scholarly journals Experimental Organism Islet Cell Adenoma Neoplasm

2020 ◽  
Author(s):  
1955 ◽  
Vol 101 (424) ◽  
pp. 673-682 ◽  
Author(s):  
D. N. Parfitt

As an approach to the problem of schizophrenia it is proposed to compare the effects and after-effects of severe hypoglycaemia due mainly to islet-cell adenoma of the pancreas in otherwise healthy people with the effects and after-effects of severe hypoglycaemia therapeutically induced in schizophrenics.The difficulties are plain. Personal experience of patients with functioning islet-cell adenoma is limited almost always to a few cases, whereas average experience of insulin coma treatment covers some hundreds of cases; moreover, there is little overlap of experience except in the post-mortem room or in the laboratory for morbid histology. During insulin treatment there is constant supervision by a trained staff, medical and nursing, so that serious developments can be met by immediate intravenous sugar and investigations are continual; with adenomata there is no observation until, perhaps, a general practitioner is called in about alarming symptoms of one kind or another and sometimes months or even years elapse before a patient gets into hospital, where the intensity of observation and even more so of investigation may exceed that available in mental hospitals. Insulin coma treatment has a more or less standard aim, to produce coma of increasing duration up to a maximum of something like an hour which is then repeated thirty times or more; dosage is built up with the greatest care. Adenomata produce conditions varying from the hardly serious to the fatal under the influence of an insulin dosage which is quite unknown.This comparison is based chiefly on an analysis of 290 serial courses of insulin coma treatment given to schizophrenic patients at Holloway Sanatorium during the four years 1950 to 1953 inclusive, and on the 258 cases of islet-cell adenoma reported by Crain and Thorn (1949) and the 398 cases, all that could be traced up to that date and including the Crain and Thorn cases, analysed by Howard, Moss and Rhoads (1950). Many separate papers have been consulted for more detailed approaches and for extra information, although of course those published before 1950 were included in the reviews already mentioned. Despite the difficulties of this comparison, it can be shown that the similarities between the two groups follow expectation and are very strong indeed, so that the differences which emerge have at least possible significance.


1979 ◽  
Vol 72 (2) ◽  
pp. 252.2-253 ◽  
Author(s):  
O. Ferrer-Roca ◽  
F. Segura ◽  
S. Nogué ◽  
J. C. Duró ◽  
E. Soriano

1952 ◽  
Vol 83 (2) ◽  
pp. 165-169
Author(s):  
Claude C. Blackwell
Keyword(s):  

PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 646-653
Author(s):  
Ezequiel D. Salinas ◽  
Henry H. Mangurten ◽  
Stuart S. Roberts ◽  
William H. Simon ◽  
Marvin Cornblath

Persistent hypoglycemia in the neonate is rare and may be due to inborn errors of carbohydrate metabolism, islet cell tumors, or unknown causes. A patient with the onset of symptomaric hypoglycemia at 36 hours of age had persistent hypoglycemia in spite of therapy with corticosteroids, A.C.T.H., Diazoxide, glucagon, parenteral glucose and fructose. She showed a normal hyperglycemic response to glucagon. Plasma insulin values were not diagnostic. At surgery, at 7 weeks of age, a discrete islet cell adenoma was found and removed with the body and tail of the pancreas. The spleen was not removed. Following surgery, she had a transient hyperglycemia and required insulin for 8 days with a wound infection. She has remained normoglycemic.


PEDIATRICS ◽  
1992 ◽  
Vol 90 (4) ◽  
pp. 636-638
Author(s):  
ANTON B. DODEK ◽  
AB SADEGHI-NEJAD

Transient hyperinsulinemic hypoglycemia of the newborn is relatively common and is seen frequently in infants of diabetic mothers.1 Erythroblastosis fetalis and Beckwith-Wiedemann syndrome are less common causes.2 By contrast, persistent hyperinsulinism is an uncommon cause of hypoglycemia in this age group.2 This form of hyperinsulinemia is often caused by nesidioblastosis, a diffuse disorder of the pancreas resulting from transformation of the pancreatic ductal tissue into insulin-producing islet cells, or rarely by an islet cell adenoma, a localized proliferation of the islets of Langerhans.2,3 In one review of 160 hyperinsulinemic infants, four adenomas were reported.4 Because an islet cell adenoma may be very small, attempts at diagnosis and localization by non-invasive techniques such as ultrasonography, computer tomography, and magnetic resonance imaging have usually been unsuccessful.


1960 ◽  
Vol 53 (1) ◽  
pp. 24-26
Author(s):  
M C GEPHARDT ◽  
H M FEINBERG ◽  
THOMAS J. HANLON

JAMA ◽  
1973 ◽  
Vol 226 (12) ◽  
pp. 1466b-1466 ◽  
Author(s):  
V. Gallardo-Navarra

Sign in / Sign up

Export Citation Format

Share Document