| pubmed-article:1471530 | pubmed:abstractText | A 38-year-old male patient with the juvenile variant of Parkinson's disease, in whom onset had occurred at the age of 24 yr, was autopsied. There were no clear symptoms of pancreatic or hepatic insufficiency during the entire clinical course. The only notable features were a slightly delayed decrease of the blood glucose level in an oral glucose tolerance test, slightly elevated levels of serum alkaline phosphatase and serum lactate dehydrogenase, and episodic loose stools. Autopsy revealed uniform enlargement of the pancreas due to massive fat replacement (lipomatous pseudohypertrophy): the exocrine glandular elements showed marked atrophy and loss, while the islets of Langerhans were preserved. The liver exhibited a histology closely mimicking alcoholic hepatitis associated with the diffuse presence of Mallory bodies (MBs), possibly indicative of a disturbance of protein metabolism. The nervous system showed the diffuse presence of Lewy bodies (LBs) in the cerebrum in addition to the ordinary lesions of Parkinson's disease. Although the etiopathogenesis of none of these three lesions has been well elucidated, common epitopes of MBs and LBs have recently been demonstrated. Therefore, the present case study suggests that a specific underlying toxic agent may cause diffuse LBs in the brain on the one hand, and diffuse MBs in the liver and lipomatous pseudohypertrophy of the pancreas on the other. | lld:pubmed |
