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Thread: [Case] A Clinical Case of New Diagnosed Diabetes

  1. #1

    Post [Case] A Clinical Case of New Diagnosed Diabetes

    A 59 yrs Asican male found his fasting serum glucose level exceeded the upper limit in June when during a regular annual physical examination (fasting serum glucose 6.32 mmol/L on Jun 17th 2013).

    After a month he re-check his fasting serum glucose and it was still higher than the upper limit (fasting serum glucose 6.62 mmol/L on Jul 18th 2013).

    So I arranged a oral glucose tolerance test (OGTT) on Aug 30th 2013 which the result was fasting plasma glucose 7.25 mmol/L, 2-h plasma glucose 14.32 mmol/L. It appears that the diagnosis of diabetes is certain. So I arrange him to a endocrinology clinic (the visit is going to be on Sep 6th 2013).

    PS: Aug 30 2013
    Fasting plasma glucose 7.25 mmol/L (130.6 mg/dL)
    0.5-h plasma glucose 13.20 mmol/L (237.8 mg/dL)
    1-h plasma glucose 16.40 mmol/L (295.5 mg/dL)
    2-h plasma glucose 14.32 mmol/L (258.0 mg/dL)

    Tom Hsiung

    Clinical Pharmacy Specialist

    Sep 1 2013
    Last edited by admin; Tue 14th July '15 at 5:43pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  2. #2


    On Sep 7th 2013 This patient tested the A1C, hepatic function, lipid metabolism, renal function, fasting plasma glucose, and urinary dialysis. Now I list their results below.

    A1C: 6.7%
    Hepatic function

    Total bilirubin: 11.8 umol/L
    Direct bilirubin: 4.8 umol/L
    In-direct bilirubin: 7.0 umol/L

    ALT: 71 IU/L
    AST: 70 IU/L

    Glutamyltranspetidase: 76 IU/L

    Albumin: 46.7 g/L
    Globulin: 34.0 g/L

    Alkaline phosphatase: 77 IU/L
    Lactate dehydrogenase: 217 IU/L

    Lipid metabolism

    Triglyceride: 3.72 mmol/L
    Cholesterol: 3.88 mmol/L
    High density lipoprotein: 0.84 mmol/L
    Low density lipoprotein: 1.97 mmol/L

    Renal function

    Blood urea nitrogen: 4.80 mmol/L
    Serum creatinine: 72.8 umol/L (0.82 mg/dL,1 mg/dL = 88.4 umol/L )
    Estimated creatinine clearance: 81.4 ml/min
    Serum uric acid: 379.0 umol/L

    Fasting plasma glucose

    FPG: 7.32 mmol/L

    Urinary dialysis

    Occult blood test: 10(+/-)
    Urinary leukocyte: 500 (+++)
    Urinary protein: (-)
    Urinary glucose: normal
    Urinary acetone bodies: negative
    Urinary bilirubin: negative

    Urinary leukocyte (microscope): 19 /HP
    Urinary red blood cell: 3 /HP
    Clinical Pharmacy Specialist - Infectious Diseases

  3. #3


    This patient should be treated as older adults. Let's make a pharmacotherapy plan for him.

    Pay attention that the elevated ALT and AST is due to allopuriol he has kept ingesting for his gout.

    Next step is to make the plan for his diabetes including the goal of glycemic control (level of A1C), and the use of medicaitons.

    The primary goals of therapy is to maintenance of independence and prevention of disability in this patient.

    I think first is to evaluate the patient's functional status including basic ADLs (e.g., dressing, bathing, transferring, feeding, toileting etc.), instrumental ADLs (e.g., use of telephone, housework, meal preparation, shopping or managing money etc.),physical function (e.g., ability to lift heavy objects, walk two or three blocks, or reaching overhead etc.), psychological state, financial resources, and social circumstances.

    Second, to evaluate his diabetes condition including microvascular complications and macrovascular comlications. In this patient both microvascular and macrovascular complications are negative.

    Third, to make the goal of glycemic control. In this patient I think we should firstly use intensive glycemic control strategy. The regimen of glycemic control consists of lifestyle change, TMN, and metformin.

