A 40-year-old male visited our hospital as polydipsia, polyuria and general fatigue developed approximately 2 months before. His body weight decreased from 72.7 kg (BMI 25.5 kg/m2) to 67.6 kg (BMI 23.8 kg/m2) during this term. He had been diagnosed with depression and taking multiple medications and dyslipidemia (T-Chol 263 mg/dl, LDL-C 186 mg/dl, HDL-C 48 mg/dl, TG 272 mg/dl) had been pointed out in the annual medical check-up conducted a year before. The blood drawn for examination presented strawberry milk-like appearance (Fig. 1a, left panel). Laboratory test revealed elevated fasting blood glucose and HbA1c; 306 mg/dl and 12.5 %, respectively. Furthermore, serum triglyceride was markedly elevated up to 5661 mg/dl, which presumably caused the dramatic change of blood color. He was admitted to our hospital for further examination about general fatigue, weight loss and hypertriglycemia. Serum amylase and lipase were both within normal range; 64 IU/l and 41 U/l, respectively and there were no symptoms which suggested pancreatitis. After admission, multiple daily insulin injection was started to obtain good glycemic control. The patient was diagnosed with type 2 diabetes as serum insulin level (3.4 μU/ml) and urinary C-peptide response (>200 µg/day) were preserved and autoantibodies related to type 1 diabetes were absent. No diabetic complications such as neuropathy, retinopathy and nephropathy were observed. Lipemia retinalis was not observed in funduscopy. We also conducted further examination to clarify the cause of extraordinarily elevated serum triglyceride. Chylomicronemia indicated that the patient had type V hyperlipoproteinemia. He had no habit of alcohol drinking and hypothyroidism was ruled out from the laboratory test (thyroid stimulating hormone (TSH) 1.065 μIU/ml, free T3 3.0 pg/ml, free T4 1.1 ng/dl). In addition, no medications which the patient was taking for depression have been reported to exacerbate diabetes or hypertriglycemia. We also checked LPL and ApoC-II to rule out any genetic factors just in case. As the results, ApoC-II was within normal range, which excluded ApoC-II deficiency. Serum heparinized lipoprotein lipase (LPL) was within normal range (255 ng/mL), which ruled out LDL deficiency, although LPL gene mutation screening was not conducted. In addition, we checked ApoE genotype to rule out any genetic factors just in case. As the results, his ApoE phenotype was E3/E3, which is not susceptible to hypertriglycemia compared to E2/E2 or E4/E4 (Kei et al. 2015; Shinozaki et al. 2005). Eruptive xanthomas were not observed probably because serum triglyceride was increased very rapidly together with acute exacerbation of type 2 diabetes. The result of treatment naive lipoprotein fraction was as shown in Fig. 1b, which revealed pre-β-band and prominently elevated VLDL fraction up to 51 %. This patient was taking a large amount of soft drinks due to polydipsia before admission, resulting in rapid exacerbation of type 2 diabetes and relative insufficiency of insulin action. Indeed, serum non-esterified fatty acid was extremely elevated up to 6.12 mEq/l (normal range is 0.14–0.85 mEq/l). We diagnosed this patient as diabetic lipemia as there was no finding suggesting genetic hypertriglycemia or secondary causes such as multiple myeloma, paraproteinemia and systemic lupus erythematosus.
After admission, in order to obtain good glycemic control, we started multiple daily insulin injection using insulin lispro and glargine. As shown in Fig. 2a, after increasing insulin dose, blood glucose level was decreased. Finally, when we increased insulin dose up to 40 U (insulin lispro 30 U, glargine 10 U), good glycemic control was obtained; fasting blood glucose levels were approximately 100 mg/dl. As shown in Fig. 2b, serum triglyceride level was markedly decreased together with the decrease of blood glucose level. Serum triglyceride level was as high as 5661 mg/dl on admission, but its level 1, 4, 6, 8, 13 days after admission was 4261, 2196, 1287, 714, 311 mg/dl, respectively. Finally, on 14th day, when he was discharged, it was improved to 272 mg/dl and blood appearance became completely normal without using any hypolipidemic agents. As shown in Fig. 1a (right panel), after insulin therapy, the serum became transparent, and there was marked difference between before and after insulin therapy, indicating that this case was truly diabetic lipemia.
