Browse

You are looking at 1 - 10 of 20 items for :

Clear All
Cun An Phang Cun An PHANG Medical Student, University of New South Wales, Sydney, Australia

Search for other papers by Cun An Phang in
Google Scholar
PubMed
Close
,
Shejil Kumar Shejil KUMAR Endocrinology Advanced Trainee, St George Hospital, Sydney, Australia

Search for other papers by Shejil Kumar in
Google Scholar
PubMed
Close
, and
Peter Rohl Peter ROHL Staff Specialist in Endocrinology, St George Hospital, Sydney, Australia

Search for other papers by Peter Rohl in
Google Scholar
PubMed
Close

Summary

The rapid rise in the use of immune checkpoint inhibitors as systemic cancer therapy has seen the emergence of immunotherapy-induced diabetes, a severe irreversible immunotherapy-related adverse event. Affected patients typically present with diabetic ketoacidosis (DKA) and low C-peptide consistent with insulin deficiency secondary to autoimmune β-cell destruction. We present the unusual case of a 61-year-old female with metastatic ampullary duodenal adenocarcinoma with primary tumour adjacent to the pancreatic head. She was commenced on immunotherapy after conventional systemic chemotherapy. Acute-onset hyperglycaemia was detected after 7 weeks on weekly blood glucose monitoring, with no glucocorticoid use or prior history of diabetes. On presentation, there was no evidence of DKA, and her glycated haemoglobin level was within the normal non-diabetic range at 5.3%, reflecting the acuity of her presentation. Initial serum C-peptide was preserved; however, it became undetectable a few weeks later, confirming insulin deficiency. We describe a case of atypical presentation of immunotherapy-induced diabetes, review the existing literature on this emerging clinical entity and discuss the differential diagnosis for new-onset diabetes mellitus in patients with metastatic cancer.

Learning points

  • Regular proactive glycaemic monitoring in patients receiving immunotherapy, particularly antibodies against programmed death ligand 1 and PD1, can facilitate very early detection of immunotherapy-induced diabetes, prompting insulin commencement and avoiding life-threatening presentations of diabetic ketoacidosis.

  • Glycated haemoglobin can be within the normal range in patients diagnosed acutely with immunotherapy-induced diabetes.

  • Serum C-peptide can be preserved initially in patients diagnosed with immunotherapy-induced diabetes but is likely to become undetectable during their illness.

  • New-onset diabetes in patients with metastatic cancer carries a broad differential diagnosis.

Open access
Matthew J Verheyden Department of Diabetes, Metabolism and Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Cancer Diagnosis and Pathology Group, Kolling Institute, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by Matthew J Verheyden in
Google Scholar
PubMed
Close
,
Natassia Rodrigo Department of Diabetes, Metabolism and Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Cancer Diagnosis and Pathology Group, Kolling Institute, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Department of Diabetes and Endocrinology, Nepean Hospital, Kingswood, New South Wales, Australia

Search for other papers by Natassia Rodrigo in
Google Scholar
PubMed
Close
,
Anthony J Gill Cancer Diagnosis and Pathology Group, Kolling Institute, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
NSW Health Pathology, Department of Anatomical Pathology, Royal North Shore Hospital, St Leonards, New South Wales, Australia

Search for other papers by Anthony J Gill in
Google Scholar
PubMed
Close
, and
Sarah J Glastras Department of Diabetes, Metabolism and Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Cancer Diagnosis and Pathology Group, Kolling Institute, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by Sarah J Glastras in
Google Scholar
PubMed
Close

Summary

Necrobiosis lipoidica (NL) is a rare and chronic disease characterised by yellow-brown, atrophic, telangiectatic plaques usually located on the lower extremities, with pathological features of collagen necrobiosis and dermal inflammation. Most cases are seen in those with diabetes mellitus, particularly type 1 diabetes (T1DM), and many without diabetes have evidence of abnormal glucose tolerance or family history of autoimmune disease. In this study, we describe four patients with NL and T1DM. A common theme is late identification and delay in diagnosis. Hence, we discuss the clinical features, need for clinicopathological correlation, and the management and prognostic implications for this distinctive entity. While most remain relatively asymptomatic, others progress to debilitating disease with pruritus, dysesthesia, and pain. Pain is often intense in the presence of ulcerated plaques, a morbid complication of NL. Diagnosis requires the integration of both clinical and histopathological findings. NL has proven a challenging condition to treat, and despite the numerous therapeutic modalities available, there is no standard of care. Hence, in this study, we provide an overview of current management strategies available for NL.

