病人姓名 : 劉 x 玲 性別 : 女 病歷號碼 : U221424340 住院日期 : 94.3.31

Chief complaint Nausea and vomitting for one day

Present illness She was 18 y/o female with previous

healthy condition. She suffered form nausea and vomitting since one week ago. And generalized weakness was also found. Dyspnea and body weight loss of 8 kg in one month ago were noted. No palpitation or hand tremor was told. She went to Dr 李 `s OPD for help. Thyrotoxicosis was suspected and T3/T4/TSH were measured on 3/29.

Present illness But nausea and generalized weakness

were getting worse .So she was sent to our ER for help. At ER, generalized weakness and Kussmauel respiration were noted. Hyperglycemia(1036 mg/dL)with blood osmorlity 344 mOsm/Kg was found. Metabolic acidosis (anion gap >12) was also noted . Urine analysis also revealed ketone body(+++). Under impression of diabetic keto-acidosis ,she was admitted to our hospital for further treatment.

Personal history Social history: a student, no history

of smoking, drinking, or betel nut chewing

Allergy history: No history of food or drua allergy

Family: Father has DM with OHA control for thirty years

Review of system General : weight loss(+), fatigue(+), weakness(+) appetite change(-), fever(-), chills(-), night

sweats(-) Skin: rashes(-), pruritus(-), bruising(-), dryness(-)

itching(-), skin cancer or other lesions(-). Head: trauma(-), headache(-), tenderness(-),

dizziness(+),syncope(-)

Review of system Eyes: glasses(-), photophobia(-), blurring(-),

diplopia(-),inflammation(-), discharge(-), dry eyes(-) excessive tearing(-), changes in visual field(-) history of cataracts or glaucoma(-)

Ears: tinnitus(-), pain(-), discharge(-), vertigo(-) history of ear infections(-), hearing

impairment(-)

Review of system Nose: epistaxis(-), obstruction(-), polyps(-), sinus

problems(-), sense of smell loss(-)

Mouth and Throat: bleeding gums(-), voice change(-),

dysphagia(-),ulcerations or other lesions of tongue(-), gums(-),or buccal mucosa(-)

Respiratory: chest pain(-)wheezing(-), dyspnea(-),

cough(-) hemoptysis(-), sputum(-), history of pneumonia(-) or TB(-)

Review of system Cardiovascular: dyspnea on exertion(-), chest pain(-),

orthopnea(-), claudication(-), varicose vein(-), palpitation(-), peripheral edema(-), History of MI(-) or murmur(-), paroxysmal noctural dyspnea(-) (-)

Gastrointestinal: abdominal pain(-), heartburn(-), nausea(-),

vomiting(-), hematemesis(-), diarrhea(-), indigestion(-),destension(-), constipation(-), melena(-), intolerace for greasy food(-), change in stool shapes and color(-)

Review of system

Musculoskeletal musculoskeletal trauma(-),

arthralgia(-), arthritis(-), redness(-), tenderness(-), back pain(+), joint swelling(-), limitation of range of motion(-)

Physical exam Blood pressure 109/63 mmHg. BT: 37.3

degree Celcius. Pulse rate 74/min, regular. Respiration rate 18/min Conciousness: dizziness (Glasgow scale:

E4M6V5) Skin: normal skin turgor, cold Lymph node: negative. Head: normal.

Physical exam Eyes: conjunctiva: pale, sclera:

anicteric, Jugular vein: no engorgement Heart: RHB without murmur Chest wall: symmetric Lung: Breathing sound: clear. Abdomen: flat, Soft, no tenderness Bowel sound: normoactive

Physical exam Liver: not palpable Spleen: not palpable. Muscle power:normal Coordination: normal. Extremities: no pitting edema

hand tremor(-)

BCS data

BCS data

Urine exam

Endocrine survy

Active problems Type 1 DM with Ketoacidosis and

hyperosmolarity

Treatment course

After admission,prompt intravenous fluid challenge and insulin injection were administerred. Her sugar was under control step by step. Jusonin had been infused due to diabetic ketoacidosis. She was transferred to ordinary ward on April 1st. Her insulin dosage escalated progressively due to poor control of serum sugar. Glucagon test was performed on April 8th to evaluate her islet cells reserved function. She was discharged with drug home on April 8th 2005.

