Functioning Islet-Cell Carcinoma of the Pancreas With Cushing's Syndrome

Balls, Kent; Nicholson, J. T.; Goodman, H. L.; Touchstone, Joseph C.

doi:10.1210/jcem-19-9-1134

Cited by 39 publications

(9 citation statements)

References 19 publications

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“…A similar case to that described here has been reported (Balls et al, 1959), in which Cushing's syndrome was associated with a large abdominal mass and hypoglycaemia. Biopsy revealed poorly differentiated carcinoma not diagnostic of the primary site of origin, but consistent with islet-cell carcinoma.…”

Section: Discussionsupporting

confidence: 83%

“…In addition to the two cases of Cushing's syndrome due to islet-cell carcinoma already cited (Balls et al, 1959), we have found accounts in the literature of 10 further cases (McLetchie and Scott, 1942-4;Castillo et al, 1950;Rosenberg, 1956;Armando, 1957;Bourgeois et al, 1959;Farrant and Insley, 1960;Meador et al, 1962;Hallwright et al, 1964;Jarett et al, 1964), and know of another; but in only four was hypoglycaemia a feature.…”

Section: Discussionmentioning

confidence: 58%

“…The mechanism of production of hypoglycaemia is unknown, and although plasma insulin-like activity is sometimes increased (Whitney and Heller, 1961), as in the case reported by Balls et al (1959), this is neither invariable nor established as being due to insulin. In the present case hyperinsulinism due to insulinoma was established conclusively both biochemically and histologically.…”

Section: Discussionmentioning

confidence: 99%

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Hyperinsulinism and Cushing's Syndrome

Marks¹,

Samols²,

Bolton³

1965

BMJ

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Many reports of the association of malignant neoplasms and Cushing's syndrome have appeared in the past few years, and a syndrome of ectopic adrenocorticotrophin production has been clearly defined (Bagshawe, 1960;Liddle et al., 1963). The purpose of this paper is to describe its occurrence with malignant insulinoma and to draw attention to certain similarities between ectopic adrenocorticotrophin production and pluriglandular syndrome. CASE REPORTA 43-year-old postman was first seen in hospital on 2 September 1962. He had been unwell for five weeks. He complained of being rather " hazy in the head " and of having " slowed-up " mentally. He Recovery was uneventful, and the patient was discharged from hospital three weeks later on maintenance (50-mg.) doses of cortisone. He was readmitted less than 24 hours later in hypoglycaemic coma, and with a blood glucose concentration of 13 mg./100 ml. He was subsequently found to be unable to withstand fasting overnight without developing severe hypoglycaemia. The fasting plasma insulin concentration on two occasions was 350 1AU/100 ml.-that is, more than five times the upper limit of normal. An attempt to make an intravenous tolbutamide tolerance test was unsuccessful, as consciousness was lost during the injection. The fasting blood glucose concentration was 20 mg./100 ml. and plasma insulin 420 pU/ml. Seven minutes after tolbutamide and glucose-given to restore consciousness-the plasma insulin was 580 p.U/ml. and blood glucose 272 mg./100 ml. Sixty minutes later the blood glucose was 37 mg./100 ml., and plasma insulin 570 ,uU/ml.The glucose assimilation coefficient K value was 3.15. A further 25 g. of glucose, given by mouth at 60 minutes, was associated with a rise in blood glucose to 44 mg./100 ml., but failed to elicit an insulinaemic response, while a second injection of tolbutamide 20 minutes later evoked an immediate (200 ,U/ml.) rise in plasma insulin to 675 pU/ml. On a three-hourly feeding regime, the patient was able to lead a more or less " normal " life at home for two months, though minor episodes of neuroglycopenia were not uncommon. Coma developed only twice, and on the second occasion (12 February 1963) he died -six and a half months after the onset of his illness, and three months after adrenalectomy.Necropsy was carried out 36 hours after death (Dr. A. Tay). The body was that of a moderately obese man with marked -cutaneous pigmentation. Pathological abnormalities were confined to the presence of a firm indurated mass, 18 mm. in diameter, in the tail of the pancreas, and multiple yellowish-white metastases in the liver. In particular, the thyroid, parathyroid, and pituitary glands were normal, as was the brain, which showed no evidence of an anoxic condition (Dr. J. B. Brierley), as is usual with death from hypoglycaemia.Histological examination of a metastasis, using special staining techniques, was thought to be typical of malignant insulinoma, a moderate number of cells containing characteristic granules (Dr.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