Learning points

  • Necrobiosis lipoidica (NL) is classically seen in patients with type 1 diabetes.

  • Koebner phenomenon, defined as the appearance of new skin lesions on previously unaffected skin secondary to trauma, is a well-recognised feature in NL.

  • Background skin phototype contributes to variable yellow appearance of lesions in NL.

  • Diagnosis of NL requires careful clinicopathological correlation.

  • NL is a chronic disease often refractory to treatment leading to significant morbidity for the patient and a management conundrum for the multidisciplinary healthcare team.

  • No standard therapeutic regimen has been established for the management of NL.

Open access
Jenny S W Yun Department of Surgical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

Search for other papers by Jenny S W Yun in
Google Scholar
PubMed
Close
,
Chris McCormack Department of Surgical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

Search for other papers by Chris McCormack in
Google Scholar
PubMed
Close
,
Michelle Goh Department of Surgical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

Search for other papers by Michelle Goh in
Google Scholar
PubMed
Close
, and
Cherie Chiang Department of Internal Medicine, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
University of Melbourne, Parkville, Victoria, Australia

Search for other papers by Cherie Chiang in
Google Scholar
PubMed
Close

Summary

Acanthosis nigricans (AN) is a common dermatosis associated with hyperinsulinemia and insulin resistance. However, AN has been rarely reported in patients with insulinoma, a state of persistent hyperinsulinemia. We present a case of metastatic insulinoma, in whom AN manifested after the first cycle of peptide receptor radionuclide therapy (PRRT). A 40-year-old man was diagnosed with metastatic insulinoma after 5 months of symptomatic hypoglycemia. Within 1 month post PRRT, the patient became euglycemic but developed a pigmented, pruritic rash which was confirmed on biopsy as AN. We discuss the rare manifestation of AN in subjects with insulinoma, the role of insulin in the pathogenesis of AN, malignant AN in non-insulin-secreting malignancies and association with other insulin-resistant endocrinopathies such as acromegaly.

Learning points

  • Acanthosis nigricans (AN) is a common dermatosis which is typically asymptomatic and associated with the hyperinsulinemic state.

  • Malignant AN can rapidly spread, cause pruritus and affect mucosa and the oral cavity.

  • AN is extremely rare in patients with insulinoma despite marked hyperinsulinemia.

  • Peptide receptor radionuclide therapy might have triggered TGF-α secretion in this subject which led to malignant AN.

  • Rapid spread or unusual distribution of pruritic AN warrants further investigation to exclude underlying malignancy.

Open access
Annabelle G Hayes Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, South Australia, Australia
University of Adelaide, Adelaide, South Australia, Australia

Search for other papers by Annabelle G Hayes in
Google Scholar
PubMed
Close
,
Mahesh M Umapathysivam Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, South Australia, Australia
University of Adelaide, Adelaide, South Australia, Australia

Search for other papers by Mahesh M Umapathysivam in
Google Scholar
PubMed
Close
, and
David J Torpy Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, South Australia, Australia
University of Adelaide, Adelaide, South Australia, Australia

