<b>Non‐islet cell tumour‐associated hypoglycaemia: <sup>111</sup>In‐octreotide imaging and efficacy of octreotide, growth hormone and glucocorticosteroids</b>

Perros, Petros; Simpson, John; Ja, Innes; Jd, Teale; Ja, McKnight

doi:10.1046/j.1365-2265.1996.721542.x

Cited by 59 publications

(55 citation statements)

References 15 publications

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“…The presence of somatostatin receptors has been demonstrated previously in a pleural fibroma causing NICTH (Perros et al 1996) and in w40-55% of hepatocellular carcinomas (Reubi et al 1999, Cebon 2006. However, in NICTH the administration of somatostatin analogues such as octreotide, generally does not restore glucose levels, probably because somatostatin receptors, if present at all in the hypoglycaemia causing tumour, are non-functional (Hunter et al 1994, Perros et al 1996, Morbois-Trabut et al 2004.…”

Section: Somatostatin Analoguesmentioning

confidence: 96%

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Groot¹,

Rikhof²,

Doorn³

et al. 2007

Endocrine Related Cancer

202

326

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This review focuses on the tumour types and symptoms associated with non-islet cell tumourinduced hypoglycaemia (NICTH) as well as the pathogenesis, diagnosis and treatment of this rare paraneoplastic phenomenon. In addition, we report two illustrative cases of patients suffering from NICTH caused by a solid fibrous tumour and a haemangiopericytoma respectively. In the first case, NICTH resolved following complete resection of the tumour, but in the second case the patient needed long-term treatment aimed at controlling hypoglycaemia because of nonresectable metastases. Many tumour types have been associated with NICTH. The crucial event in the development of NICTH seems to be overexpression of the IGF-II gene by the tumour. NICTH is characterised by recurrent fasting hypoglycaemia and is associated with the secretion of incompletely processed precursors of IGF-II ('big'-IGF-II) by the tumour. This induces dramatic secondary changes in the circulating levels of insulin, GH, IGF-I and IGF-binding proteins, resulting in an insulin-like hypoglycaemic activity of 'big'-IGF-II.

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Section: Somatostatin Analoguesmentioning

confidence: 96%

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Groot¹,

Rikhof²,

Doorn³

et al. 2007

Endocrine Related Cancer

202

326

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“…Patients with NICTH may undergo complete remission following surgical removal of the tumour; even partial removal often may reduce or abolish the hypoglycaemia . This is followed by a rise in IGF1 levels, restoration of the IGF2/IGF1 ratio, blood glucose and plasma insulin levels (Perros et al 1996. Both hGH and prednisolone can induce a substantial and seemingly specific effect in alleviating the symptoms of hypoglycaemia (Mitchell et al 1968, Teale et al 1992, Perros et al 1996.…”

Section: Ectopic Igf1mentioning

confidence: 99%

“…This is followed by a rise in IGF1 levels, restoration of the IGF2/IGF1 ratio, blood glucose and plasma insulin levels (Perros et al 1996. Both hGH and prednisolone can induce a substantial and seemingly specific effect in alleviating the symptoms of hypoglycaemia (Mitchell et al 1968, Teale et al 1992, Perros et al 1996. Although a therapeutic role of long-acting somatostatin analogues seems feasible, they should be used with caution as they may inhibit other counter-regulatory responses to hypoglycaemia hormones (Kaltsas et al 2004b).…”

