Diabetes

New-onset diabetes after renal transplant (NODAT) presenting as diabetic ketoacidosis (DKA) in a patient with sickle cell disease (2015)

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Type of publication:
Conference abstract

Author(s):
*Kaldindi S.R., *Moulik P., *Macleod A.

Citation:
Diabetic Medicine, March 2015, vol./is. 32/(117-118)

Abstract:
A 42-year-old Afro-Caribbean female presented with 1 week history of polyuria, polydypsia and vomiting. She had a background of transfusion associated iron overload and renal failure secondary to sickle cell disease. She underwent a live donor renal transplant 8 months prior to admission. Immunosuppressive therapy included tacrolimus, mycophenolate, prednisolone 5mg once a day. There was no family history of diabetes. She had a normal body mass index. Results revealed a pH of 7.08, bicarbonate of 6.6mmol/l, capillary blood glucose tests recorded as greater than 28.7mmol/l, ketones 7.0mmol/l, Hb 84 g/l. Her creatinine was 101mumol/l (baseline 90), eGFR 52 and tacrolimus levels were within therapeutic range. No obvious precipitant for diabetic ketoacidosis (DKA) was found. She responded well to intravenous fluids and insulin. Her glutamic acid decarboxylase (GAD) and islet antigen 2 (IA2) antibodies were negative. Possible causes for her diabetes include iron overload, steroid therapy, tacrolimus. In her case, she presented with a short timeline of symptoms along with severe DKA. This is typical of Type 1 diabetes, even though her antibodies were negative. NODAT usually behaves like Type 2 diabetes but, rarely, such patients can also present with an insulin deficient state similar to Type 1 diabetes. The Renal Association suggests lower levels of tacrolimus to decrease NODAT risk and screening for diabetes post-transplant. A steroid sparing immunosuppressive regimen may help in reducing the incidence of NODAT.

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Selective diabetic gastroparesis (2015)

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Type of publication:
Conference abstract

Author(s):
*Rai D., *Kalidindi S., *Moulik P., *Macleod A.

Citation:
Diabetic Medicine, March 2015, vol./is. 32/(118)

Abstract:
Up to 5% of people with Type 1 diabetes have been reported to have gastroparesis. We present the case of a 19-year-old female who presented to hospital with diabetic ketoacidosis due to intractable vomiting. She developed Type 1 diabetes aged 8. Initial diabetes control was very poor, with a peak HbA1c of 167mmol/ mol and she developed severe non-proliferative diabetic retinopathy. One year prior to admission, she actively improved her blood sugars and dropped her HbA1c gradually down to 105mmol/mol. Paradoxically this seems to have worsened her vomiting. She denied any other symptoms of enteropathy and had no signs of autonomic or peripheral neuropathy. A CT and MRI brain were negative. She developed malnutrition requiring total parenteral nutrition and trials of prokinetics, dietary modifications were unsuccessful. A percutaneous endoscopic gastrotomy-jejunal tube was inserted which allowed simultaneous post pyloric feeding and gastric decompression. After a period of stable blood glucose with an HbA1c of 48mmol/mol, she had a formal gastric emptying study which confirmed severe delayed gastric emptying with a time (lag) of 87 min (normal <55) and half-life of 119 min (normal <80). Gastroscopy showed severe reflux oesophagitis consistent with delayed gastric emptying. She is currently awaiting a gastric pacemaker and manages to have small frequent meals with supplemental jejunal feeding. Diabetic gastroparesis is usually associated with peripheral and autonomic neuropathy, but she seems to have isolated gastroparesis. She also developed severe depression, psychological issues which required cognitive behavioural therapy. These issues could have worsened her symptoms.

Link to full-text: http://onlinelibrary.wiley.com/doi/10.1111/dme.12668_1/pdf