    Four, we should monitor the laboratory tests including serum glucose level to prevent hypoglycemia , A1C to assess the response to treatment, and tests (renal function, hepatic function) to predict and prevent side effects of metformin (drug-disease interactions such as lactic acidosis).

    Lactic acidosis is a rare, but potentially severe, consequence of therapy with metformin; it is characterized by elevated blood lactate levels, decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio.

    For this patient, he has no issues with basic ADLs and instrumental ADLs, but he has a mild problem with physical function - he feels tired when climbing stairs.
    Last edited by Janis.Y.Chen; Mon 9th September '13 at 7:42pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  4. #4


    Medical History (targeting for risk factors such as overuse, inappropriate prescribing, underuse, or medication nonadherence)

    The patient has kept on allopurinol for about 7 months (began on Feb 27th 2013), occasional mild acute gouty flare documented which relieved after colchicine.

    Initial liver function showed (examed on Jun 15th) that the two transaminases both ALS and AST had elevated (ALT 85.0 U/L, AST 65.8 U/L). The latest liver function showed (examed on Sep 7th 2013) ALT: 71 IU/L, AST: 70 IU/L, and glutamyltranspetidase: 76 IU/L. The reason for this lab abnormalities is believed to be allopurinol (reversible asymptomatic clinical hepatotoxicity).


    1.Gout (with renal stones)
    2.Type 2 diabetes (duration of disease is at least shorter than 2 years and 4 months)


    1.Allopuriol 300 mg po Qd

    2.Metformin (pre-use) 500 mg po Q12h initial, increasse Q1-2Weeks; maintenance: 1500-2550 mg/day po divided q8-12h with meal. Dosage increases should be made in increments of 500 mg weekly or 850 mg every 2 weeks.

    3.Colchicine 1 mg po SATA, and 0.5 mg po SATA after a period of 1 hr within 24 hrs of an acute gouty flare if it happened. Repeat 12 hrs late if acute gouty flare didn't relieve.

    Assessing and monitoring drug therapy

    1.Match the medical problems and the drug list via MAI.

    a.Is there an indication for the medication (allopuriol, metformin, and colchicine)? - Yes

    b.Is the medication effective for the condition (allopuriol, metformin, and colchicine)? - Yes

    c.Is the dosage correct (allopuriol, metformin, and colchicine)? - Yes

    d.Are the direction correct (orally)? - No first-pass effect; absorption and bioavailability might be decreased and prolonged by food.

    e.Are the directions practical? - Yes

    f.Are there clinical significant drug-drug interactions? - No interactions found

    g.Are there clinical significant drug-disease/condition interactions? - Not yet

    However, be care of lactic acidosis and hypoglycemia due to metformin, irreversible hepatotoxicity due to the allergic of allopurinol, and colchicine-induced neuromuscular toxicity and rhabdomyolysis, and vitamin B12 deficiency and hypoglycemia due to metformin.

    h.Is there unnecessary duplication with other medication(s)? - No

    i.Is the duration of therapy acceptalbe? - Yes

    j.Is this medication the least expensive alternative compared with others of equal utility? - Yes

    2.To determine whether the patient has a chronic condition and is not taking an evidence-based medication


    3.Lab monitoring

    a.Allopurinol - Liver function (long interval and if necessary), serum uric acid level.

    b.Metformin - Renal function (if necessary), liver function (if necessary), Vitamin B12 level (if necessary), A1C and/or basal, postprandial plasma glucose.

    c.Colchicine - None

    Documenting problems and formulating a therapeutic plan

    Documenting interventions and monitoring patient progress

    (more coming soon)
    Last edited by Janis.Y.Chen; Mon 9th September '13 at 9:07pm.
    Clinical Pharmacy Specialist - Infectious Diseases

  5. #5


    On Sep 10th 2013 the patient visit his doctor. And the regimen for his diabetes was to change life sytel, without any drugs or insulin.
    Clinical Pharmacy Specialist - Infectious Diseases

  6. #6
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    Chengdu, Sichuan, China


    On Feb 12th 2014, after 5 months of life-style intervention (enhanced physical activities, including walking and riding), his A1C fell back to 6.2%, with a fasting serum glucose of 134.59 mg/dL (7.47 mmol/L).

