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View Full Version : [Case] A Clinical Case of New Diagnosed Diabetes



Janis.Y.Chen
Sun 1st September '13, 11:11pm
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

Janis.Y.Chen
Mon 9th September '13, 5:49pm
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

Janis.Y.Chen
Mon 9th September '13, 6:48pm
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.

Janis.Y.Chen
Mon 9th September '13, 8:43pm
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).

Problems:

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

Medications:

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

No

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)

Janis.Y.Chen
Thu 19th September '13, 5:00pm
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.

admin
Wed 12th February '14, 7:58pm
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)

Tom

TomHsiung
Thu 6th November '14, 3:58pm
A1c on Dec 6th 2014 is 6.7%

Rx:

Enhancing the intensity and duration of physical activity

and

Repeat the A1c 3 months later

TomHsiung
Fri 26th June '15, 10:34pm
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.

Regimen,

http://www.tomhsiung.com/wordpress/wp-content/uploads/2014/07/Dosage-of-Statin-Therapy.png

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.

http://ww1.sinaimg.cn/large/724661c7gw1eq4h7nrt5cj20jm0iq0w2.jpg

TomHsiung
Fri 26th June '15, 10:39pm
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

and

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

TomHsiung
Fri 26th June '15, 10:41pm
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

and

4.Changes in Components of Response Distal to The Receptor

TomHsiung
Fri 26th June '15, 11:03pm
References:
1.DailyMed - ATORVASTATIN CALCIUM- atorvastatin calcium tablet (http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=901550e6-22be-68c9-eb86-f85a9c9dd998)

Contraindications

4.1 Active Liver Disease which may include Unexplained Persistent Elevations of Hepatic Transaminase Levels
4.2 Hypersensitivity to any component of this medication
4.3 Pregnancy
and
4.4 Nursing mothers

Warnings

5.1 Skeletal Muscle
Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with atorvastatin calciumand with other drugs in this class. A history of renal impairment may be a risk factor for the development of rhabdomyolysis. Such patients merit closer monitoring for skeletal muscle effects.

Atorvastatin, like other statins, occasionally causes myopathy, defined as muscle aches or muscle weakness in conjunction with increases in creatine phosphokinase (CPK) values >10 times ULN. The concomitant use of higher doses of atorvastatin with certain drugs such as cyclosporine and strong CYP3A4 inhibitors (e.g., clarithromycin, itraconazole, and HIV protease inhibitors) increases the risk of myopathy/rhabdomyolysis.

There have been rare reports of immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, associated with statin use. IMNM is characterized by: proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment; muscle biopsy showing necrotizing myopathy without significant inflammation; improvement with immunosuppressive agents.

Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever or if muscle signs and symptoms persist after discontinuing atorvastatin. Atorvastatin calcium therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected.

The risk of myopathy during treatment with drugs in this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, erythromycin, clarithromycin, the hepatitis C protease inhibitor telaprevir, combinations of HIV protease inhibitors, including saquinavir plus ritonavir, lopinavir plus ritonavir, tipranavir plus ritonavir, darunavir plus ritonavir, fosamprenavir, and fosamprenavir plus ritonavir, niacin, or azole antifungals. Physicians considering combined therapy with atorvastatin calcium and fibric acid derivatives, erythromycin, clarithromycin, a combination of saquinavir plus ritonavir, lopinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir, or fosamprenavir plus ritonavir, azole antifungals, or lipid-modifying doses of niacin should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs or symptoms of muscle pain, tenderness, or weakness, particularly during the initial months of therapy and during any periods of upward dosage titration of either drug. Lower starting and maintenance doses of atorvastatin should be considered when taken concomitantly with the aforementioned drugs (see Drug Interactions (7)). Periodic creatine phosphokinase (CPK) determinations may be considered in such situations, but there is no assurance that such monitoring will prevent the occurrence of severe myopathy.