Section: Ectopic Igf1mentioning

confidence: 99%

Paraneoplastic syndromes secondary to neuroendocrine tumours

Kaltsas

Androulakis²,

Herder³

et al. 2010

Endocrine-Related Cancer

100

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Neuroendocrine tumours may be either benign or malignant tumours, and have the ability to synthesise and secrete biologically active substances characteristic of the cell of origin that can cause distinct clinical syndromes. The term 'paraneoplastic syndromes' (PNSs) is used to denote syndromes secondary to substances secreted from tumours not related to their specific organ or tissue of origin and/or production of autoantibodies against tumour cells; such syndromes are mainly associated with hormonal and neurological symptoms. Appreciation of the presence of such syndromes is important as clinical presentation, if not identified, may delay the diagnosis of the underlying neoplasia. Conversely, early recognition can allow for more rapid diagnosis, particularly as the coexistence of a neoplasm with a clinical or biochemical marker offers an additional determinant of tumour status/progression. PNSs can complicate the patient's clinical course, response to treatment, impact prognosis and even be confused as metastatic spread. Their diagnosis involves a multidisciplinary approach, and detailed endocrinological, neurological, radiological and histological studies are required. Correct diagnosis is essential as the treatment of choice will be different for each disorder, particularly in the case of malignant tumours; it is therefore important to develop appropriate means to correctly identify and localise these tumours. Clinical awareness and the incorporation into clinical practise of 111 In-octreotide scintigraphy, chromogranin A and other evolving biochemical marker measurement techniques have substantially contributed to the identification of patients harbouring such syndromes. Diseasespecific medical therapies are mandatory in order to prevent recurrence and/or further tumour growth. Owing to their rarity, central registration of these syndromes is very helpful in order to be able to provide evidence-based diagnostic and therapeutic approaches.

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“…Previously documented cases of NICTH have been associated with variable results from imaging with 111 In-labelled octreotide (10,11), although a recent report of autoradiographic studies on sections of tumour suggested that negative imaging with 111 In-labelled octreotide does not exclude the possibility of low levels of expression of somatostatin receptors on the tumour cells (11). To date, there have been no reported cases of a beneficial effect of octreotide on glucose levels in NICTH, and, moreover, in our first patient a test dose of octreotide of 100 mg led to a fall in glucose.…”

Section: Discussionmentioning

confidence: 99%

Dose-related effects of growth hormone on IGF-I and IGF-binding protein-3 levels in non-islet cell tumour hypoglycaemia

Drake

Miraki

Siddiqi

et al. 1998

European Journal of Endocrinology

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Mesenchymal tumours are a well recognised cause of spontaneous hypoglycaemia. The mechanism is thought to relate to hypersecretion by tumour cells of high molecular mass insulin-like growth factor-II (pro-IGF-II), with consequent suppression of growth hormone (GH) secretion. The use of recombinant human (rh)GH has been reported to alleviate hypoglycaemia in non-islet cell tumour hypoglycaemia, and the mechanism is thought to relate to GH-mediated increments in serum levels of IGF-binding protein-3 (IGFBP-3), thereby reducing the bioavailability of IGF-II. We report the effect of increasing doses of rhGH on the clinical condition and serum IGF-I and IGFBP-3 levels in two patients with solitary pleural fibrous tumours causing severe hypoglycaemia. Hypoglycaemia was successfully alleviated in each patient although, despite using large doses of rhGH, the observed increments in IGFBP-3 were only modest. We postulate that the beneficial effects of rhGH in this situation are likely to be multifactorial and not simply related to increments in serum IGFBP-3 levels.

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Non‐islet cell tumour‐associated hypoglycaemia: ¹¹¹In‐octreotide imaging and efficacy of octreotide, growth hormone and glucocorticosteroids

Cited by 59 publications

References 15 publications

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Paraneoplastic syndromes secondary to neuroendocrine tumours

Dose-related effects of growth hormone on IGF-I and IGF-binding protein-3 levels in non-islet cell tumour hypoglycaemia

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Non‐islet cell tumour‐associated hypoglycaemia: 111In‐octreotide imaging and efficacy of octreotide, growth hormone and glucocorticosteroids

Cited by 59 publications

References 15 publications

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Non-islet cell tumour-induced hypoglycaemia: a review of the literature including two new cases

Paraneoplastic syndromes secondary to neuroendocrine tumours

Dose-related effects of growth hormone on IGF-I and IGF-binding protein-3 levels in non-islet cell tumour hypoglycaemia

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Non‐islet cell tumour‐associated hypoglycaemia: ¹¹¹In‐octreotide imaging and efficacy of octreotide, growth hormone and glucocorticosteroids