A Pentamidine-Treated Acquired Immunodeficiency Syndrome Patient Associated With Sudden Onset Diabetes mellitus and High Tumor Necrosis Factor α Level

• Published in: Journal of diabetes and its complications Vol. 11; no. 4; pp. 256 - 258
• Main Authors: Ubukata, Eiichi, Mokuda, Osamu, Nagata, Megumi, Ogino, Yoshio, Sakamoto, Yoshikazu, Tanaka, Koushi, Shimizu, Naokata
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.07.1997; Elsevier Science; Elsevier Limited
• Subjects: Acquired immune deficiency syndrome; Acquired Immunodeficiency Syndrome - complications; Adult; AIDS; Biological and medical sciences; Case reports; Diabetes; Diabetes Mellitus - chemically induced; Glucose; HIV; Human immunodeficiency virus; Human viral diseases; Humans; Infectious diseases; Insulin resistance; Male; Medical sciences; Necrosis; Pentamidine - adverse effects; Pentamidine - therapeutic use; Pneumonia, Pneumocystis - complications; Pneumonia, Pneumocystis - drug therapy; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Endocrinopathy; Human; Immunopathology; Toxicity; Diabetes mellitus; Cytokine; Biological marker; Male; AIDS; Pentamidine; Immune deficiency; Insulin; Infection; Case study; Antiprotozoal agent; Target tissue resistance; Association; Viral disease; Parasiticid; Tumor necrosis factor α
• ISSN: 1056-8727; 1873-460X
• DOI: 10.1016/1056-8727(95)00111-5

We report one patient with a very high level of plasma TNF-α who acquired diabetes mellitus following pentamidine treatment for pneumocystis pneumoniae.2 Case report A 29-year-old heterosexual man with a 4-week history of fever, dyspnea, and productive cough was admitted to our hospital. [...]Human Immunodeficiency Virus (HIV) antibodies were found, and the CD4/CD8 lymphocyte ratio was 0.05 (CD4 8 cells/μL, CD8 165 cells/μL). [3]reported that TNF-α led to downregulation of glucose transporter type 4 (Glut-4), and caused the insulin resistance,[3]but TNF-α can inhibit insulin-stimulated glucose transport at doses that have no effect on the cellular content of Glut-4.