Search for other papers by David J Torpy in
Google Scholar
PubMed
Close

Summary

Sulphonylureas are insulinotropic and are not only useful in patients with diabetes but also act in non-diabetic individuals where hypoglycaemia and hyperinsulinism mimic insulinoma. We present a 63-year-old man who presented with inadvertent sulphonylurea-induced life-threatening hypoglycaemia on two occasions, resulting in hazardous and invasive investigation. Biochemistry revealed endogenous hyperinsulinaemia, with elevated serum c-peptide and insulin concentrations during symptomatic hypoglycaemia, and plasma glucose of 1.7 mmol/L. There was no history of sulphonylurea use prompting anatomical insulinoma studies to locate an insulinoma. However, a routine plasma insulinoma screen-detected glimepiride. Directed history implicated a medication taken for erectile dysfunction prior to disturbed consciousness, with alcohol. The tablets, obtained online, were analysed by mass spectrometry and contained tadalafil and dapoxetine as advertised but also contained glimepiride.

Learning points

  • Symptomatic unexplained hypoglycaemia requires investigation with plasma glucose level, c-peptide, insulin level, pro-insulin, beta-hydroxybutyrate, and a sulphonylurea screen regardless of known exposure to sulphonylureas.

  • Consider contamination of alternative or undisclosed medication, including PDE-5 inhibitor erectile dysfunction drugs.

  • Concomitant alcohol may impair glycogenolysis and gluconeogenesis, exacerbating hypoglycaemia.

Open access
Anneke Graf Department of Endocrinology, London, UK

Search for other papers by Anneke Graf in
Google Scholar
PubMed
Close
,
Eleni Armeni Department of Endocrinology, London, UK

Search for other papers by Eleni Armeni in
Google Scholar
PubMed
Close
,
Louise Dickinson Department of Radiology, London, UK

Search for other papers by Louise Dickinson in
Google Scholar
PubMed
Close
,
Matthew Stubbs Department of Haematology, University College London Hospitals NHS Foundation Trust, London, UK

Search for other papers by Matthew Stubbs in
Google Scholar
PubMed
Close
,
Brian Craven Department of Haematology, University College London Hospitals NHS Foundation Trust, London, UK

Search for other papers by Brian Craven in
Google Scholar
PubMed
Close
,
Umasuthan Srirangalingam Department of Endocrinology, London, UK

Search for other papers by Umasuthan Srirangalingam in
Google Scholar
PubMed
Close
, and
Teng-Teng Chung Department of Endocrinology, London, UK

Search for other papers by Teng-Teng Chung in
Google Scholar
PubMed
Close

Summary

Rare cases of vaccine-induced Immune thrombocytopenia and thrombosis (VITT) are being identified after vaccination with the SARS-CoV-2 Oxford–AstraZeneca vaccination. We report on two such patients with associated adrenal involvement, which is now being recognised. Both patients presented with abdominal pain, back pain and vomiting. Case 1 was a 46-year-old male who had received the first dose of the Oxford–AstraZeneca vaccination 8 days earlier. Imaging demonstrated a number of serious thrombotic complications including evolving bilateral adrenal haemorrhage (right adrenal haemorrhage identified at presentation, with the left-sided changes only evident on day 4 of the admission). Case 2 was a 38-year-old female who had received the first dose of Oxford–AstraZeneca vaccination 11 days prior. Imaging demonstrated left renal vein thrombosis and left adrenal infarction. VITT was diagnosed in both cases given these changes and other consistent haematological findings. Both patients were treated empirically for adrenal insufficiency, a diagnosis subsequently confirmed in case 1. We report these two cases of VITT presenting with adrenal complications (haemorrhage and infarction) after Oxford–AstraZeneca vaccination to highlight the association and the need for prompt management of co-existing adrenal insufficiency, especially given the potential for evolving adrenal involvement.

Learning points

  • Adrenal complications (thrombosis/infarction/haemorrhage) may develop as a part of vaccine-induced immune thrombocytopenia (VITT) after SARS-CoV-2 Oxford–AstraZeneca vaccination.

  • Evolving adrenal involvement is possible and ongoing assessment is required to identify this promptly.

  • Cortisol levels may be difficult to interpret when assessing for adrenal insufficiency, given high doses of corticosteroids may be used to manage VITT.

