PMID- 12114788
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230315
IS  - 1559-0097 (Electronic)
IS  - 1046-3976 (Linking)
VI  - 8
IP  - 4
DP  - 1997 Winter
TI  - Insulin-Dependent Diabetes Mellitus: Islet Changes in Relation to Etiology and 
      Pathogenesis.
PG  - 273-282
AB  - Type and type II diabetes are the most common types of diabetes. The ratio of 
      type I to type II diabetes is about 1:9. Type I diabetes is caused by absolute 
      insulin deficiency and is therefore referred to as insulin-dependent diabetes. 
      The disease becomes manifest clinically in childhood or adolescence ("juvenile 
      diabetes"), though onset in adulthood is increasingly being observed. 
      Morphologically a subtotal (>80%) to total loss of B-cells in the pancreatic 
      islets occurs. Lymphocytic insulitis, which disappears after the B-cells have 
      been totally destroyed, is pathogneumonic of type I diabetes. This insulitis is 
      an expression of an autoimmune event that is triggered by a multitude of factors. 
      An important factor appears to be a genetic predisposition (human leukocyte 
      antigen [HLA] DR3/DR4/DQ8) in connection with as-yet-unknown environmental 
      factors (e.g., viruses). Autoantibodies, such as islet cell cytoplasmic 
      antibodies (ICA). insulin autoantibodies (IAA) and/or autoantibodies to the 
      gamma-aminobutyric acid (GABA)-synthesizing enzyme glutamic acid carboxylase 
      (GAD), are already detectable in a prediabetic phase, though it is not possible 
      to predict the time of clinical onset. The course of the disease is dependent on 
      age. Young children require insulin therapy sooner than juveniles or adults.
FAU - Kloppel, Gunter
AU  - Kloppel G
AD  - MD, PhD.
FAU - Clemens, Andreas
AU  - Clemens A
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocr Pathol
JT  - Endocrine pathology
JID - 9009288
EDAT- 1997/01/01 00:00
MHDA- 2002/07/13 10:00
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 2002/07/13 10:00 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - EP0804273 [pii]
AID - 10.1007/BF02739929 [doi]
PST - ppublish
SO  - Endocr Pathol. 1997 Winter;8(4):273-282. doi: 10.1007/BF02739929.