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Hyperinsulinism and Cushing's Syndrome

Marks¹,

Samols²,

Bolton³

1965

BMJ

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“…Serum potassium was 2.1 meq/liter and serum bicarbonate was 37.5 meq/liter. A 24-hour urinary cortisol was 5119 pg (normal, 0-120 pg/24 hours), and the plasma cortisol was 74.3 pg/lOO ml a t 08:OO hours (normal 0-29 pg/IOO ml) and 131.3 pg/lOO ml, at 20:OO hours (normal, [0][1][2][3][4][5][6][7][8][9][10] …”

mentioning

confidence: 99%

Electron microscopy of an acth-secreting islet cell carcinoma

Rawlinson

1973

Cancer

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A metastasizing ACTH‐secreting islet cell carcinoma was examined at autopsy. During life, the patient had elevated plasma ACTH and urinary and plasma cortisol. ACTH was assayed postmortem in the primary tumor. With the light microscope, the histologic features of the primary and metastatic tumor were characteristic of an islet cell carcinoma. Special stains for alpha granules, beta granules, and ACTH granules were negative. With the electron microscope, dense‐core granules were easily identified in the tumor. The granules were morphologically similar to those seen in the pituitary gland, in pituitary adenomas, and in other tumors known to produce ACTH.

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“…The first case of this association was described by Castillo, del Trucco, and Manzuoli (1950). Eight further cases have been reported by Rosenberg (1956), Armando (1957), Bourgeois, Roge, Clement, Martin and, Descamps (1959), Balls, Nicholson, Goodman, and Touchstone (1959), Farrant and Insley (1960), Meador, Liddle, Island, Nicholson, Lucas, Nuckton, and Luetscher (1962), Jarett, Lacey, and Kipnis (1964), and Marks, Samols, and Bolton (1965). The literature contains no account of this syndrome in a child.…”

Section: Discussionmentioning

confidence: 99%

Cushing's syndrome associated with an islet-cell tumour of the pancreas in a boy aged 2 years.

Burkinshaw¹,

O’Brien²,

Pendower³

1967

Archives of Disease in Childhood

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We present this case because, so far as we can discover, no similar one has yet been reported in a child.Case History This boy was born in June 1963. He presented at the out-patient clinic in September of 1965 at the age of 2 years and 3 months, on account of sudden excessive weight gain. He had been healthy and free of symptoms until 6 weeks before, when he had suddenly developed a ravenous appetite ('he will eat two of every meal I offer him'). He had become very fat and his face had become very red. His weight four weeks before his attendance had been 12 7 kg.: now he weighed 15-9 kg. There were no other symptoms, and he was lively and cheerful, with no polydipsia or polyuria. He had never had a fit, faint, or episode of disordered consciousness, such as might be caused by hypoglycaemia. His birthweight had been 2-7 kg., and the perinatal period and infancy had been uneventful. The parents were both alive and well, and not of abnormal size or weight. The paternal great grandfather was short and fat. He had one brother aged 4 years alive and well, weighing at present 13-5 kg.Examination. He was very fat (Fig. 1), weight 15 9 kg. (97th centile), height 88 cm. (50th centile). He had a red moon face, and there was a faint brownish pigmentation of the entire skin, but no pigment inside the mouth. The genitalia were not enlarged and there was no hirsutes. Blood pressure estimations were difficult owing to the excessive amount of fat and to the child's dislike of the procedure. Two readings of 110 mm. Hg were recorded by the flush and palpation methods using a 10 cm. cuff. A firm, non-tender rounded mass about the size of an orange could be felt in the left hypochondrium. It did not move on respiration and did not extend backward into the loin. No other abnormalities were found. A provisional diagnosis was made of a rapidly growing, probably suprarenal tumour, and the child was admitted at once into the ward.Investigations. Table I

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Functioning Islet-Cell Carcinoma of the Pancreas With Cushing's Syndrome

Cited by 39 publications

References 19 publications

Hyperinsulinism and Cushing's Syndrome

Hyperinsulinism and Cushing's Syndrome

Electron microscopy of an acth-secreting islet cell carcinoma

Cushing's syndrome associated with an islet-cell tumour of the pancreas in a boy aged 2 years.

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