Case Report:

A 66-year-old woman presented with impaired consciousness. Her past medical history was no specific findings. She had a family history of type 2 diabetes mellitus in her grandmother, grandfather, and cousin. She was living  alone, working as a care worker, non-smoker, and her alcohol consumption was 350 ml/day of beer.

Around November X-24 (at the age of 43 years), the patient visited a nearby clinic with chief complaints of dry mouth, polydipsia, and polyuria. Her blood glucose level was 600 mg/dl, and the patient was diagnosed with diabetes mellitus. Treatment with oral sulfonylurea was started on an outpatient basis because the patient refused hospitalization. However, the patient lost 8 kg of body weight in six months, and insulin was started in March X-23 (at the age of 44 years). In X-22, the patient was referred to our hospital due to a high hemoglobin A1c (HbA1c) of 10.6% to 11.6% (National Glycohemoglobin Standardization Program), and she was subsequently diagnosed with type 1 diabetes mellitus, thereafter continuing with insulin treatment at our outpatient clinic. The patient was admitted to our hospital in August X-17 and May X for ketoacidosis. Peripheral neuropathy and simple retinopathy were observed as diabetic complications, along with stage 1 nephropathy.

Around November 15, X,the patient presented with epigastric pain and vomiting. Upper gastrointestinal endoscopy on November 17 showed no abnormalities. Insulin aspart in the morning (6 units), at lunchtime (10 units), and in the evening (12 units), as well as glargine before bedtime (8 units), resulted in poor glycemic control with an HbA1c of 9.6% and a casual blood glucose level of 412 mg/dl. The urinary ketone level was 2+. During a regular outpatient check-up on December 4, hepatobiliary enzyme levels were elevated [aspartate transaminase (AST) 136 U/l, alanine transaminase (ALT) 127 U/l, alkaline phosphatase (ALP) 392 U/l, and lactate dehydrogenase (LDH) 326 U/l)]. Contrast-enhanced computed tomography (CT) showed hepatomegaly and elevated CT numbers in the hepatic parenchyma.

While the blood glucose level was 242 mg/dl, the urinary ketone level was still 2+.The day after the check-up, the patient vomited once at night on December 5 and vomited again, twice, on December 7 at work. In the evening on December 7, a coworker of the patient noticed the patient’s finger tremors and incoherent speech, and the patient came to the emergency room of our hospital at around 7 PM. At the time of the checkup, the patient presented with findings of diabetic ketoacidosis (blood glucose level 1110 mg/dl; blood ketone bodies 10,926 μmol/l; pH 7.247), and she was immediately hospitalized on the same day.

Conditions at visit: height 155 cm, body weight 50 Kg, body mass index (BMI) 20.8 kg/m², blood pressure 82/39 mmHg, pulse rate 84 beats/min, respiratory rate 20 breaths/min, temperature 37.6°C, level of consciousness (restless), Japan Coma Scale Grade 1, Glasgow Coma Scale 14 out of 15 (eye opening 4, best verbal response 4, best motor response 6). No specific abnormalities in the head, neck, and chest areas were evident. Pressure pain was noted in the epigastric region. On neurological examination, the pupil size was 3 mm/3 mm with a prompt response to light. No other neurological abnormalities were noted.

A markedly elevated blood glucose level (1110 mg/dl), high total blood ketone bodies (10,926 μmol/l), and urinary ketones (3+) were noted. Metabolic acidosis was observed, as shown by the venous blood gas results (pH 7.160 and BE-19.1 mmol/l). Compared to the results during the outpatient check-up on December 4, the patient had low Na levels (126 mEq/l), elevated K levels (5.5 mEq/l), and elevated hepatobiliary enzyme levels (AST 239 IU/l, ALT 169 IU/l, ALP 434 IU/l, LDH 508 IU/l, γ-GTP 383 IU/l). A slight increase in the inflammatory response (WBC 9030/mm³, CRP 0.59 mg/dl) was also observed, There were no abnormal findings on plain chest X-rays, electrocardiograms, and head CT at that visit.

The patient in the present study was 66 years of age, much older than patients in previously reported studies. While the patient had a high blood glucose level (1110 mg/dl) at the time of hospitalization, HbA1c (9.6%) was lower than previously reported studies, suggesting that there was a very wide fluctuation in blood glucose levels. Although the elevated liver enzyme levels and hepatomegaly improved in the process of glycemic control, it was extremely difficult to achieve glycemic control in this case, as described in the course of events after hospitalization. Even though the trigger for hepatic glycogenosis is not yet known, appropriately adjusting the amount of insulin and continuing glycemic control should prevent future relapse of hepatic damage.

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Valentina Rose
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Endocrinology and Metabolism: Open Access
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