  • Clinicians should have a low threshold for starting empirical replacement with corticosteroids until reliable assessment of adrenal function can be performed.

Open access
Elaine E Sanderson Department of Endocrinology and Diabetes, Perth Children’s Hospital, Perth, Western Australia, Australia

Search for other papers by Elaine E Sanderson in
Google Scholar
PubMed
Close
,
Mark Shah Department of Endocrinology and Diabetes, Perth Children’s Hospital, Perth, Western Australia, Australia

Search for other papers by Mark Shah in
Google Scholar
PubMed
Close
,
Amanda J Hooper Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital and Fiona Stanley Hospital Network, Perth, Australia
School of Medicine, University of Western Australia, Perth, Australia

Search for other papers by Amanda J Hooper in
Google Scholar
PubMed
Close
,
Damon A Bell Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital and Fiona Stanley Hospital Network, Perth, Australia
School of Medicine, University of Western Australia, Perth, Australia

Search for other papers by Damon A Bell in
Google Scholar
PubMed
Close
, and
Catherine S Choong Department of Endocrinology and Diabetes, Perth Children’s Hospital, Perth, Western Australia, Australia
School of Medicine, University of Western Australia, Perth, Australia

Search for other papers by Catherine S Choong in
Google Scholar
PubMed
Close

Summary

We report a case of an 11-year-old girl presenting with a new diagnosis of diabetes associated with a heterozygous missense mutation in the insulin receptor (INSR) gene. This case highlights that INSR gene variants can be a cause for monogenic diabetes in children and adolescents and the need for genetic evaluation in atypical presentations of diabetes. We also describe the possible role of metformin in treating individuals with type A insulin resistance syndrome due to INSR gene variants.

Learning points

  • Insulin receptor (INSR) gene variants can be a cause of monogenic diabetes in children and adolescents.

  • Genetic evaluation should be considered in children and adolescents with type 2 diabetes (T2D), particularly where there is an atypical presentation and/or positive family history.

  • Metformin may have a role in the treatment of type A insulin resistance syndrome due to heterozygous mutation of the INSR gene.

Open access
Arunan Sriravindrarajah Royal Prince Alfred Hospital, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

Search for other papers by Arunan Sriravindrarajah in
Google Scholar
PubMed
Close
,
Amelia Fernandes Royal Prince Alfred Hospital, Sydney, Australia
Faculty of Medicine, University of New South Wales, Sydney, Australia

Search for other papers by Amelia Fernandes in
Google Scholar
PubMed
Close
,
Ted Wu Royal Prince Alfred Hospital, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

Search for other papers by Ted Wu in
Google Scholar
PubMed
Close
, and
Samantha Hocking Royal Prince Alfred Hospital, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Charles Perkins Centre, University of Sydney, Sydney, Australia

Search for other papers by Samantha Hocking in
Google Scholar
PubMed
Close

Summary

Maturity-onset diabetes of the young type 3 (MODY3) accounts for approximately 50% of cases of MODY. First-line treatment with sulfonylureas has been well established for individuals with MODY3. In contrast, the use of sodium-glucose co-transporter 2 (SGLT2) inhibitors in the treatment of individuals with MODY3 remains unclear. This case illustrates the in vivo effect of an SGLT2 inhibitor in a 30-year-old woman with MODY3 with poor glycaemic control despite the treatment with supramaximal doses of sulfonylurea and metformin. The addition of a SGLT2 inhibitor resulted in a rapid improvement in glycaemic control without any hypoglycaemic episodes. This case suggests that SGLT2 inhibitors may be an effective and potent treatment option in addition to sulfonylureas for individuals with MODY3.

Learning points

  • Maturity-onset diabetes of the young type 3 (MODY3) arises from mutations in the hepatocyte nuclear factor-1alpha gene, which controls the expression of sodium-glucose co-transporter 2 (SGLT2) in the kidneys.

  • Paradoxically, despite individuals with MODY3 having reduced expression of SGLT2, SGLT2 inhibitors induce higher glycosuria in individuals with MODY3 compared to individuals with type 2 diabetes mellitus.

