Serum angiotensin-converting enzyme and frequency of severe hypoglycaemia in Type 1 diabetes: does a relationship exist?

Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be renoprotective. We determined whether urinary ACE2 enzyme activity and protein levels (ELISA), as well as angiotensinogen and ACE, are elevated during clamped euglycemia (4–6 mmol·L–1) in patients with uncomplicated type 1 diabetes (T1D, n = 58) compared with normoglycemic controls (n = 21). We also measured the effect of clamped hyperglycemia (9–11 mmol·L–1) on each urinary factor in T1D patients. Urinary ACE2 activity and protein levels were higher during clamped euglycemia in T1D compared with the controls (p < 0.0001). In contrast, urinary angiotensinogen levels (p = 0.27) and ACE excretion (p = 0.68) did not differ. In response to clamped hyperglycemia in T1D, urinary ACE2 protein decreased (p < 0.0001), whereas urinary ACE2 activity as well as angiotensinogen and ACE levels remained unchanged. Urinary ACE2 activity and protein expression are increased in T1D patients prior to the onset of clinical complications. Further work is required to determine the functional role of urinary ACE2 in early T1D.

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Case Report: Isolated hepatosplenic sarcoidosis treatment improving glycaemic control in a type 1 diabetic patient

F1000Research ◽

10.12688/f1000research.21798.1 ◽

2020 ◽

Vol 9 ◽

pp. 50

Author(s):

Sérgio Pina ◽

Teresa Salero ◽

Mariana Figueiras ◽

Rui Osório ◽

Sofia Amálio

Keyword(s):

Type 1 Diabetes ◽

Glycaemic Control ◽

Angiotensin Converting Enzyme ◽

Ct Scan ◽

Enzyme Inhibitor ◽

Systemic Disease ◽

Insulin Dose ◽

Beta Thalassemia ◽

Converting Enzyme

Sarcoidosis is a multi-systemic disease characterized by non-caseating granulomas in various organs. The aetiology is still unknown. Although the liver is the third most commonly affected organ, hepatosplenic sarcoidosis without lung involvement is very uncommon. There is a high frequency of certain autoimmune illnesses observed in sarcoidosis, but association with type 1 diabetes is infrequent. We present the case of a 31-year-old woman, with type 1 diabetes mellitus diagnosed 22 years before with a glycated haemoglobin (HbA1c) above 14%, diabetic nephropathy, retinopathy and neuropathy, hypercholesterolemia and beta thalassemia. She was medicated with an angiotensin-converting enzyme inhibitor, a dihydropyridine calcium antagonist and insulin. The patient presented with a 4-month history of tiredness, abdominal pain, weight lost and hepatosplenomegaly. Abdominal ultrasound revealed hepatomegaly with regular contours, diffuse heterogeneous texture, containing numerous nodules with slight enlargement of the spleen. Serum angiotensin converting enzyme (ACE) was 67 IU/L and a sedimentation rate of 120 mm/h. Computer tomography (CT) scan confirmed hepatosplenomegaly and suggested infiltration in both organs. Liver biopsies were compatible with sarcoidosis. After ruling other organ involvement, a diagnosis of isolated hepatosplenic sarcoidosis was provided and prednisolone (40mg/day) was started. After a few months the patient developed a corticoid-induced myopathy confirmed with electromyography. Prednisolone was reduced to 20mg/day and azathioprine (50mg/day) treatment initiated. After a 7-month treatment, chest-abdomen-pelvis CT scan showed a marked reduction of the nodularity and hepatosplenomegaly and after 1 year the patient was completely asymptomatic (HbA1c, 7.5%; ACE, 24IU/L). At 18-month follow-up there was no evidence of recurrence (HbA1c, 7%), with optimum glycaemic control with total daily insulin dose lowered to half. This is an uncommon case in which the treatment of hepatosplenic sarcoidosis with regression of sarcoid tissue can help explain the improvement of glycaemic control in this patient.

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