Irreversible Hypoglycaemic Coma in Islet-Cell Adenoma and in Schizophrenia

1955 ◽  
Vol 101 (424) ◽  
pp. 673-682 ◽  
Author(s):  
D. N. Parfitt
Keyword(s):  
Personal Experience ◽  
Islet Cell ◽  
Severe Hypoglycaemia ◽  
Insulin Dosage ◽  
Cell Adenoma ◽  
After Effects ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Trained Staff ◽  
Hypoglycaemic Coma

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.

THERAPIE EINES METASTASIERENDEN INSELZELLTUMORS MIT STREPTOZOTOCIN

1971 ◽  
Vol 67 (2) ◽  
pp. 405-416 ◽  
Author(s):  
E. Nieschlag ◽  
H. Wombacher ◽  
F. J. Kroeger ◽  
L.V. Habighorst
Keyword(s):  
Liver Metastases ◽  
Blood Sugar ◽  
Mechanism Of Action ◽  
Islet Cell ◽  
Plasma Insulin ◽  
Severe Hypoglycaemia ◽  
Islet Cells ◽  
Intravenous Injections ◽  
High Affinity ◽  
Methyl Nitrosourea

A patient with a metastazing functional islet cell tumour suffering from severe hypoglycaemia was treated with streptozotocin. Four intravenous injections of 1.5 g streptozotocin each were administered in 4 to 6 days intervals. After the 4th injection there were no further episodes of hypoglycaemia, parenteral glucose administration could be stopped and blood sugar and plasma insulin, showing concentrations of up to 405 μU/ml before treatment, reached normal levels. The tumours in the pancreas disappeared and the liver metastases decreased in size and number as judged by arteriography. A hypothesis for the mechanism of action of streptozotocin is proposed. The glucose moiety is considered to facilitate a high affinity to the islet cells whereas the N-methyl-nitrosourea residue serves the active antitumour part of the molecule.

Modification of Insulin Resistance

1956 ◽  
Vol 102 (428) ◽  
pp. 576-588 ◽  
Author(s):  
Edward Marley
Keyword(s):  
Deep Coma ◽  
Insulin Dosage ◽  
Insulin Resistant ◽  
Significant Difference ◽  
High Insulin ◽  
Insulin Coma ◽  
The Central Nervous System ◽  
Resistance To Insulin ◽  
High Doses ◽  
Special Instance

Sakel (1938a) drew attention to the difficulty of establishing satisfactory comas in a minority of patients attending for Deep Insulin therapy. This phenomenon has since been confirmed by other workers including Tillim (1938) whose patient received 500 units of insulin without the production of deep coma, by Hall (1940) who reported an instance in which 1,000 units of insulin was equally unsuccessful, by Reznikoff and Scott (1942) who described how neither 120 nor 1,000 units of insulin when injected intravenously produced any significant difference in hypoglycaemia in insulin resistant patients, and more recently by Fogarty (1953) whose case required 5,000 units of insulin for the production even of sopor. Other recorded examples of resistance to massive doses of insulin include those of Bantinget al.(1938) and Tennent (1944).Various explanations of this perverse response to insulin have been formulated, including that of Jones (1939) who proposed that resistance to insulin was both a problem of true insulin insensitivity and also of an anomalous response of the central nervous system to hypoglycaemia. Medunaet al.(1942) preferred to ascribe it to anti-insulin factors in the blood, but a more interesting interpretation derived from Freudenberg (1952) who suggested that if the effects of high insulin dosage employed in insulin coma treatment were regarded as a special instance of a stress response, then the fluctuations and differences in response could be equated in terms of the General Adaptation Syndrome of Selye. High doses were thus an index of an effective “alarm stage” characterized by a discharge from plentiful adrenocortical reserves.