Drug Interactions Associated with Increased Risk of Myopathy/Rhabdomyolysis


Interacting Agents
Prescribing Recommendations


Cyclosporine, HIV protease inhibitors (tipranavir plus ritonavir), hepatitis C protease inhibitor (telaprevir)
Avoid atorvastatin


HIV protease inhibitor (lopinavir plus ritonavir)
Use with caution and lowest dose necessary


Clarithromycin, itraconazole, HIV protease inhibitors (saquinavir plus ritonavir*, darunavir plus ritonavir, fosamprenavir, fosamprenavir plus ritonavir)
Do not exceed 20 mg atorvastatin daily


HIV protease inhibitor (nelfinavir)
Hepatitis C protease inhibitor (boceprevir)
Do not exceed 40 mg atorvastatin daily



5.2 Liver Dysfunction
Statins, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (>3 times the upper limit of normal [ULN] occurring on 2 or more occasions) in serum transaminases occurred in 0.7% of patients who received atorvastatin calcium in clinical trials. The incidence of these abnormalities was 0.2%, 0.2%, 0.6%, and 2.3% for 10, 20, 40, and 80 mg, respectively.

One patient in clinical trials developed jaundice. Increases in liver function tests (LFT) in other patients were not associated with jaundice or other clinical signs or symptoms. Upon dose reduction, drug interruption, or discontinuation, transaminase levels returned to or near pretreatment levels without sequelae. Eighteen of 30 patients with persistent LFT elevations continued treatment with a reduced dose of atorvastatin calcium.

It is recommended that liver enzyme tests be obtained prior to initiating therapy with atorvastatin calcium and repeated as clinically indicated. There have been rare postmarketing reports of fatal and non-fatal hepatic failure in patients taking statins, including atorvastatin. If serious liver injury with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment with atorvastatin calcium, promptly interrupt therapy. If an alternate etiology is not found, do not restart atorvastatin calcium.

Atorvastatin calcium should be used with caution in patients who consume substantial quantities of alcohol and/or have a history of liver disease. Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of atorvastatin calcium [see Contraindications (4.1)].

5.3 Endocrine Function
Increased in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including atorvastatin calcium.

Statins interfere with cholesterol synthesis and theoretically might blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin calcium does not reduce basal plasma cortisol concentration or impair adrenal reserve. The effects of statins on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown. Caution should be exercised if a statin is administered concomitantly with drugs that may decrease the levels or activity of endogenous steroid hormones, such as ketoconazole, spironolactone, and cimetidine.

5.4 CNS Toxicity
Brain hemorrhage was seen in a female dog treated for 3 months at 120 mg/kg/day. Brain hemorrhage and optic nerve vacuolation were seen in another female dog that was sacrificed in moribund condition after 11 weeks of escalating doses up to 280 mg/kg/day. The 120 mg/kg dose resulted in a systemic exposure approximately 16 times the human plasma area-under-the-curve (AUC, 0-24 hours) based on the maximum human dose of 80 mg/day. A single tonic convulsion was seen in each of 2 male dogs (one treated at 10 mg/kg/day and one at 120 mg/kg/day) in a 2-year study. No CNS lesions have been observed in mice after chronic treatment for up to 2 years at doses up to 400 mg/kg/day or in rats at doses up to 100 mg/kg/day. These doses were 6 to 11 times (mouse) and 8 to 16 times (rat) the human AUC (0-24) based on the maximum recommended human dose of 80 mg/day.

CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other members of this class. A chemically similar drug in this class produced optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in clinically normal dogs in a dose-dependent fashion at a dose that produced plasma drug levels about 30 times higher than the mean drug level in humans taking the highest recommended dose.

