A 79-year-old Japanese woman was brought to an emergency room with symptoms of nausea and vomiting. She was diagnosed as MAC pulmonary disease at the age of 52, and as polymyalgia rheumatic at 73 and rheumatoid arthritis at 75. She was taking 150 mg/day of rifampicin, 250 mg/day of ethambutol, 400 mg/day of clarithromycin and 5 mg/day of prednisolone for the treatment of MAC pulmonary disease and 3 mg/day of tacrolimus and 100 mg/day of pregabalin for polymyalgia rheumatic and rheumatoid arthritis. She had no remarkable family history. She had no drinking and smoking. Her height, body weight and BMI were 155.4 cm, 33.5 kg and 13.9 kg/m2, respectively. Her vital signs were as follows: temperature, 36.8°C; blood pressure, 118/62 mmHg; heart rate, 84 beats/min; oxygen saturation, 98 % (room air). Table 1 shows laboratory data in an emergency room. Her infection markers were markedly elevated: white blood cell, 21,460 /µL (neutrophil, 88.5 %); C-reactive protein, 36.09 mg/dL. Liver and renal function was almost within the normal range: aspartate aminotransferase (AST), 34 U/L; alanine transaminase (ALT), 13 U/L; alkaline phosphatase (ALP), 250 U/L; γ-glutamyl transpeptidase (γ-GTP), 24 U/L; lactate dehydrogenase (LDH), 215 U/L; creatinine, 0.74 mg/dL; blood urea nitrogen (BUN), 39 mg/dL. In addition, her nutrition-associated data were as follows: plasma glucose, 66 mg/dL; hemoglobin A1c (HbA1c), 6.1 %; total cholesterol, 113 mg/dL; total protein, 6.1 g/dL; albumin, 2.8 g/dL; cholinesterase, 125 U/L. Moreover, her urinary test showed elevated urinary ketone body (2+), and serum ketone body concentrations were high as follows: total ketone body, 3,107.6 µmol/L; acetoacetate, 1,032.7 µmol/L; β-hydroxybuterate, 2074.9 µmol/L.
Table 1
Laboratory data in an emergency room in this subject
Variable | Result | Reference range | Variable | Result | Reference range |
Blood biochemistry | Peripheral blood |
Total protein (g/dL) | 6.1 | 6.6–8.1 | White blood cells (/µL) | 21460 | 3300–8600 |
Albumin (g/dL) | 2.8 | 4.1–5.1 | Neutrophil (%) | 88.5 | 52.0–80.0 |
Globulin (g/dL) | 3.3 | 2.2–3.4 | Red blood cells (×104/µL) | 439 | 386–492 |
Total bilirubin (mg/dL) | 0.8 | 0.4–1.5 | Hemoglobin (g/dL) | 12.0 | 11.6–14.8 |
AST (U/L) | 34 | 13–30 | Hematocrit (%) | 37.5 | 35.1–44.4 |
ALT (U/L) | 13 | 7–23 | Platelets (×104/µL) | 22.3 | 15.8–34.8 |
LDH (U/L) | 215 | 124–222 | Diabetes and Dyslipidemia markers |
ALP (U/L) | 250 | 106–322 | Plasma glucose (mg/dL) | 66 | |
γ-GTP (U/L) | 24 | 9–32 | Hemoglobin A1c (%) | 6.1 | 4.9–6.0 |
BUN (mg/dL) | 39 | 8–20 | Total cholesterol (mg/dL) | 113 | 142–248 |
Creatinine (mg/dL) | 0.74 | 0.46–0.79 | Total ketone body (µmol/L) | 3107.6 | 0.0–130.0 |
Cholinesterase (U/L) | 125 | 201–421 | Acetoacetate (µmol/L) | 1032.7 | 0.0–55.0 |
Uric acid (mg/dL) | 8.7 | 2.6–5.5 | β-Hydroxybuterate (µmol/L) | 2074.9 | 0.0–85.0 |
Creatine Kinase (U/L) | 49 | 41–153 | Urinary test |
Amylase (U/L) | 264 | 44–132 | Urinary pH | 5.5 | 5.0–7.5 |
CRP (mg/dL) | 36.09 | < 0.14 | Urinary protein | 1+ | - |
Sodium (mEq/L) | 140 | 138–145 | Urinary sugar | - | - |
Potassium (mEq/L) | 3.9 | 3.6–4.8 | Urinary ketone body | 2+ | - |
Chloride (mEq/L) | 99 | 101–108 | Urinary bilirubin | - | - |
Calcium (mg/dL) | 7.9 | 8.8–10.1 | Urinary blood | 2+ | - |
Abbreviation: AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDH, lactate dehydrogenase; ALP, alkaline phosphatase; γ-GTP, γ-glutamyl transpeptidase; BUN, blood urea nitrogen; CRP, C-reactive protein |
After admission, we started antibiotics therapy (13.5 g/day of tazobactam), because her infection markers were markedly elevated. Her fever was immediately improved next day (its peak was 37.5°C) and her infection markers were decreased (white blood cell, 5,260 /µL; C-reactive protein, 5.42 mg/dL). Surprisingly, she had been hospitalized four times within one year. Therefore, we checked details of her laboratory data during the period of hospitalization. Her body weight was decreased to under 35.0 kg about 1 years ago. Her main complaint in every hospitalization were nausea and vomiting, although she was complicated with MAC pulmonary disease. Moreover, at every hospitalization, she had slight hypoglycemia and urinary ketone bodies (Fig. 1). Based on such findings, we finally diagnosed her as acetonemic vomiting complicated with low body weight. In addition, her low body weight was caused by MAC pulmonary disease. We started the education and diet therapy for her (total 1,500 kcal/day (about 30 kcal per ideal body weight) and without skipping meals including carbohydrate), and after then she was not hospitalized for one year.