Pharmacy Education

The Plan to Future (ongoing updating)

May 7, 2015 Pharmacy Education No comments , ,

552519_10150623880396074_321083388_nThe good news is that I got the offer to the master degree program of clinical pharmacy in China Pharmaceutical University. The university is a pharmacy university as a whole. In China there are lots of Medical Universities but only two the pharmacy universities exist in China – China Pharmaceutical University and Shenyang Pharmaceutical University. It is apparent that the China Pharmaceutical University is one of the most top pharmacy schools in China. The master degree of clinical pharmacy just began in two or three of years ago, which is a professional degree program. Within the program of Master Degree of Clinical Pharmacy two direction are there, including direction of Hospital Pharmacy and direction of Clinical Trial. I was so lucky that I was distributed to the direction of Hospital Pharmacy, the last one person (29th). OK, you must know that I quitted my job to participate the Graduate School Admission Exam 2015. Therefore if I failed the exam, I both lost my job and the chance to graduate school.

Now I tell myself that the affair to get the offer to graduate school has ended and I must have a plan for next three years. So now I sit in front of my hackintosh to think the future plans. The nearest plan in my brain is that I should get the TOEFL done with a score as enough as NABP (National Association of Boards of Pharamcy) requires. NABP requires the TOEFL should be as minimal as 93 in total to meet the preretirement of foreign pharmacist license certification. Yes, as what I just said it’s obvious that I am interested in U.S. Pharmacist license and I want to become a U.S. licensed pharmacist. The detail schedule for TOEFL has not been determined but I think I should get it done during the three years of study. I wrote a letter to NABP to consult for the license program for foreign pharmacists and I am wait for their reply. I remembered that I shipped the mail on about April 20th 2015. It would take about 20 days to reach NABP.

So in summary my primer plan til now is that I should get the TOEFL down with a minimal score as enough as NABP requires. I will update this thread in future while the future plan gets more detail in my mind.

Update on 11:18pm May 7th 2015

Just a minute ago I notice that the “phonics” is a good way to improve my oral English. Therefore during the last time before the September I should master the way of phonics to improve my English.

Update on 10:57pm May 22nd 2015

There are so many textbooks to read but the time is not very enough for me. So I shall focus on my major disciplines that include critical care, infectious diseases, and hematology. Time is limited, so efficacy of learning is important.

Update on 5:38pm May 24th 2015

I just took Nancy and Van’s suggestion to improve oral English by watching TED videos. That’s go great, though most of the time I must watch the subtle. However, it is a good start. I think great improvement needs a period of time to accumulate. I will keep on.

The Management of Dyslipidemia

July 26, 2014 Cardiology, Diabetes, Pharmacotherapy, Pharmacy Education, Therapeutics No comments , , ,

Let's talk about ATP IV first, then we shall discuss how to detect, evaluate, and manage patients with lipid disorders.

This thread is based on the latest clinical guideline (Circulation. 2014:S1-S45) for therapy of dyslipidemia to reduce atherosclerotic cardiovascular risk in adults (>21 years of age) and the guideline is based on the Full Panel Report. Because RCT data were used to identify those most likely to benefit from cholesterol-lowering statin therapy, the recommendations will be of value to primary care clinicians as well as specialists concerned with ASCVD prevention.

These recommendations in the guideline are intended to provide a strong, evidence-based foundation for the treatment of cholesterol for the primary and secondary prevention of ASCVD in women and men. Of note, to manage the patients with dyslipidemia successfully and appropriately, besides the guideline clinicians should also know the detection, evaluation, and treatment of lipid disorders of these patients, with strategies for each specific individual.

Basically, the latest guideline or ATP IV is quite different from any previous guidelines such as ATP III. The latest ATP IV guideline only focus on the treatment of dyslipidemia to reduce risk of ASCVD, based on evidence-based medicine, RCTs.

