Showing posts with label Medications. Show all posts
Showing posts with label Medications. Show all posts

Coupons for Allergy and Asthma Medications - As Supplied by Manufacturer

Editor: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago

Coupons for asthma medications by MyCouponDoc.com http://goo.gl/pTJZB

Coupons for allergy medications by MyCouponDoc.com http://goo.gl/wjoWG


Asthma Medications (in alphabetical order)

Advair


Astepro


Antihistamines (pills)

Benadryl

Published: 01/22/2011
Updated: 03/09/2012

Immunosuppressive drugs: Mycophenolate (CellCept)

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport) Department of Allergy and Immunology

Mycophenolate (CellCept) is often used as an alternative to azathioprine.


Mycophenolic acid. Image source: Wikipedia, public domain.

Mycophenolate mofetil is increasingly being used in place of azathioprine in organ transplantation, as it is associated with less bone marrow suppression, fewer opportunistic infections, and a lower incidence of acute rejection.

Mycophenolic acid is commonly marketed under the trade names CellCept (mycophenolate mofetil; Roche) and Myfortic (mycophenolate sodium; Novartis).

Mycophenolate is derived from the fungus Penicillium stoloniferum.

Mycophenolate blocks lymphocyte proliferation by inhibiting guanine nucleotide synthesis in lymphocytes. Mycophenolate affects purine nucleotide synthesis and metabolism. It is used in organ transplantation and is available in oral and intravenous form.

Mycophenolate was shown to be effective in severe atopic dermatitis, with some responders
showing lasting remission.

What is the molecule that tacrolimus binds to in order to exert its therapeutic effect?

(A) NFkB
(B) calcium
(C) ipraimmunophilin
(D) NFAT
(E) calcineurin
(F) calmodulin
(G) AP-1

Answer: E.

References

Immunosuppressive drugs. Wikipedia.
Abbas' Immunology, edition 6, 2009.
Mycophenolic acid. Wikipedia.

Published: 05/20/2009
Updated: 08/20/2010

Monoclonal antibodies (mAb)

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU

Monoclonal antibodies are produced by hybridomas. A hybridoma is a product of cell fusion between:

- normal antibody producing B cell (plasma cell)
- myeloma cell

Typically, spleen cells from an immunized mouse are fused with myeloma cells by using polyethylene glycol (PEG) to produce a hybrid cell line called a hybridoma.

Each hybridoma is descended from a single cell and all the antibodies produced by that cell are identical. These antibodies are called monoclonal antibodies (mAbs).

Monoclonal antibodies (mAbs) nomenclature related to sufix

-omab - murine, only of mouse origin. Murine component is 100%

-ximab - chimeric human/mouse. mAb combines murine mAb variable regions with the constant region of human antibody. Murine component is 30%

-zumab - humanized. mAb combines murine mAb variable regions with a portion of a human IgG molecule. Murine component is less than 10%

-umab - "fully" human mAb cloned into a bacteriophage

-cept - fusion of a receptor to the Fc part of human IgG1

Examples of monoclonal antibodies (mAb) in clinical practice

- Rituximab - against CD20. Used in autoimmune diseases, B cell lymphomas
- Anti-CD20 monoclonal antibody ocrelizumab helps patients with relapsing-remitting multiple sclerosis (MS) (Lancet, 2011).
- Omalizumab - againts FcεRI (cε3). Used in asthma
- Adalimumab - against TNF-α. Used in rheumatoid arthritis
- Palivizumab - against RSV. Used to prevent RSV infection in infants with bronchopulmonary dysplasia
- Mepolizumab - against IL-5. Used in hypereosinophilic syndrome and patients with eosinophilic asthma
- Daclizumab - against IL-2 receptor α chain (CD25). Used to prevent renal allograft rejection
- Natalizumab - against α 4 chain of integrin molecule. Used in multiple sclerosis (MS)
- Abciximab - against integrin αIIβ3. Used in acute coronary syndromes (ACS)
- Anti-IL-17 Receptor Antibody Brodalumab Helps Patients with Psoriasis - NEJM, 2012.
- Anti–Interleukin-17 Monoclonal Antibody Ixekizumab Improves Chronic Plaque Psoriasis - NEJM, 2012.
- Natalizumab-Associated Progressive Multifocal Leukoencephalopathy (PML) - NEJM lists the risk factors
- In 2014, FDA Approved New Drug for Crohn Disease and UC: vedolizumab (Entyvio), an injectable monoclonal antibody. Vedolizumab, an integrin receptor antagonist http://buff.ly/1lFuRtv

References

Online Book of Biologic Therapies (monoclonal antibodies, etc.) by the Clinical Immunology Society

Related reading

Allergy to monoclonal antibodies: cutting-edge desensitization methods - Expert Reviews, 2012.

mAb: If it ends in -mumab, it's a fully human protein, -zumab is humanized (10% mouse), -ximab is chimeric (33% mouse). ACP blog, 2012.