5.5 Use in Patients with Recent Stroke or TIA
In a post-hoc analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) study where atorvastatin calcium 80 mg vs. placebo was administered in 4,731 subjects without CHD who had a stroke or TIA within the preceding 6 months, a higher incidence of hemorrhagic stroke was seen in the atorvastatin calcium 80 mg group compared to placebo (55, 2.3% atorvastatin vs. 33, 1.4% placebo; HR: 1.68, 95% CI: 1.09, 2.59; p=0.0168). The incidence of fatal hemorrhagic stroke was similar across treatment groups (17 vs. 18 for the atorvastatin and placebo groups, respectively). The incidence of nonfatal hemorrhagic stroke was significantly higher in the atorvastatin group (38, 1.6%) as compared to the placebo group (16, 0.7%). Some baseline characteristics, including hemorrhagic and lacunar stroke on study entry, were associated with a higher incidence of hemorrhagic stroke in the atorvastatin group [see Adverse Reactions (6.1)].

TomHsiung
Fri 26th June '15, 11:32pm
Basic pharmacokinetics parameters,

Absorption:Atorvastatin calcium is rapidly absorbed after oral administration.

The absolute bioavailability of atorvastatin (parent drug) is approximately 14%.

Distribution:Mean volume of distribution of atorvastatin calcium is approximately 381 liters. Atorvastatin calcium is ≥98% bound to plasma proteins.

Metabolism:Atorvastatin calcium is extensively metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin calcium. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites.

In vitro studies suggest the importance of atorvastatin calcium metabolism by cytochrome P450 3A4.

Excretion:Atorvastatin calcium and its metabolites are eliminated primarily in bile following hepatic and/or extra-hepatic metabolism; however, the drug does not appear to undergo enterohepatic recirculation.

Mean plasma elimination half-life of atorvastatin calcium in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites. Less than 2% of a dose of atorvastatin calcium is recovered in urine following oral administration.

According to the information above, we get the primary pharmacokinetic parameters as follows,

Original data from references,
F: 14%
tin: approximately 2 hours
V: 381 L
fu: 2%
t1/2: approximately 14 hrs (besides, there exists active metabolites and enterohepatic recirculation)

Estimated data according to original data,
k: 0.0495
Cl: 18.86 L/hr

As the tin <1/6 of t1/2, we use bolus model as the pharmacokinetic mode for this patient. So relevant equations are below,

Css ave =(S)(F)(Dose/τ)/Cl
Cl: Clearance represents the theoretical volume of blood or plasma which is completely cleard of drug in a given period.
Css ave: The average steady-state drug concentration
τ: Dosing interval

Css max =[(S)(F)(Dose)/V]/(1-e-kτ)
τ(tau): Dose interval, a period
k: k is the fraction or percentage of the total amount of drug in the body removed per unit of time and is a function of clearance and volume of distribution (k=Cl/V).
(1-e-kτ): (1-e-kτ) represents the fraction of drug that is eliminated in the dosing interval
Cl: Clearance
F: Bioavailability factor
S: Fraction of the administered dose that is the active drug
V: Volume of Distribution

Css min =[(S)(F)(Dose)/V]/(1-e-kτ)*(e-kτ)
τ(tau): Dose interval, a period
k: k is the fraction or percentage of the total amount of drug in the body removed per unit of time and is a function of clearance and volume of distribution (k=Cl/V).
(1-e-kτ): (1-e-kτ) represents the fraction of drug that is eliminated in the dosing interval
Cl: Clearance
F: Bioavailability factor
S: Fraction of the administered dose that is the active drug
V: Volume of Distribution

Css 1 =[(S)(F)(Dose)/V]/(1-e-kτ)*(e-kt1)
Css 1 is concentration obtained at time (t1) other than the peak or trough, within a dose interval
τ(tau): Dose interval, a period
k: k is the fraction or percentage of the total amount of drug in the body removed per unit of time and is a function of clearance and volume of distribution (k=Cl/V).
(1-e-kτ): (1-e-kτ) represents the fraction of drug that is eliminated in the dosing interval
Cl: Clearance
F: Bioavailability factor
S: Fraction of the administered dose that is the active drug