PS: ASCVD includes coronary heart disease (CHD), stroke, and peripheral arterial disease, all of presumed atherosclerotic origin.

In the figure on the left are new changes in ATP IV guideline. Here we shall keep in mind for those ones:

1.This guideline is based on a comprehensive set of data from RCTs from which 4 statin benefit groups were identify that focus efforts to reduce ASCVD event in secondary and primary prevention;

2.This guideline identifies high-intensity and moderate-intensity statin therapy for use in secondary and primary prevention;

3. The Expert Panel was unable to find RCT evidence to support continued use of specific LDL-C or non-HDL-C treatment target;(For secondary prevention the Expert Panel reviewed 19 RCTs to answer the question of specific LDL-C and non-HDL-C targets. No data were identified for treatment or titration to a specific LDL-C goal in adults with clinical ASCVD since no any RCTs compared 2 LDL-C treatment targets [<100 mg/dL or <70 mg/dL]. For primary prevention the Expert Panel reviewed 6 RCTs but did not find any RCTs that evaluated titration of all individuals in a treatment group to specific LDL-C targets <100 mg/dL or <70 mg/dL)

4.Nonstatin therapies, as compared with statin therapy, do not provide acceptable ASCVD risk-reduction benefits relative to their potential for adverse effects in the routine prevention of ASCVD. For safety of nonstatin please refer to the thread here

There are more updates in ATP IV guideline. They are listed at left side.

The Management of Lipid Disorders


All adults older than age 20 year should have plasma levels of cholesterol, triglyceride, LDL-C, and HDL-C measured after a 12-hour overnight fast, at least once every five years. If the profile is obtained in the nonfasted state, only total cholesterol and HDL-C will be usable because LDL-C is usually a calculated value. If total cholesterol is >=200 mg/dL, or if HDL-C is <40 mg/dL, a followup fasting lipoprotein profile should be obtained.

Patient Evaluation

After a lipid abnormality is confirmed, we shall try efforts to define the category of the lipid disorder and to rule out any possible secondary causes of the hyperlipidemia. The Fredrickson classfication can be helpful in this regard.

Thereafter, major components of the evaluation are the history, physical examination, and laboratory investigations. A complete history and physical exam should assess:

(1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual; Major risk factors for ASCVD include: Age >=45 years (male) or>=55 years or premature menopause without estrogen replacement (female); High total choesterol; Low HDL-C; Hypertension, or use of antihypertensive therapy; Diabetes; Current smoking.

Additional factors contributing to ASCVD risk including: Family history of premature CHD (definite myocardial infarction or sudden death before 55 years of age in father or other male first-degree relative, or before 65 years of age in mother or other female first-degree relative); Primary LDL-C >=160 mg/dL or other evidence of genetic hyperlipidemias; High-sensitivity C-reactive protein >=2 mg/L, coronary artery calcium score >=300 Agatston units or >=75th percentile for age, sex, and ethnicity; Ankle-brachial index <0.9; or Elevated lifetime risk of ASCVD (see in following text).

(2) family history of premature cardiovascular disease or lipid disorders;

(3) presence or absence of secondary causes of lipid abnormalities, including concurrent medications (see;

(4) presence or absence of xanthomas or abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack).

(5) baseline lab value such as fasting lipid profile, liver function, renal function, and creatine kinase;

(6) history of previous statin intolerance or muscle disorders;

(7) whether the individual had comorbidities, possible concurrent medications and DDIs.

To evaluate the potential risk for ASCVD, ATP IV guideline suggest using the new Pooled Cohort Risk Assessment Equations developed by the Risk Assessment Work Group to estimate the 10-year ASCVD risk (defined as first-occurrence nonfatal and fatal MI and nonfatal and fatal stroke) or the lifetime ASCVD risk (more detail see Pharmacy Profession Forum at The predicted 10-year ASCVD risk is defined as first-occurrence nonfatal and fatal MI and nonfatal and fatal stroke.