  • SGLT2 inhibitors may be an effective treatment for achieving glycaemic control in individuals with MODY3.

Open access
R K Dharmaputra Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia

Search for other papers by R K Dharmaputra in
Google Scholar
PubMed
Close
,
K L Wan Monash Health Pathology, Monash Health, Victoria, Australia

Search for other papers by K L Wan in
Google Scholar
PubMed
Close
,
N Samad Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia

Search for other papers by N Samad in
Google Scholar
PubMed
Close
,
M Herath Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia
Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Victoria, Australia

Search for other papers by M Herath in
Google Scholar
PubMed
Close
,
J Wong Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia
Department of Endocrinology, Monash Health, Victoria, Australia

Search for other papers by J Wong in
Google Scholar
PubMed
Close
,
S Sarlos Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia
Department of Endocrinology, Monash Health, Victoria, Australia
Department of Medicine, School of Clinical Sciences, Monash University, Victoria, Australia

Search for other papers by S Sarlos in
Google Scholar
PubMed
Close
,
S R Holdsworth Department of Immunology, Monash Health, Victoria, Australia

Search for other papers by S R Holdsworth in
Google Scholar
PubMed
Close
, and
N Naderpoor Diabetes and Vascular Medicine Department, Monash Health, Victoria, Australia
Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Victoria, Australia

Search for other papers by N Naderpoor in
Google Scholar
PubMed
Close

Summary

Insulin autoimmune syndrome (IAS) is a rare cause of non-islet cell hypoglycaemia. Treatment of this condition is complex and typically involves long-term use of glucocorticoids. Immunotherapy may provide an alternative in the management of this autoimmune condition through the suppression of antibodies production by B-lymphocyte depletion. We present a case of a 62-year-old male, with refractory hypoglycaemia initially presenting with hypoglycaemic seizure during an admission for acute psychosis. Biochemical testing revealed hypoglycaemia with an inappropriately elevated insulin and C-peptide level and no evidence of exogenous use of insulin or sulphonylurea. Polyethylene glycol precipitation demonstrated persistently elevated free insulin levels. This was accompanied by markedly elevated anti-insulin antibody (IA) titres. Imaging included CT with contrast, MRI, pancreatic endoscopic ultrasound and Ga 68-DOTATATE position emission tomography (DOTATATE PET) scan did not reveal islet cell aetiology for hyperinsulinaemia. Maintenance of euglycaemia was dependent on oral steroids and dextrose infusion. Complete resolution of hypoglycaemia and dependence on glucose and steroids was only achieved following treatment with plasma exchange and rituximab.

Learning points

  • Insulin autoimmune syndrome (IAS) should be considered in patients with recurrent hyperinsulinaemic hypoglycaemia in whom exogenous insulin administration and islet cell pathologies have been excluded.

  • Biochemical techniques play an essential role in establishing high insulin concentration, insulin antibody titres, and eliminating biochemical interference. High insulin antibody concentration can lead to inappropriately elevated serum insulin levels leading to hypoglycaemia.

  • Plasma exchange and B-lymphocyte depletion with rituximab and immunosuppression with high dose glucocorticoids are effective in reducing serum insulin levels and hypoglycaemia in insulin autoimmune syndrome (IAS).

  • Based on our observation, the reduction in serum insulin level may be a better indicator of treatment efficacy compared to anti-insulin antibody (IA) titre as it demonstrated greater correlation to the frequency of hypoglycaemia and to hypoglycaemia resolution.