TomHsiung
Sat 27th June '15, 12:01am
Regimen 1, 20 mg Q24h

Css ave = 1*0.14*20/24/18.86 = 0.0062 ug/mL
Css max = 1*0.14*20/381/[1-e(-0.0495*24)] = 0.0106 ug/mL
Css min = 1*0.14*20/381/[1-e(-0.0495*24)]*e(-0.0495*24) = 0.0035 ug/mL

Regimen 2, 40 mg Q24h

Css ave = 1*0.14*40/24/18.86 = 0.0124 ug/mL
Css max = 1*0.14*40/381/[1-e(-0.0495*24)] = 0.0211 ug/mL
Css min = 1*0.14*40/381/[1-e(-0.0495*24)]*e(-0.0495*24) = 0.0070 ug/mL

Regimen 3, 80 mg Q24h

Css ave = 1*0.14*80/24/18.86 = 0.0247 ug/mL
Css max = 1*0.14*80/381/[1-e(-0.0495*24)] = 0.0423 ug/mL
Css min = 1*0.14*80/381/[1-e(-0.0495*24)]*e(-0.0495*24) = 0.0141 ug/mL

admin
Tue 14th July '15, 5:58pm
Early Jun 2015

A1c: 6.6%

Hepatic function

Total bilirubin: 12.3 umol/L (0.72 mg/dL)
Direct bilirubin: 4.2 umol/L (0.25 mg/dL)
In-direct bilirubin: 8.1 umol/L (0.47 mg/dL)

ALT: 62 U/L
AST: NA IU/L

Albumin: NA g/L
Globulin: NA g/L

Lipid Profile

Triglyceride: 5.33 mmol/L (471.7 mg/dL)
Total cholesterol: 4.15 mmol/L (160.2 mg/dL)
High density lipoprotein: 0.67 mmol/L (25.9 mg/dL)
Low density lipoprotein: 1.48 mmol/L (57.1 mg/dL)

admin
Tue 14th July '15, 6:22pm
Patient history changed.

On early Jun 2015, regular annually checkup. Primary medical condition was microscopic hematuria.

Urinary analysis

Color: yellow
Transparency: Transparent
pH: 7.0
Nitrite: (-)
Glucose: (-)
Specific gravity: 1.010
Blood: (+++)
Protein: (+)
Bilirubin: (-)
Urobilinogen: (-)
Ketones: (-)
White cell: (+), 5-10/HP
Red cell: 10-20/HP
Urinary crystal: no seen
Hyaline cast: no seen
Granular cast: no seen

Renal function

Serum nitrogen: 3.4 mmol/L (9.5 mg/dL)
Serum creatinine: 85 umol/L (0.96 mg/dL)
Serum uric acid: 249 umol/L (4.2 mg/dL)

admin
Tue 14th July '15, 6:34pm
Patient history changed.

On 17 Jun 2015, the patient sought for medical examination because the urinary protein (+) of the regular annually checkup. Primary medical condition was microscopic hematuria. The physician prescribed amoxicillin 500 mg Q12h.

Urinary analysis

Color: faint yellow
Transparency: Transparent
pH: 7.0
Nitrite: (-)
Glucose: (-)
Specific gravity: 1.010
Blood: (++)
Protein: (-)
Bilirubin: (-)
Urobilinogen: (-)
Ketones: (-)
White cell: (+-), 72.70/HP
Red cell: 727.5/HP
Epithelial cell: 7.8/HP
Bacteria: 28.20 /HP
Urinary crystal: 0.3
Cast: 0.77
Pathologic cast: 0.12

admin
Tue 14th July '15, 6:42pm
Patient history changed.

On Jun 20th 2015 the patient discovered that the color of his blood looked like tea (after 4 days therapy of amoxicillin 500 mg Q12h). Therefore the suspected microscopic hematuria became macroscopic hematuria on that day. After two days of continued therapy of amoxicillin regimen, the patient went to the hospital seeking for medical help again, on Jun 23rd 2015. The physician prescribed a urinary dialysis.

According to the following result of urinary analysis, the patient was hospitalized on Jun 23rd 2015.