Estimates of 10-year risk for ASCVD are based on data from multiple community-based populations and are applicable to African-American and non-Hispanic white men and women 40 through 79 years of age. For other ethnic groups, we recommend use of the equations for non-Hispanic whites, though these estimates may underestimate the risk for persons from some race/ethnic groups, especially American Indians, some Asian Americans (e.g., of south Asian ancestry), and some Hispanics (e.g., Puerto Ricans), and may overestimate the risk for others, including some Asian Americans (e.g., of east Asian ancestry) and some Hispanics (e.g., Mexican Americans)Estimates of lifetime risk for ASCVD are provided for adults 20 through 59 years of age and are shown as the lifetime risk for ASCVD for a 50-year old without ASCVD who has the risk factor values entered into the spreadsheet. The estimates of lifetime risk are most directly applicable to non-Hispanic whites. We recommend the use of these values for other race/ethnic groups, though as mentioned above, these estimates may represent under- and overestimates for persons of various ethnic groups. Because the primary use of these lifetime risk estimates is to facilitate the very important discussion regarding risk reduction through lifestyle change, the imprecision introduced is small enough to justify proceeding with lifestyle change counseling informed by these results.

Note that 10-year risk estimation is only calculated for the 40 to 79 year range. Life-time risk estimation is only calculated for the 20 to 59 year range.

Also there is iPad app of this new tool, completely free –

General Approach

Therapeutic lifestyle change (TLC) should be implemented in all patients prior to considering drug therapy. Many persons should be given a three-month trial (two visits spaced 6 Weeks apart) of TLC unless patients are at very high risk.

PS: Very high risk for ASCVD is defined as the presence of established CVD plus one or more of:
1. multiple major risk factors (especially diabetes)
2. severe and poorly controlled risk factors (especially continued cigarette smoking)
3. multiple risk factors of the metabolic syndrome (especially high triglycerides >=200 mg/dL plus non-HDL-C>=130 mg/dL with low HDL-C [<40 mg/dL])
4. on the basis of PROVE IT, patients with acute coronary syndromes.

However, this criteria is derived from ATP III guideline. The ATP IV guideline has changed largely and according to a clinical pharmacy specialist/BCPS/Cardiology, whose name is Brent Reed, the very high risk category is no longer valid in the new guidelines (Clinical Practice Guideline of ATP IV).

If drug therapy to further reduce lipid profile is necessary, before initiation of drug therapy the patient shall be evaluation, not only the potential risk for ASCVD, but also ASCVD risk-reduction benefits, adverse effects, DDIs, and patient preferences (e.g., comorbidities, age >75 years, etc.)

In the latest ATP IV guideline, generally, four groups of patients would definitely benefit from statin therapy (ASCVD risk reduction clearly outweighs the risk of adverse events based on a strong body of evidence). They are 1.secondary prevention in individuals with clinical ASCVD; 2. primary prevention in individuals with primary elevations of LDL-C >=190 mg/dL; 3.primary prevention in individuals with diabetes 40 to 75 years of age who have LDL-C 70 to 189 mg/dL; and 4.primary prevention in individual without diabetes and with estimated 10-year ASCVD risk>=7.5%, 40 to 75 years of age who have LDL-C 70 to 189 mg/dL. Patient with heart failure or hemodialysis are excluded and no suggestion would be made to these two cohorts.

PS: clinical ASCVD is defined by the inclusion criteria for the secondary-prevention statin RCTs, which include acute coronary syndromes, a history of Mi, stable or unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin.

Also, moderate evidence supports the use of statin for primary prevention in individuals with 5% to <7.5% 10-year ASCVD risk, 40 to 75 years of age with LDL-C 70 to 189 mg/dL. Selected individuals with <5% 10-year ASCVD risk, or <40 or >75 years of age may also benefit from statin therapy, but in these circumstances clinicians shall consider the potential ASCVD risk reduction benefits, adverse effects, DDIs, and patient preferences.

