Emaciated Patient with Slowly Progressed Type 1 Diabetes Mellitus Who Had Hypoglycemia Despite Impaired Insulin Secretion

23 Case Report Emaciated Patient with Slowly Progressed Type 1 Diabetes Mellitus who had Hypoglycemia Despite Impaired Insulin Secretion Takeshi Ito, MD, FACP, Nobuya Fujita, MD, PhD, Naoki Maeda, MD, Masayoshi Komura, MD, Hideto Tomioka, MD, Nobuki Ohnishi, MD, Kunihiko Arai, MD, Mizue Yokoyama, MD, Ryoji Yoshida, MD, PhD Department of Internal Medicine, Saiseikai Utsunomiya Hospital, Tochigi, Japan ABSTRACT：We describe a 38-year-old, severely emaciated female with slowly progressive type 1 diabetes mellitus （SPIDDM), who had hypoglycemia due to fasting and an extremely low energy intake. After being diagnosed with diabetes mellitus（DM), she took in only 300-500 kcal per day and her weight had decreased to 30 kg, with a body mass index（BMI）of 11.4 kg／m2. She was admitted with hypoglycemia, and SPIDDM was confirmed by nearly- completely ceased insulin secretion and seropositivity towards anti-GAD antibody. After appropriate dietary therapy and insulin administration, she recovered from a state of emaciation and her glucose metabolism was restored. With this patient it proved very effective for the general physician to coordinate treatment for both diabetes and an eating disorder. KEY WORDS：slowly progressive type 1 diabetes mellitus, eating disorder, hypoglycemia, emaciation, insulin therapy Gen Med：2009；10：23-27 disorder is serious in females, and is considered to cause INTRODUCTION obesity or emaciation, as well as impaired glucose lowly progressive type 1（insulin-dependent）dia- metabolism that leads to hyper- or hypoglycemia, and betes mellitus（SPIDDM）starts in the non-insulin- diabetes-related complications6. Therefore, further studies of Sdependent state and ultimately becomes insulin- the relationship between type 1 DM and eating disorders are dependent diabetes mellitus（IDDM）with exhausted intrin- required to improve patient mortality7. sic insulin secretion over several years. Positivity for Here, we describe a severely emaciated female with an pancreatic islet-related auto-antibodies characterizes eating disorder who had survived SPIDDM without insulin SPIDDM, which accounts for about 5% of all diabetes therapy despite nearly ceased endogenous insulin production, mellitus（DM）that is considered type 21,2. Eating disorders and whose emaciation and impaired glucose metabolism that are diagnosed according to the Diagnostic and Statistical were repaired by administering insulin. Manual for Mental Disorders Text Revision（DSM-Ⅳ-TR)3 are more prevalent in type 1 diabetic, rather than non- diabetic, females4,5. Type 1 diabetes with a concurrent eating Author for correspondening：Takeshi Ito, MD, FACP Department of Internal Medicine, Saiseikai Utsunomiya Hospital, 911-1 Takebayashi, Utsunomiya, Tochigi, 321-0974, Japan, Phone：＋81-28-626-5500, Fax：＋81-28-626-5573, E-mail：[email protected] Received for publication 30 August 2008 and accepted in revised form 19 November 2009 24 General Medicine, Vol. 10, No. 1, 2009 Table 1. Laboratory data upon admission. CASE REPORT Urinalysis Blood chemistry A38-year-female was transferred to our hospital for a Protein ― TP 5.3 g／dl detailed examination of weight loss and hypoglycemia Glucose ― Alb 3.5 g／dl despite her diabetes mellitus. Her personality was inflexible Blood ― BUN 9.4 mg／dl and methodical and she exhibited compulsive neurosis-like Ketone ― UA 3.7 mg／dl symptoms, but showed no anxiety or depression. Diabetes Cr 0.4 mg／dl and psychological illness was unknown in her family history. Blood cell count T-chol 117 mg／dl Four years before admission she had chronic thyroiditis, WBC 2600／ml TG 65 mg／dl 4 but fasting plasma glucose（FPG）of 130 mg／dl, HbA1c of RBC 362×10 ／ml T-Bil 1.0 mg／dl 7.5%, and sugars detected in her urine led to a diagnosis of Hb 11.0 g／dl ALP 1440 U／l diabetes mellitus（DM）at the hospital to which she was Ht 32.8% ChE 74 U／l Plt 22.3×104／ml AST 221 U／l previously admitted. At that time a physician specializing in ALT 371 U／l diabetes care took charge of her, and a 1,400 kcal dietary HBs Ag ― g-GTP 322 U／l restriction was advised. However, she became pathologically HCV Ab ― LDH 461 U／l fixated on the notion of zero calories and thus consumed FPG＊ 53 mg／dl only boiled vegetables. We estimated that she had taken in HbA1c 5.9% 300-1, 000 kcal／day during prior to hospitalization. Two Na 135 mEq／l years and 8 months before admission, glimepiride（1mg） K 3.6 mEq／l and supplemental thyroid hormone treatment（levothyroxine Cl 95 mEq／l sodium）were prescribed, but she visited her previous CRP ＜0.3 mg／dl hospital irregularly. During the next 4 years, her weight ＊FPG, fasting plasma glucose gradually declined from 54 to 40 kg. One year and 6 months before admission menstruation ceased. Two weeks before admission the patient weighed approximately 40 kg, and she became intractable and the patient was transferred to our was an active mother. Due to family problems, she ate hospital. nothing for 5 days before admission to her previous hospital. At transfer to our facility, a physical examination revealed On the day of admission to the hospital, she lost the following：height 162 cm, body weight 30 kg and BMI consciousness while driving and had a traffic accident. 