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Autonomic and sensory ganglionopathy occurring in a patient with fulminant type 1 diabetes mellitus
Author(s) -
Makino Mutsuki,
Hiwatashi Dai,
Minemura Kesami,
Kawaguchi Kenji
Publication year - 2016
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12373
Subject(s) - medicine , fulminant , autopsy , diabetes mellitus , pathology , pancreas , etiology , pancreatitis , gastroenterology , endocrinology
A 63‐year‐old male with a previous infection was admitted to our hospital because of acute pancreatitis. Although he had no history of diabetes mellitus, laboratory examinations revealed marked hyperglycemia on admission, and intensive insulin treatment was required. After 2 weeks, he developed severe pandysautonomia and sensory impairment, and eventually died from colonic perforation caused by paralytic ileus at 1 year after onset. Autopsy findings showed a complete loss of pancreatic islet beta cells with mild fibrosis of the exocrine pancreas. Neuropathological examination showed myelin loss of the dorsal fasciculus at all levels of the spinal cord and ganglionopathy of the dorsal root and sympathetic truncus, revealing degeneration of ganglion cells and a decrease in their number with the formation of N ageotte nodules. On the basis of this clinicopathological evidence, fulminant type 1 diabetes mellitus ( T 1 DM ) and idiopathic immune‐mediated autonomic neuropathy were suspected. Here, we suggest a close etiological relationship between both diseases.