Nonpharmacologic Therapy

It must be emphasized that lifestyle modification (i.e., heart-healthy diet, regular exercise habits, avoidance of tobacco products, and maintenance of a healthy weight) remains a crucial component of health promotion and ASCVD risk reduction, both prior to and in concert with the use of cholesterol-lowering drug therapies. Individualized diet counseling that provides acceptable substitutions for unhealthy foods and ongoing reinforcement by a registered dietitian are necessary for maximal effect.

Generally, lifestyle modification includes stopping excessive dietary intake of cholesterol and saturated fatty acids, weight control, increasing physical activity, increasing intake of soluble fiber, intake of fish oil supplementation, fat substitutes, and plant sterols & stanols.

Excessive dietary intake of cholesterol and saturated fatty acids leads to decreased hepatic clearance of LDL and deposition of LDL and oxidized LDL in peripheral tissues. Compared with polyunsaturated and saturated fat, intake of cholesterol has been found to have a greater effect on the concentration of LDL. Note that changes in blood lipid levels may change before three months, but may require a longer period time too. If all of the recommended dietary changes from NCEP are made, the estimated reduction, on average, in LDL-C would range from 20-30%.

Thus, ideally, lifestyle modification shall reduced intake of saturated fats and cholesterol. Weight control plus increased physical activity reduces risk beyond LDL-C and non-HDL lowering, but also can raises HDL.

Increased intake of soluble fiber can result in useful adjunctive reductions in total and LDL cholesterol. However, increased fiber intake has little or no effect on HDL-C or triglyceride concentrations. It is unclear whether the reduction in CHD risk associated with large amount of cold water, oily fish is the same with commercially prepared fish oil products. Note that fish oil supplementation has fairly large effect in reducing triglycerides and VLDL-C but it either has no effect on total and LDL-C or may cause elevations in these fractions.

Fat substitutes is similar in composition to triglycerides, but is not hydrolyzed in the gastrointestinal tract by pancreatic lipase, and, consequently, is not taken up by the intestinal mucosa. However, the absorption of lipophilic drugs or vitamins (A, D, E, and K) would be kept in the tract and excreted in the feces.

Plant sterols and stanols have demonstrated LDL-lowering effect in recent studies. The two are efficaciously comparable.

Pharmacotherapy Therapy

Nonstatin therapies, as compared with statin therapy, do not provide acceptable ASCVD risk-reduction benefits relative to their potential for adverse effects in the routine prevention of ASCVD. For patients with clinical ASCVD and within age of 75 years, high-intensity statin therapy should be initiated if they are not on statin therapy, or the intensity shall be increased in those receiving a low- or moderate-intensity statin therapy unless they have a history of intolerance to high-intensity statin therapy or other characteristics that could influence safety. If high-intensity statin therapy would otherwise be used, either when high-intensity statin therapy is contraindicated or when characteristics predisposing to statin-associated adverse effects are present, moderate-intensity statin should be used as the second option, if tolerated.

Dosage of Statin TherapyPatients with clinical ASCVD

For patients with clinical ASCVD and >75 years of age, RCTs data of high-intensity versus moderate-intensity statin therapy is few. However, there was no clear evidence of an additional reduction in ASCVD events from high-intensity statin therapy. In contrast, individuals >75 years of age did experience a reduction in ASCVD events in  moderate-intensity statin therapy, as compared with control. Thus, moderate-intensity statin therapy should be considered for individual >75 years of age with clinical ASCVD.

Although atorvastatin 40 mg reduces LDL-C by approximately >=50%, this dose was used in only 1 RCT if the participant was unable to tolerate atorvastatin 80 mg/dL. Whether an individual receiving atorvastatin 40 mg should be uptitrated to atorvastatin 80 mg shall be based on the potential for adverse effects, DDIs, and patient preferences.

