Clinical Overview > Condition/ Syndrome

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  • Diabetic hypoglycaemia x
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Naoya Toriu Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Masayuki Yamanouchi Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Rikako Hiramatsu Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Noriko Hayami Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Junichi Hoshino Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Akinari Sekine Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Masahiro Kawada Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Eiko Hasegawa Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Tatsuya Suwabe Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Keiichi Sumida Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Toshiharu Ueno Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Naoki Sawa Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan

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Kenichi Ohashi Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan
Department of Pathology, Yokohama City University, Graduate School of Medicine, Yokohama, Japan

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Takeshi Fujii Department of Pathology, Toranomon Hospital, Tokyo, Japan

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Kenmei Takaichi Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan
Okinaka Memorial Institute for Medical Research, Tokyo, Japan

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Motoko Yanagita Department of Nephrology, Kyoto University Graduate School of Medicine, Japan

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Tetsuro Kobayasi Okinaka Memorial Institute for Medical Research, Tokyo, Japan

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Yoshifumi Ubara Nephrology Center and Department of Rheumatology, Toranomon Hospital, Tokyo, Japan
Okinaka Memorial Institute for Medical Research, Tokyo, Japan

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Summary

We report the case of a 67-year-old Japanese woman with type 1 diabetes mellitus. At 47 years of age, her hemoglobin A1c (HbA1c) was 10.0%, and she had overt nephropathy. The first renal biopsy yielded a diagnosis of diabetic nephropathy. Intensive glycemic control was initiated and her HbA1c improved to 6.0%. Renal dysfunction showed no progression for 15 years. At 62 years of age, a second renal biopsy was performed. Glomerular lesions did not show progression but tubulointerstitial fibrosis and vascular lesions showed progression compared with the first biopsy. Intensive glycemic control can prevent the progression of glomerular lesions, but might not be effective for interstitial and vascular lesions.

Learning points:

  • Intensive control of blood glucose can prevent the progression of glomerular lesions.

  • Intensive control of blood glucose may not be able to prevent progression of interstitial and vascular lesions.

  • CSII reduces HbA1c without increasing the risk of hypoglycemia.

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N Jassam Harrogate District Hospital, Harrogate HG2 7SX, UK

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N Amin Leeds Children's Hospital NHS Trust, Leeds, UK

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P Holland Leeds Children's Hospital NHS Trust, Leeds, UK

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R K Semple Wellcome Trust, Cambridge University Hospital, Cambridge, UK

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D J Halsall Clinical Biochemistry Department, Addenbrooke's Hospital, Cambridge, UK

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G Wark SAS Peptides Hormone Section, Royal Surrey County Hospital, Surrey, UK

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J H Barth Blood Sciences Department, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Summary

A lean 15-year-old girl was diagnosed with type 1 diabetes based on symptomatic hyperglycaemia and positive anti-islet cell antibodies. Glycaemia was initially stabilised on twice-daily mixed insulin. After 11 months from the time of diagnosis, she complained of hyperglycaemia and ketosis alternating with hypoglycaemia. This progressively worsened until prolonged hospital admission was required for treatment of refractory hypoglycaemia. A high titre of anti-insulin antibodies was detected associated with a very low recovery of immunoreactive (free) insulin from plasma after precipitation with polyethylene glycol, suggesting the presence of insulin in bound complexes. Insulin autoimmune syndrome was diagnosed and metabolic fluctuations were initially managed supportively. However, due to poor glucose control, immunosuppressive therapy was initiated first with steroids and plasmapheresis and later with anti-CD20 antibody therapy (Rituximab). This treatment was associated with a gradual disappearance of anti-insulin antibodies and her underlying type 1 diabetes has subsequently been successfully managed with an insulin pump.

Learning points

  • Anti-insulin antibodies may result in low levels of free insulin.

  • Polyclonal anti-insulin antibodies can interfere with the pharmacological action of administered insulin, resulting in hypoglycaemia and insulin resistance, due to varying affinities and capacities.

  • In this patient, rituximab administration was associated with a gradual disappearance of anti-insulin antibodies.

  • It is hypothesised that this patient had subcutaneous insulin resistance (SIR) caused by insulin capture at the tissue level, either by antibodies or by sequestration.

  • A prolonged tissue resistance protocol may be more appropriate in patients with immune-mediated SIR syndrome.

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