellitus, Type 1 / Q000150:complications*; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D005968:Glutamate Decarboxylase / Q000276:immunology; D019382:Human Growth Hormone / Q000172:deficiency*; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism; D008214:Lymphocytes; D008279:Magnetic Resonance Imaging; D008297:Male; D010900:Pituitary Diseases / Q000150:complications / Q000473:pathology; D011388:Prolactin / Q000172:deficiency*; D013972:Thyrotropin / Q000172:deficiency*; D050817:Transcription Factor Pit-1; D014157:Transcription Factors / Q000235:genetics
chemical_list: D001323:Autoantibodies; D004268:DNA-Binding Proteins; C494187:POU1F1 protein, human; D050817:Transcription Factor Pit-1; D014157:Transcription Factors; D019382:Human Growth Hormone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D005968:Glutamate Decarboxylase