11. 4 kg／m2, with distinct skeletal emaciation. The ocular Though no injuries or epilepsy were apparent, she was conjunctivas were free of anemia and jaundice, the thyroid admitted to the previous hospital for detailed testing due to was not palpable, the chest and abdomen were free of severe emaciation（37 kg）and hypoglycemia［plasma glu- abnormalities, and fine hair was absent. Table 1 shows the cose of（PG）20 mg／dl, measured using a portable blood blood and urinary findings at admission to our hospital, glucose meter during transport to the Emergency Room]. which indicate leukocytopenia, hypoproteinemia, and liver Upon admission, because her level of consciousness on the damage. Fasting plasma glucose（FPG）was low（53 mg／dl） Glasgow Coma Scale was 13（E4 V4 M5), glucose was and HbA1c was within the normal range（5.8%）without infused intravenously and she became alert immediately. ketosis［urinary ketone（−）］or acidosis（pH 7.49, pCO2 8 − Based on conditions that matched Whippleʼs triad , hospital 45. 3 mmHg, HCO3 33. 9 mmol／／／L, BE 9. 5 mmol／L).To staff determined that she was likely to have suffered a treat the diabetes and emaciation, we, along with a hypoglycemia attack. Although neither insulin nor an oral psychiatrist, initially counseled the patient and made antidiabetic agent was administered, the low trend in plasma substantial effort to change her harmful perception that glucose levels continued. Despite 1 month of hospitalization, skipping meals would prevent an increase in blood glucose her weight declined to 30 kg［（body mass index（BMI）11. and the use of insulin and to help her understand that her 4kg／m2, degree of obesity −48. 0%）]. At the hospital, progressive emaciation was life-threatening. Physicians although a physician specializing in diabetes care took charge specializing in diabetes care, members of a nutrition support of her and encouraged her to keep up an appropriate energy team, nursing staff, and psychiatrists all offered suggestions intake, she only ate vegetables（300-500 kcal／day）and during the case conference. However, some of the advice refused blood tests, drip infusions, and psychiatric consulta- given was conflicting. For patients greatly obsessive about tion, insisting that it was much better to skip meals than to eating disorders and blood glucose levels, it is not wise to receive insulin infusions. The patient-doctor relationship consult without coordination；therefore, the attending doctor, Ito T, et al. Emaciated patient with slowly progressed type 1 diabetes mellitus 25 Table 2. Endocrinological data before treatment IRI ＜1.00 mU／ml TSH 0.487 mIU／ml S-CPR＊＜0.05 ng／ml freeT4 1.83 ng／dl U-CPR＊＊ 7.8 mg／day freeT3 1.55 pg／ml anti-GAD Ab 99.0 U／ml Anti-Tg Ab 16.5 U／ml anti-IA-2Ab 11 U／ml Anti-TPO Ab ＜0.3 U／ml anti-insulin Ab 3.6% ACTH 58.2 pg／ml Cortisol 47.4 mg／dl Adrenaline 94 pg／ml Noradrenaline 421 pg／ml Glucagon 131 pg／ml GH 36.8 ng／ml ＊S-CPR, serum-C-peptide immunoreactivity；＊＊U-CPR, urinary-C-peptide immunoreactivity 75g-oral glucose tolerant test（OGTT) Time（min) PG†（mg／dl) IRI （mU／ml) S-CPR（ng／ml) Cortisol（mg／dl) 0 59 ＜1.00 0.08 47.7 30 101 ＜1.00 0.35 46 60 69 ＜1.00 0.15 39.9 90 163 ＜1.00 0.53 36.4 120 193 ＜1.00 0.67 36.2 180 2031.14 0.87 29.8 †PG, plasma glucose HLA DNA typing DRB1＊04051-080302／DQB1＊0401-060101 a general physician, coordinated advice and medical care to counteracting a tendency to hypoglycemia（Table 2).In with various professionals playing their own roles in one the 75 g-oral glucose tolerance test（OGTT）（Table 2), team. plasma glucose increased in a bimodal manner, indicating Thereafter, she changed her attitude to eating dramatically, impaired glucose tolerance. Plasma glucose again increased and 2 or 3 days after her admission to our hospital she started in delayed phases, accompanied by a slight increase in taking in 1, 200 kcal／day or more. She no longer needed insulin secretion. These findings suggested an imbalance in intravenous drips and did not experience further severe glucose metabolism and insulin secretion. S-CPR levels 6 hypoglycemia resulting in a loss of consciousness. Her minutes after 1 mg glucagon injection was 0. 68 ng／ml, endocrine data measured on Days 6-7 of our hospitalization consistent with S-CPR and U-CPR depletion.

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