Systemic Fibrosclerosis with Intracranial Involvement and Pancreatic Islet Cell Adenoma

1979 ◽  
Vol 72 (2) ◽  
pp. 252.2-253 ◽  
Author(s):  
O. Ferrer-Roca ◽  
F. Segura ◽  
S. Nogué ◽  
J. C. Duró ◽  
E. Soriano
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Pancreatic Islet Cell ◽  
Cell Adenoma ◽  
Intracranial Involvement

Islet cell adenoma with hyperinsulinism

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

FUNCTIONING ISLET CELL ADENOMA IN THE NEWBORN

PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 646-653
Author(s):  
Ezequiel D. Salinas ◽  
Henry H. Mangurten ◽  
Stuart S. Roberts ◽  
William H. Simon ◽  
Marvin Cornblath
Keyword(s):  
Wound Infection ◽  
Carbohydrate Metabolism ◽  
Islet Cell ◽  
Plasma Insulin ◽  
The Body ◽  
Islet Cell Tumors ◽  
Inborn Errors ◽  
Cell Adenoma

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.

Value of Selective Pancreatic Angiography in the Evaluation of Hyperinsulinemic Hypoglycemia in Infancy

PEDIATRICS ◽  
1992 ◽  
Vol 90 (4) ◽  
pp. 636-638
Author(s):  
ANTON B. DODEK ◽  
AB SADEGHI-NEJAD
Keyword(s):  
Islet Cell ◽  
Islet Cells ◽  
Hyperinsulinemic Hypoglycemia ◽  
Cell Adenoma ◽  
Non Invasive ◽  
Common Causes ◽  
Group 2 ◽  
Invasive Techniques ◽  
Ductal Tissue ◽  
Diabetic Mothers

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.

Studies on the Physiology of Awareness: An Oximetric Investigation of the Anoxaemia Accompanying Insulin Coma Therapy

1952 ◽  
Vol 98 (412) ◽  
pp. 411-420 ◽  
Author(s):  
John W. Lovett Doust ◽  
Robert A. Schneider
Keyword(s):  
Clinical Symptoms ◽  
Venous Blood ◽  
Insulin Injection ◽  
Personal Contact ◽  
Blood Oxygen Saturation ◽  
The Real ◽  
Arterial Blood ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Insulin Coma Therapy

This investigation deals with the measurement, by a peripheral method of discontinuous spectroscopic oximetry, of the arterial blood oxygen saturation levels in a group of schizophrenic patients undergoing insulin coma therapy.The association between tissue anoxia and insulin hypoglycaemia was first established by Campbell and Dudley in 1924. Dameshek and Meyerson (1935), using the arterio-venous oxygen difference method with the internal jugular vein as the source of venous blood, showed that the injection of insulin in coma doses was accompanied by an anoxaemia in the schizophrenic patients they studied. This work was confirmed by Himwich, Bowmanet al.(1939), and in another paper Himwich (1951, p. 277) and his co-workers found that the correlation of progressively developing clinical symptoms with the decrease of cerebral oxygen uptake was a closer one than the correlation with the more acute fall in the blood-sugar curve. An important symptomatic aspect of insulin hypoglycaemia includes the progressive changes in the levels of consciousness accompanying the approach towards coma. Wilder (1943) has outlined some of these changes, and Frostig (1940) and Himwich (1951, pp. 258-265) have delineated these awareness thresholds and discussed their relationship to the Hughlings Jackson theory of the phyletic organization of the central nervous system. Thus, during thefirst hourfollowing insulin injection, somnolence and lassitude appear to be associated with suppression of cortical and cerebellar activity; in thesecond hourfurther clouding of consciousness, sometimes with excitement, perceptual disturbances, periods of confusion, exacerbations of previously existing hallucinations and latent psychotic syndromes are seen; in thethird hourmotor restlessness and loss of consciousness suggest the release of basal ganglia and hypothalamus; in thefourth hourdeepening stupor and depression of exteroceptive sensitivity indicate a probable release of the midbrain and suppression of pyramidal function; in thefifth hourthe deep pre-mortal coma presages medullary release. Similarly, it is with awareness changes that many workers prefer to diagnose the “real coma” level in a patient under treatment. Thus Sakel (1937) held that coma was to be diagnosed when no further personal contact with the patient was possible, and Kalinowsky and Hoch (1946) agree that the real coma level is reached when it is completely impossible to awaken the patient.

Islet Cell Adenoma: A Review and Illustrative Case

1960 ◽  
Vol 53 (1) ◽  
pp. 24-26
Author(s):  
M C GEPHARDT ◽  
H M FEINBERG ◽  
THOMAS J. HANLON
Keyword(s):  
Islet Cell ◽  
Illustrative Case ◽  
Cell Adenoma
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