    Well, this is an absolutely good news. My therapeutic goal is to control his A1C below 6.5%. So we should keep on the life-style intervention without any anitdiabetic drugs.

    Due to that his fasting serum glucose was a bit higher than last visit, I consider to enhance his life-style intervention (adding dietary intervention).

    Rx: life-sytle intervention (enhanced physical activities plus dietary interventions)

    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease. Chengdu, Sichuan, China.

    Twitter: @TomHsiung
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  7. #7
    PharmD Year 1 TomHsiung's Avatar
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    Jan 2013
    Chengdu, Sichuan, China


    A1c on Dec 6th 2014 is 6.7%


    Enhancing the intensity and duration of physical activity


    Repeat the A1c 3 months later
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

  8. #8
    PharmD Year 1 TomHsiung's Avatar
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    Chengdu, Sichuan, China


    Jun 26th 2015

    Due to hematuria the patient hospitalized on Jun 23rd 2015. The cause of the hematuria is believed to the nephrolithiasis (uric-induced probable).

    According to the medical conditions of this patient, the high-intensity dose regimen is recommended and I am going to raise the dosage gradually.


    Because atorvastatin has an adverse effect of urinary tract infection (see below) and because the patient does have urinary tract infection, I decide to delay the treatment of atorvastatin until his urinary tract infection completely resolved.

    Table 2. Clinical adverse reactions occurring in ≥ 2% in patients treated with any dose of atorvastatin calcium and at an incidence greater than placebo regardless of causality (% of patients).
    Adverse Reaction* Any dose N=8755 10 mg N=3908 20 mg N=188 40 mg N=604 80 mg N=4055 Placebo N=7311
    Nasopharyngitis 8.3 12.9 5.3 7 4.2 8.2
    Arthralgia 6.9 8.9 11.7 10.6 4.3 6.5
    Diarrhea 6.8 7.3 6.4 14.1 5.2 6.3
    Pain in extremity 6 8.5 3.7 9.3 3.1 5.9
    Urinary tractinfection 5.7 6.9 6.4 8 4.1 5.6
    Dyspepsia 4.7 5.9 3.2 6 3.3 4.3
    Nausea 4 3.7 3.7 7.1 3.8 3.5
    Musculoskeletal pain 3.8 5.2 3.2 5.1 2.3 3.6
    Muscle Spasms 3.6 4.6 4.8 5.1 2.4 3
    Myalgia 3.5 3.6 5.9 8.4 2.7 3.1
    Insomnia 3 2.8 1.1 5.3 2.8 2.9
    Pharyngolaryngeal pain 2.3 3.9 1.6 2.8 0.7 2.1
    * Adverse Reaction 2% in any dose greater than placebo

    Of note is that the adverse effects of statins are significant sever, i.e., rhabdomyolysis, myopathy. With the intention to monitor the adverse effects of atorvastatin, I use the Naranjo method to evaluate the potential adverse effect of atorvastatin.

    Last edited by TomHsiung; Fri 26th June '15 at 11:21pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

  9. #9
    PharmD Year 1 TomHsiung's Avatar
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    Chengdu, Sichuan, China

    Exclamation The Analysis of Potential Adverse Effects

    1.Beneficial and Toxic Effects Mediated by the Same Receptor-Effector Mechanism

    2.Beneficial and Toxic Effects Mediated by Identical Receptors but in different Tissues or by Different Effector Pathways


    3.Beneficial and Toxic Effects Mediated by Different Types of Receptors

    Factors contributing to drug-induced diseases

    1.Pharmacokinetics and pharmacodynamics, including:

    • Concurrent Diseases
    • Physiologic Conditions
    • DDIs
    • Drug-Food Interactions
    • Lifestyle Factors
    • Genetic Variability

    2.Adherence To Prescribed Therapy

    3.Medication Errors
    Last edited by admin; Tue 30th June '15 at 7:47pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

  10. #10
    PharmD Year 1 TomHsiung's Avatar
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    Chengdu, Sichuan, China

    Exclamation Variation in Drug Responsiveness

    1.Alteration in Concentration of Drug That Reaches The Receptor

    2.Variation in Concentration of an Endogenous Receptor Ligand

    3.Alterations in Number of Function of Receptors


    4.Changes in Components of Response Distal to The Receptor
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

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