Urinary analysis

Color: faint red
Transparency: muddy
pH: 6.5
Nitrite: (-)
Glucose: (-)
Specific gravity: 1.020
Blood: (+++)
Protein: (+)
Bilirubin: (-)
Urobilinogen: (-)
Ketones: (-)
White cell: (+), 87.80/HP
Red cell: 3332.2/HP
Epithelial cell: 24.1/HP
Bacteria: 27.20 /HP
Urinary crystal: 0.0
Cast: 0.88
Pathologic cast: 0.44

admin
Tue 14th July '15, 7:06pm
After hospitalized, the surgeons thought the macroscopic hematuria was caused by kidney calculus. Both kidney has big calculus, primarily located on renal pelves of both sides. And on Jun 29th 2015 the patient received a surgery (PCNL/Percutaneous Nephrolithotomy) on the right side kidney. Stones were removed from the right side renal pelvis and calyxes.

A stone analysis was performed later. The result surprised me that the stones were not made up of uric acid and uric acid relative substances.

During the hospitalization, we found that the patient's BP was abnormal. The patient was diagnosed with hypertension.

Surgery on the right side kidney on Jun 29th 2015, finished.

Hospitalization during Jun 23rd 2015 to Jul 7th 2015.



All diagnoses

1.Urinary calculus
2.Urinary tract infection (clinical diagnosis, not laboratory diagnosis)
3.Gout
4.Hypertension
5.Type 2 diabetes
6.Hyperlipidemia


BP records

The highest systolic BP was: 174 mm Hg and the highest diastolic BP was 98 mm Hg. The average BP was: 149/83 mm Hg (n=25).

Renal Stone Analysis

Result: Calcium oxalate monohydrate and carbonate apatite.

Liver function (Jun 24th 2015)

ALT: 54 U/L
AST: 51 U/L
Albumin: 48.5 g/L
Globin: 28.3 g/L

Total bilirubin: 8.4 umol/L (0.49 mg/dL)
Direct bilirubin: 3.8 umol/L (0.21 mg/dL)
In-direct bilirubin: 4.6 umol/L (0.27 mg/dL)

gamma-Glutamy transpeptidase: 68 U/L
Alkaline phosphatase: 81 U/L
Lactate dehydrogenase: 216 U/L
5-Nucleotidase: 6.60 U/L

Renal function (Jun 24th 2015)

Serum urea: 4.3 mmol/L
Creatinine: 84 umol/L (0.95 mg/dL)
Uric acid: 259 umol/L (4.4 mg/dL)

Lipid profile

Triglyceride: 7.83 mmol/L (692.9 mg/dL)
Total cholesterol: 4.69 mmol/L (181.1 mg/dL)
High density lipoprotein: 0.80 mmol/L (30.9 mg/dL)
Low density lipoprotein: 1.37 mmol/L (52.9 mg/dL)

ApoA1: 0.88 g/L
apoB: 0.54 g/L
LPa: 52 mg/L

Others

Serum Glucose: 7.36 mmol/L (132.6 mg/dL), fasting

Serum potassium: 3.90 mmol/L
Serum sodium: 138.0 mmol/L
Serum chlorine: 103.0 mmol/L
Serum Calcium: 2.27 mmol/L
Serum magnesium: 0.93 mmol/L
Serum phosphorus: 0.80 mmol/L
Serum bicarbonate: 22.7 mmol/L

Medication history

Note: Some of the medications are not available in United States so they are not listed out here.

Part 1 Long-time medications

1.Allopurinol 200 mg b.i.d, long time

Part 2 Medications during these new medical conditions (not during the surgery)

1.Amoxicillin 500 mg, q12h, Jun 16-23, 7 days
2.Cefoxitn
3.Pantoprazole

Part 3 Medications during these new medical conditions (during the surgery)

1.Phenylephrine
2.Midazolam
3.Flumazenil
4.Cefoxitin
5.Rocuronium
6.Propofol
7.Sevoflurane
8.Dyclonine mucilage
9.Neostigmine
10.Pantoprazole
11.Metoclopramide
12.Iohexol

TomHsiung
Sat 8th August '15, 11:40pm
Today we begin the drug therapy indicating for dyslipidemia. We start the Atorvastatin Calcium tablet at dosage of 20 mg Qd. We will increase the dose of the drug from 20 mg gradually to 80 mg per day, in order to use the drug safely.