Open access
Jennifer R Snaith Department of Diabetes and Endocrinology, Westmead Hospital, Westmead, New South Wales, Australia
Department of Diabetes and Endocrinology, St Vincent’s Hospital, Darlinghurst, New South Wales, Australia
Healthy Ageing, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by Jennifer R Snaith in
Google Scholar
PubMed
Close
,
Duncan McLeod Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Department of Anatomical Pathology, Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, New South Wales, Australia
Westmead Institute for Medical Research, Sydney, New South Wales, Australia

Search for other papers by Duncan McLeod in
Google Scholar
PubMed
Close
,
Arthur Richardson Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Department of Surgery, Westmead Hospital, Sydney, New South Wales, Australia
Department of Surgery, Sydney Adventist Hospital, Sydney, New South Wales, Australia

Search for other papers by Arthur Richardson in
Google Scholar
PubMed
Close
, and
David Chipps Department of Diabetes and Endocrinology, Westmead Hospital, Westmead, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by David Chipps in
Google Scholar
PubMed
Close

Summary

Insulinomatosis is a rare cause of hyperinsulinaemic hypoglycaemia. The ideal management approach is not known. A 40-year-old woman with recurrent symptomatic hyperinsulinaemic hypoglycaemia was diagnosed with an insulinoma. A benign 12 mm pancreatic head insulinoma was resected but hypoglycaemia recurred 7 years later. A benign 10 mm pancreatic head insulinoma was then resected but hypoglycaemia recurred within 2 months. Octreotide injections were trialled but exacerbated hypoglycaemia. After a 2-year interval, she underwent total pancreatectomy. A benign 28 mm pancreatic head insulinoma was found alongside insulin-expressing monohormonal endocrine cell clusters (IMECCs) and islet cell hyperplasia, consistent with a diagnosis of insulinomatosis. Hypoglycaemia recurred within 6 weeks. There was no identifiable lesion on MRI pancreas, Ga-68 PET or FDG PET. Diazoxide and everolimus were not tolerated. MEN-1 testing was negative. Insulinomatosis should be suspected in insulinomas with early recurrence or multifocality. De novo lesions can arise throughout the pancreas. Extensive surgery will assist diagnosis but may not provide cure.

Learning points:

  • Insulinomas are usually benign and managed surgically.

  • Insulinomatosis is characterised by multifocal benign insulinomas with a tendency to recur early. It is rare.

  • Multifocal or recurrent insulinomas should raise suspicion of MEN-1 syndrome, or insulinomatosis.

  • Insulinomatosis is distinguished histologically by insulin-expressing monohormonal endocrine cell clusters (IMECCs) and tumour staining only for insulin, whereas MEN-1 associated insulinomas stain for multiple hormones.

  • The ideal treatment strategy is unknown. Total pancreatectomy may not offer cure.

Open access
Annabelle M Warren Department of Endocrinology and Diabetes, Alfred Health, Melbourne, Victoria, Australia

Search for other papers by Annabelle M Warren in
Google Scholar
PubMed
Close
,
Duncan J Topliss Department of Endocrinology and Diabetes, Alfred Health, Melbourne, Victoria, Australia
Monash University, Central Clinical School, Melbourne, Victoria, Australia

Search for other papers by Duncan J Topliss in
Google Scholar
PubMed
Close
, and
Peter Shane Hamblin Department of Endocrinology and Diabetes, Alfred Health, Melbourne, Victoria, Australia
Monash University, Central Clinical School, Melbourne, Victoria, Australia
Department of Endocrinology and Diabetes, Western Health, Melbourne, Victoria, Australia
Department of Medicine, Western Clinical School, The University of Melbourne, Melbourne, Victoria, Australia

Search for other papers by Peter Shane Hamblin in
Google Scholar
PubMed
Close

Summary

Despite improvements in localisation techniques and surgical advances, some patients with insulinoma will not be cured by surgery or may not be suitable for surgery. Medical management with diazoxide is an option for such cases. This case report details 27 years of successful management of insulinoma using diazoxide. It has been effective and safe, with only minor adverse effects.

Learning points:

  • Long term diazoxide use can be a safe, effective option for insulinoma when it cannot be localised or removed surgically.

  • Common adverse effects include peripheral oedema, hyperuricaemia, and hirsutism.

  • 68Ga-NOTA-exendin-4 PET/CT scan should be considered for insulinoma localisation when other modalities have been unhelpful.

Open access