Patients with LDL-C >=190 mg/dL

For patient >=21 years of age without clinical ASCVD but with LDL-C >=190 mg/dL (primary), severe elevation of LDL-C have a high lifetime risk for ASCVD events. Thus, at age 21, these individuals should receive statin therapy if they have not already been diagnosed and treated before. Patients with primary elevations of LDL-C >=190 mg/dL require even more substantial reductions in their LDL-C levels and intensive management of other risk factors to reduce their ASCVD event rates. Therefore, it is reasonable to use high-intensity statin therapy to achieve at least 50% reduction. It is recognized that maximal statin therapy might not be adequate to lower LDL-C sufficiently to reduce ASCVD event risk in individuals with primary severe elevations of LDL-C. In addition to a maximally tolerated dose of statin, nonstatin cholesterol level medications are often needed to lower LDL-C to acceptable levels in these individuals. It is also important that secondary causes, if it were exist, can contribute to the degree and severity of LDL-C >=190 mg/dL. Therefore these secondary causes should be corrected if possible.

Patients with diabetes and LDL-C is between 70 and 189 mg/dL

A high level of evidence supports the use of moderate-intensity statin therapy in persons with diabetes who are 40 to 75 years of age. The only trial of high-intensity statin therapy in primary prevention was performed in a population without diabetes. However, a high level of evidence existed for event reduction with statin therapy in individuals with a >=7.5% estimated 10-year ASCVD risk who did not have diabetes to recommend high-intensity statin therapy preferentially for individuals with diabetes and a >=7.5% estimated 10-year ASCVD risk. This consideration for those with diabetes who are 40 to 75 years of age recognizes that these individuals are at substantially increased lifetime risk for ASCVD events and death. Moreover, individuals with diabetes experience greater morbidity and worse survival after the onset of clinical ASCVD. For patients with diabetes but the 10-year ASCVD risk <7.5% moderate-intensity is recommended.

In patients with diabetes who are <40 years of age or >75 years of age, or whose LDL-C is <70 mg/dL, statin therapy should be individualized on the basis of considerations of ASCVD risk-reduction benefits, the potential for adverse effects and drug-drug interactions, and patient preferences.

Patients without diabetes and with LDL-C between 70 and 189 mg/dL

In individuals 40 to 75 years of age with LDL-C 70 to 189 mg/dL who do not have clinical ASCVD or diabetes, initiation of statin therapy based on estimated 10-year ASCVD risk is recommended, regardless of sex, race, or ethnicity. A high level of evidence for an ASCVD restriction benefit from initiation of moderate- or high-intensity statin therapy in individuals 40 to 75 years of age with >=7.5% estimated 10-year ASCVD risk was found. The reduction in ASCVD risk clearly outweighs the potential for adverse effects. Thus, it is recommended that individuals 40 to 75 years of age, who are not already candidates for statin therapy on the basis of the presence of clinical ASCVD, diabetes, or LDL-C >=190 mg/dL, receive statin therapy if they have a >=7.5% estimated 10-year risk for ASCVD and LDL-C 70 to 189 mg/dL.

For patients in this group (age 40-75) with estimated risk of 5-7.5%, although a similar level of evidence of a reduction in ASCVD events from moderate- and high-intensity statin therapy is present, the potential for adverse effects may outweigh the potential for ASCVD risk-reduction benefit when high-intensity statin therapy is used. Thus, it is recommended that moderate-intensity statin therapy should be used in this cohort since ASCVD risk-reduction benefit from moderate-intensity statin therapy clearly exceeds the potential for adverse effects.

For patients in this group (age 40-75) with estimated risk of <5%, patients 21 to 39 years of age, patients >75 years of age, or patients with LDL-C <70 mg/dL, the decision to initiate statin therapy and the starting dosage should based on ASCVD risk-reduction benefits, adverse effects, DDIs, and patient preferences.