Glucagon test ( C-peptide level)

Glucagon test ( Glucose level)

Journal of Clinical Endocrinology and Metabolism, Vol. 80, No. 21995

Modified Glucagon Test Allowing Simultaneous Estimation of Insulin Secretion and Insulin Sensitivity: Application to Obesity, Insulin-Dependent Diabetes Mellitus, and Noninsulin-Dependent Diabetes Mellitus

Preface The test is based on the ability of iv glucagon

to stimulate insulin secretion and the efficiency of insulin to decrease the blood glucose levels previously raised by glucagon.

Indices of insulin secretion and insulin sensitivity have been compared in various populations: lean controls, nondiabetic obese subjects, IDDM patients, and NIDDM patients with or without weight excess.

Materials and Methods Subjects: The following groups of individuals were examined: 1) 11 lean [body mass index (BMI), <25 kg/m*] and healthy

volunteers, 2) 5 obese (BMI, >30 kg/m2 ,1 subjects with normal fasting

blood glucose and normal to mildly impaired glucose tolerance 3) 9 IDDM patients, 4) 7 nonobese NIDDM patients, and 5) 8 moderately obese (BMI, >25 kg/m2) NIDDM subjects.

Materials and Methods Diabetic patients with marked

hyperglycemia were connected to glucose-controlled insulin infusion (GCII) system during the night preceding the study to control fasting blood glucose.

Instrumentation The glucose-controlled insulin infusion

system used in this study was the Biostator (Miles Martin Laboratories, Eklhart, IN). This is a closed loop device that continuously samples blood for glucose analysis and infuses insulin to mimic insulin secretion.

Test glucagon (Nova-Nordisk, Copenhagen,

Denmark) at a dose of 1 mg/m’ corporeal surface.

During the 20 min after glucagon injection, blood glucose levels were allowed to rise freely, i.e. blood glucose levels were continuously recorded by the Biostator, but insulin was not infused.

After that time, the Biostator was allowed to infuse insulin in a glucose-controlled basis (static and dynamic mode).

Test This insulin infusion was maintained for

the next 30 min, and then the test was completed.

Two continuous blood collections were obtained: from O-20 min and from 20-50 min.

Computations Evaluation of the hepatic response. The

hepatic ability to increase glucose output in response to glucagon was estimated as the rate of increase in blood glucose when this increase was linear, that is from l0-20 min of the test.

Computations Evaluation of the B-cell response. The

C-peptide concentration was measured in plasma from both tubes of continuous blood collection (from O-20 min and from 20-50 min)

Computations Evaluation of the sensitivity to insulin.

An index of insulin sensitivity was obtained by dividing the rate of decrease in blood glucose (when this decrease was linear, i.c. from 40-50 min) by the total amount of insulin entering the circulation (insulin secreted + insulin infused)

Results Maximum blood glucose levels (9.6 2

0.3 mmol/L) were attained in 16-38 min (mean, 30 2 1 min).

No significant differences were seen in the rising blood glucose profile of the different groups of subjects studied.

Most subjects exhibited a similar hepatic response to glucagon.

Results In the subsequent decline in blood

glucose, both normal controls and IDDM patients showed faster decreases than obese or NIDDM subjects.

Results The rates of decrease in blood glucose

concentration were significantly (P <

0.001) higher in normal controls (0.208 ± 0.018 mmol/L.min) and IDDM patients (0.155 ± 0.030 mmol/L.min) than in obese subjects (0.110 ± 0.015 mmol/L.min ) or NIDDM patients (0.094 ± 0.011 mmol/L.min).

Results the obese subjects showed a

significantly greater endogenous insulin secretion

In the nonobese NIDDM group, the

endogenous insulin secretion tended to be slightly lower than that in lean controls or overweight NIDDM patients

Results The index of sensitivity to insulin,

calculated by dividing the rate of decrease in blood glucose in the last 10 min of the test by the total amount of insulin entering the circulation, is lower in obese subjects and even more decreased in NIDDM patients than in normal controls and IDDM patients (Table 4).

Discussion The estimate of insulin sensitivity was

obtained by comparing the decline in blood glucose levels and the total amount of insulin entering the circulation.

As insulin secretion is markedly deficient in some diabetic patients, we used a glucose-controlled insulin infusion in the last 30 min of the test to induce a rapid decrease in blood glucose levels.

Discussion The endogenous insulin secretion was

increased in obese subjects. In IDDM patients, the index of insulin

sensitivity was slightly lower than that in normal controls.

In most of the NIDDM patients, the insulin efficiency to decrease blood glucose was very low, lower than that observed in obese nondiabetic patients.