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

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Chris McCormack Department of Surgical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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Michelle Goh Department of Surgical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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Cherie Chiang Department of Internal Medicine, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
University of Melbourne, Parkville, Victoria, Australia

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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.

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Nishant Raizada Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India

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S H Rahaman Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India

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D Kandasamy Department of Radiology, All India Institute of Medical Sciences, New Delhi, India

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V P Jyotsna Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India

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Summary

Insulin autoimmune syndrome (IAS) is a rare cause of hyperinsulinemic hypoglycaemia, which is known to occur in association with the use of sulfhydryl-containing drugs and autoimmune disorders. We describe a patient with hitherto an unreported association of IAS with ankylosing spondylitis. We have also performed and described a simplified method of polyethylene glycol (PEG) precipitation of an insulin bound antibody in the serum.

Learning points

  • IAS should be considered in differential diagnosis of endogenous hyperinsulinemic hypoglycaemia.

  • Ankylosing spondylitis can be associated with IAS apart from several other autoimmune diseases.

  • Very high serum insulin levels (100–10 000 μU/ml) are frequently seen in IAS.

  • When faced with very high serum insulin before suspecting insulinoma, it is advisable that PEG precipitation of serum be done to identify antibody bound insulin.

  • A clinical suspicion of IAS can avoid expensive imaging and unnecessary surgery in affected patients.

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Soham Mukherjee Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Anuradha Aggarwal Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Ashu Rastogi Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Anil Bhansali Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Mahesh Prakash Department of Radiology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Kim Vaiphei Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Pinaki Dutta Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India

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Summary

Spontaneous diabetic muscle infarction (DMI) is a rare and under diagnosed complication of diabetes mellitus. Clinically it presents with acute to subacute onset swelling, pain and tenderness of muscle(s) without systemic manifestations. MRI is helpful in diagnosis, exclusion of other causes and for localization of affected muscle for biopsy in atypical cases. Muscles of the thighs are commonly affected in diabetic myonecrosis (DMN). Here we present the summary of four cases seen in the last 3 years in a tertiary care centre with simultaneous or sequential involvement of multiple groups of muscles or involvement of uncommon sites. All these patients had advanced duration of diabetes with microvascular complications and poor glycemic control. Conservative management including rest and analgesics is the treatment of choice. Short-term prognosis is good but there may be recurrence.

Learning points

  • A high index of suspicion is required for the diagnosis of DMN which can avoid inadvertent use of antibiotics.

  • Acute–subacute onset severe focal muscle pain in the absence of systemic symptoms in a female patient with long-standing diabetes with microvascular complications suggests DMI.

  • MRI is the most sensitive test for diagnosis.

  • Muscle biopsy should be reserved for atypical cases.

  • Conservative management including rest and analgesics has good outcome.

  • Improvement usually occurs within 6–8 weeks, but there may be recurrence.

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Pinaki Dutta Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Anuradha Aggarwal Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Yashpal Gogate Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Uma Nahar Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Viral N Shah Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Mandeep Singla Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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N Khandelwal Radiodiagnosis, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Anil Bhansali Departments of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

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Summary

We describe the clinical presentation, diagnostic and management issues in five cases of non-islet cell tumor hypoglycemia (NICTH), diagnosed at a tertiary care institute over a period of 15 years. The clinical, laboratory, and histopathological findings of these patients along with diagnostic utility of IGF2:IGF1 ratio are discussed. The mean age of presentation was 52 years, with a male predominance (3:2). Three patients presented with recurrent episodes of fasting hypoglycemia and it was detected in other two patients during hospitalization. Two patients had acromegaloid features that regressed following treatment. One patient had hypokalemia. Low levels of insulin, C-peptide, GH, and IGF1 were invariably found in all. The IGF2 level was elevated in only one patient; however, IGF2:IGF1 ratio was more than 10 in four of the five patients. The mean tumor size was 16.4 cm and mean weight was 3.6 kg. Four patients had mesenchymal tumors and one had epithelial tumor. NICTH is a rare cause of hypoglycemia. Hypoinsulinemic hypoglycemia with low IGF1 and IGF2:IGF1 ratio more than 10 is suggestive of this entity.

Learning points

  • NICTH should be considered in patients presenting with tumor of mesenchymal origin and hypoglycemia.

  • Hypoinsulinemic hypoglycemia with low IGF1 is a strong biochemical evidence of NICTH.

  • IGF2:IGF1 ratio of more than 10 is a complementary investigation in the absence of an assay facility for IGF2.

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