Combination Therapy

No evidence support the routine use of nonstatin drugs combined with statin therapy to further reduce ASCVD events. However, high-risk patients who have a less than-anticipated response to statins, who are unable to tolerate a less-than-recommended intensity of a statin, or who are completely statin intolerant, may be added a nonstatin cholesterol level therapy. High-risk patients include those with ASCVD, those with LDL-C >=190 mg/dL, and those with diabetes 40-75 years of age. Due to that the potential benefits and safety are not clear in combination therapy, ASCVD risk-reduction benefits, adverse effects, DDIs, and patient preferences should be considered.


Once pharmacotherapy for dyslipidemia initiates, clinicians should monitor the efficacy, safety, adherence of the choosen regimen. To monitor the efficacy, the evidence is less clear with regard to the most appropriate tests for determining whether an anticipated therapeutic response to statin therapy has occurred on the maximally tolerated dose. However, it is reasonable to use following as indicators of anticipated therapeutic response for the monitor of statin therapy. The percent LDL-C reduction may not only indicate adherence, but also may reflect biological variability in the response to statin therapy.

1.High-intensity statin therapy generally results in an average LDL-C reduction of >=50% from the untreated baseline.

2.Moderate intensity statin therapy generally results in an average LDL-C reduction of 30% to <50% from the untreated baseline.

3.If the baseline levels of LDL-C of the patients are unknown and already on a statin, an LDL-C of <100 mg/dL was observed in most individuals receiving high-intensity statin therapy in RCTs.

The most important issue in statin safety is to manage the muscle symptoms. The recommendation is list in the table below.

Statin Safety RecommendationsSome recommendation shall be emphasized here.

Routine measurement of creatine kinase is not recommended. To monitor it when patients have symptoms and signs of muscle problems.

If the 2 consecutive values of LDL-C are <40 mg/dL, clinicians shall consider decreasing the statin dose. This recommendation was based on the approach taken in 2 RCTs. However, no data were identified that suggest an excess of adverse events occurred when LDL-C levels were below this level.

The frequency of monitor should be every 3 to 12 months as clinical indicated, with the first re-check 4 to 12 Weeks after initiation of statin therapy.


Feb 11 2016

Major cardiovascular risk factors

  • Advanced age (>55 years for men, >65 years for women)
  • Cigarette smoking (no information available)
  • Diabetes mellitus
  • Dyslipidemia (no information available)
  • Familiy history of premature atherosclerotic vascular disease (men <55 years or women <65 years) in primary relatives
  • Hypertension
  • Kidney disease (microalbuminuria or estimate GFR <60 mL/min/1.73 m2)
  • Obesity (BMI >=30 kg/m2)
  • Physical inactivity (no information available)

Additional cardiovascular rsik factors

  • Family history of premature CHD (definite myocardial infarction or sudden death before 55 years of age in father or other male first-degree relative, or before 65 years of age in mother or other female first-degree relative)
  • Primary LDL-C >=160 mg/dL or other evidence of genetic hyperlipidemias
  • High-sensitivity C-reactive protein >=2 mg/L, coronary artery calcium score >=300 Agatston units or >=75th percentile for age, sex, and ethnicity
  • Ankle-brachial index <0.9
  • Elevated lifetime risk of ASCVD

Make a provider and patient education for levothyroxine

February 13, 2013 Adverse Drug Reactions, Cardiology, Drug Informatics, Drug Interactions, Pharmacokinetics, Pharmacotherapy, Pharmacy Education, Therapeutics 3 comments , , , ,

Today I would like to write something about levothyroxine. My hospital uses levothyroxine often. Everyday there are lots of patients prescribed with levothyroxine. I do believe it is necessary to write below for education, which is not only for patients but also providers. The reference I use comes from U.S. FDA’s official drug information database.