Rx:

Atorvastatin 20 mg Qd

admin
Sat 26th September '15, 9:50pm
The patient went to hospital owing to seek help for his hypertension on Sep 22nd 2015. Physical examination and some laboratory testes had been interpreted that day. Below are their results:

All diagnoses

1.Urinary calculus
2.Urinary tract infection (clinical diagnosis, not laboratory diagnosis)
3.Gout
4.Hypertension
5.Type 2 diabetes
6.Hyperlipidemia


BP records

The highest systolic BP was: waiting for updating mm Hg and the highest diastolic BP was waiting for updating mm Hg. The average BP was: waiting for updating mm Hg (n=25).


Liver function (Sep 22nd 2015)

ALT: 77 U/L
AST: 60 U/L
Albumin: 51.9 g/L
Globin: 31.7 g/L

Total bilirubin: 13.5 umol/L (0.79 mg/dL)
Direct bilirubin: 4.9 umol/L (0.29 mg/dL)
In-direct bilirubin: 8.6 umol/L (0.50 mg/dL)


Renal function (Sep 22nd 2015)

Serum urea: 3.9 mmol/L (10.92 mg/dL)
Creatinine: 101 umol/L (1.14 mg/dL)
Uric acid: 261 umol/L (4.39 mg/dL)

Lipid profile

Triglyceride: 2.81 mmol/L (248.67 mg/dL)
Total cholesterol: 2.76 mmol/L (106.56 mg/dL)
High density lipoprotein: 0.93 mmol/L (35.91 mg/dL)
Low density lipoprotein: 1.20 mmol/L (46.33 mg/dL)

Others

Serum Glucose: 8.08 mmol/L (145.59 mg/dL), fasted.

admin
Sat 26th September '15, 10:07pm
On Sep 22nd 2015 the patient's Rx had some changes.

Former Rx (since Aug 15th 2015)
Allopurinol 200 mg Bid
Atorvastatin 20 mg Qd

Current Rx (since Sep 23rd 2015)
Allopurinol 200 mg Bid
Atorvastatin 20 mg Qod
Irbesartan/Hydrochlorothiazide 150/12.5 mg Qd
Nifedipine XL 30 mg Qn

Because the patient has tachycardia after the ingestion of nifedipine XL, tonight I asked him to stop drug of nifedipine XL 30 mg Qn. I think the tachycardia probable was caused by nifedipine induced hypotension during sleep. The reduction in dose of atorvastatin was due to the increased level of AST/ALT and bilirubin, which was modified by the physician on Sep 23rd 2015.

Rx:
Allopurinol 200 mg Bid
Atorvastatin 20 mg Qod
Irbesartan/Hydrochlorothiazide 150/12.5 mg Qd

CheneyHsiung
Wed 7th October '15, 7:12pm
The patient has a over-normal response to Irbesartan/Hydrochlorothiazide 150/12.5 mg Qd with the most apparent clinical presentation of fatigue, which is a adverse effect of Irbesartan/Hydrochlorothiazide. So The dose had been cut half on Sep 23rd.

And according to continuing self BP monitoring, the blood pressure are controlled within the therapeutic target of below 130/80 mm Hg for the most of time.

BP records:

1.Date 2.Morning(before ingestion of Irbesartan/Hydrochlorothiazide) 3.Noon 4.Evening 5.Bedtime






Morning
Noon
Evening
Evening
Bedtime


Sep 29












Sep 30
129/76










Oct 1
122/79




122/71




Oct 2
137/79










Oct 3
120/74










Oct 4
113/73










Oct 5












Oct 6
118/80










Oct 7
121/69
125/68