Indications and Usage

Levothyroxine sodium is used for the following indications:

Hypothyroidism – As replacement or supplemental therapy in congenital or acquired hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. Specific indications include: primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) hypothyroidism. Primary hypothyroidism may result from functional deficiency, primary atrophy, partial or total congenital absence of the thyroid gland, or from the effects of surgery, radiation, or drugs, with or without the presence of goiter.

Pituitary TSH Suppression – In the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic thyroiditis, multinodular goiter and, as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer.


Levothyroxine is contraindicated in patients with untreated subclinical (suppressed serum TSH level with normal T3 and T4 levels) or overt thyrotoxicosis of any etiology and in patients with acute myocardial infarction. Levothyroxine is contraindicated in patients with uncorrected adrenal insufficiency since thyroid hormones may precipitate an acute adrenal crisis by increasing the metabolic clearance of glucocorticoids. Finally, levothyroxine is contraindicated in patients with hypersensitivity to any of the inactive ingredients in levothyroxine.

Dosage and Administration

  • The goal of replacement therapy is to achieve and maintain a clinical and biochemical euthyroid state.
  • The goal of suppressive therapy is to inhibit growth and/or function of abnormal thyroid tissue.

To acheive the two goals above, it depends on variety of factors including the patient’s age, body weight, cardiovascular status, concomitant medical conditions (e.g., pregnancy, concomitant medications, and the specific nature of the condition being treated). As a result Dosing must be individualized and adjustments made based on periodic assessment of the patient’s clinical response and laboratory parameters.

Levothyroxine sodium tablets are administered as a single daily dose.

Table 1 The Indication and Dosages of Levothyroxine

Indication and UsageDosage
1HypothyroidismIndividuals who are at low risk of coronary artery diseaseStarting at 1.7 mcg/kg/day (Full dose). Adjusting dosage in 12.5-25 mcg increments until clinically euthyroid and serum TSH has normalized.
If myxedema coma, administer intravenously rather than orallyIndividuals older than 50 yrs or under 50 yrs with underlying cardiac diseaseStarting from 25-50 mcg/day, with increments of 12.5-25 mcg/day at 6-8 week intervals until clinical euthyroid and the serum TSH has normalized
Elderly individualsStarting from 12.5-25 mcg/day, with increments of 12.5-25 mcg/day at 4-6 week intervals until clinical euthyroid and the serum TSH has normalized
Individuals with severe hypothyroidismStarting from 12.5-25 mcg/day, with increments of 25 mcg/day at 2-4 week intervals until clinical euthyroid and the serum TSH has normalized
Secondary or tertiary hypothyroidismDosage as above but titrated until clinically euthyroid and serum free-T4 level is restored to the upper half of the normal range
2TSH Suppression – various types of euthyroid goiters and thyroid cancerWell-differentiated thyroid cancer> 2 mcg/kg/day (Target: TSH suppressed to <0.1 mU/L)
Contraindicated if the serum TSH is already suppressedWell-differentiated thyroid cancer (high risk)Target: TSH suppressed to <0.01 mU/L
Benign nodules and nontoxic multinodular goiter (controversial)Target: TSH suppressed to between 0.1 to either 0.5 or 1.0 mU/L


The adequacy of therapy is determined by periodic assessment of appropriate laboratory tests and clinical evaluation. In adult patients with primary (thyroidal) hypothyroidism, serum TSH levels alone may be used to monitor therapy. The frequence of TSH monitoring during levothyroxine dose titration depends on the clinical situation but it is generally recommended at 6-8 week intervals until normalization.

Monitor (more…)

A Whole New Pharmacy Profession Forum

January 3, 2013 Pharmacy Education, Social Network 2 comments

Hi, everyone. I just built a whole new website recent couple of days. It’s named “Pharmacy Profession Forum”. The forum welcome pharmacist, residents, students, and anyone who is interested in the profession of pharmacy all over the world. Join us today, Pharmacy Profession Forum (


Top docs provide free online advice for rare leukemia

July 14, 2012 Hematology, Pharmacy Education No comments , ,

July 11, 2012 — Seven hematologists from leading cancer centers have volunteered to provide free medical advice to patients with myeloproliferative neoplasms (MPNs), a rare form of leukemia, and to their healthcare providers.

The physicians have signed on with the online MPNforum Magazine, which is published monthly by an MPN patient collective. They offer help to patients and caregivers on MPN Clinic, an online roundtable hosted by the publication.

The term MPN covers a rare set of disorders occurring in about 5 people per million, according to a press release from the publication, which operates on a shoestring budget. This rarity means that community-based clinicians may never see a case and if one comes along, help is needed.

The initial volunteers for the project are Richard Silver, MD (Weill-Cornell in New York City), Srdan Verstovsek, MD (M.D. Anderson in Houston, Texas), Ruben Mesa, MD (Mayo Clinic in Scottsdale, Arizona), Claire Harrison, DM (Guy’s and St. Thomas’ in London, United Kingdom), Jason Gotlib, MD (Stanford Medical Center in Palo Alto, California), Ross Levine, MD (Sloan-Kettering in New York City), and Attilio Orazi, MD (Weill-Cornell).

“It’s amazing that we have this group of doctors,” said Zhenya Senyak, the founder and editor of MPNforum, about the eminence of the participating experts. “They are really concerned about getting this information out,” he told Medscape Medical News in an interview. Senyak, who lives in Asheville, North Carolina, is a writer who has myelofibrosis.

I’ve never waited more than a day for a response.

The service is free. Patients, caregivers, and healthcare providers can email questions to, which are then forwarded to all members of the panel. One of the experts responds, and circulates that response among the other panel members for review and comment. The final response is then forwarded to the individual who submitted the question. “I’ve never waited more than a day for a response,” said Senyak. The volunteer experts have even responded while on vacation, he said, adding that the answers are highly detailed and “powerful.”

All the questions, answers, and comments will eventually be published in the monthly MPN Clinic section of MPNforum Magazine. The entries will be archived in a searchable, publicly available online database.

The first MPN Clinic report will be published on September 15. However, Senyak said that responses to 27 questions have already been received and forwarded to patients in the United States and England. He is delighted by the volunteer experts’ helpfulness. “They have nothing to gain. It is purely altruistic of them,” he said.

MPNforum is financed by small donations, which, to date, amount to about $2000.

More About MPNs

MPNs are caused by one or more mutations, usually acquired after middle age. However, increasing numbers of younger adults and children are being diagnosed with the disorder, according to an MPNforum press statement. In MPNs, an overproduction of blood cells disrupts normal hematopoiesis. The various MPNs are differentiated by what is overproduced, such as erythrocytes in polycythemia vera or platelets in essential thrombocythemia.

If treated properly, many patients can live a normal life span with minimal suffering, according to the organization; however, some forms, such as myelofibrosis, can be debilitating and even fatal.

Myelofibrosis is associated with the dysregulation of 2 enzymes — janus-associated kinase (JAK)1 and 2 — which are involved in regulating blood and immunologic functioning. As the disease progresses, bone marrow is replaced with scar tissue, leading to anemia and thrombocytopenia. However, the scarred bone marrow tissue accumulates in other organs, most notably the spleen and liver. This collagen fibrosis can also cause bone pain, intense fatigue, and loss of appetite.

The only cure for myelofibrosis has been stem cell transplantation. However, since the implication of a genetic mutation in this disease was discovered, there have been developments in drug treatment. In 2011, the first drug treatment ever for myelofibrosis, ruxolitinib (Jakafi, Incyte Corp.), was approved by the US Food and Drug Administration.

Ruxolitinib has shown results that are “unprecedented” in the treatment of this disorder, according to Dr. Harrison, who is one of the volunteers and one of the drug’s principal investigators.

While research continues, access to MPN specialists remains the surest means of securing optimal treatment, said Senyak.