Published: 08/12/2008
Updated: 05/25/2012

Allergic and "pseudoallergic" reactions to NSAIDs

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D, Allergist/Immunologist and Assistant Professor at NSU

NSAIDs are the drugs most commonly involved in hypersensitivity drug reactions. http://buff.ly/1tI92CZ

NSAIDs can cause several allergic and "pseudoallergic" reactions. Allergic reactions are immunologic reactions to NSAIDs that are presumed IgE-mediated. Pseudoallergic reactions are non-immunologic.

Pseudoallergic reactions are non-immunologic abd are related to the COX-1 inhibition. They can be elicited by any NSAID that inhibits COX-1, including aspirin. Precise mechanism has not been established.

Allergic NSAID reactions are presumed to be IgE-mediated. They are elicited by a single NSAID in a susceptible individual.


Allergic and "pseudoallergic" reactions to NSAIDs (click to enlarge the image).

Pseudoallergic NSAID reactions

Pseudoallergic reactions can be caused by any COX-1 inhibiting NSAID, and the likelihood of these reactions is related to the degree of COX-1 inhibition. Pseudoallergic reactions are usually seen in patients with one of the following comorbidities: the combination of asthma and chronic rhinosinusitis with nasal polyposis; or chronic urticaria.

Pseudoallergic reactions are divided into 4 types:

- Type 1: NSAID-induced asthma and rhinosinusitis
- Type 2: NSAID-induced urticaria/angioedema in patients with chronic urticaria
- Type 3: NSAID-induced urticaria/angioedema in otherwise asymptomatic individuals
- Type 4: Blended reactions in otherwise asymptomatic individuals

Type 3: NSAID-induced urticaria/angioedema in otherwise asymptomatic individuals

There is a small subsets of patients without chronic urticaria who develop acute urticaria and/or angioedema with COX-1 inhibiting NSAIDs/ASA. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth. This condition is uncommon. These patients may develop urticaria and/or angioedema only after NSAID ingestion or may have intermittent episodes of unexplained urticaria unrelated to NSAID ingestion, but they do not have chronic urticaria.

The probable mechanism is related to COX-1 inhibition, as patients with type 3 pseudoallergy can react to their very first dose of a COX-1 inhibitor and to structurally different COX-1 inhibiting NSAIDs. They are able to tolerate highly selective COX-2 inhibiting NSAIDs (eg, celecoxib).

Allergic NSAID reactions (presumed IgE-mediated)

Allergic reactions to NSAIDs range from urticaria/angioedema to life-threatening anaphylaxis. In contrast to pseudoallergic reactions, these reactions are elicited by a single NSAID, or rarely by more than one agent with similar molecular structures.

These reactions are believed to be IgE-mediated via a drug hapten/carrier protein phenomena. While most of these reactions have been associated with ibuprofen, the first NSAID to become available over the counter in the United States, they can happen with any COX-1 inhibitor. There are no practical available tests to detect IgE to NSAIDs (such as skin testing or drug-specific serum IgE tests).

Allergic reactions may be divided into two types, based on the severity of the symptoms:

- Type 5: Urticaria/angioedema to a single NSAID - urticaria and/or angioedema within minutes to one hour of taking a particular NSAID or ASA. These patients generally do not have underlying chronic urticaria.

- Type 6: Anaphylaxis to a single NSAID (not ASA) - Type 6 reactions are distinguished from type 5 reactions based only upon severity. Typical symptoms of anaphylaxis include shortness of breath/wheezing due to bronchospasm or laryngeal edema and hypotension due to vascular collapse.

It is notable that there are no confirmed cases of anaphylaxis to aspirin itself.

Diagnosis

There are no in vitro or skin testing methods available. Definitive diagnosis requires a challenge procedure, although this is only indicated if the patient has a specific need for regular NSAID therapy (ie, usually NSAIDs for rheumatologic disease or aspirin for cardiovascular disease).

Management of pseudoallergic reactions

Challenge procedures

If a definitive diagnosis is required, then a provocative challenge procedure must be performed.

Without additional information, the clinician must advise the patient to avoid all NSAIDs. However, a challenge procedure with aspirin would clarify whether the patient reacts to all COX-1 inhibitors (pseudoallergic), or only to ibuprofen (allergic).

Alternative to the challenge

An alternative to the challenge is to administer a highly selective COX-2 inhibitor. Highly selective COX-2 inhibitors (eg, celecoxib) are tolerated by patients with pseudoallergic reactions. These agents demonstrate at least a 200 to 300-fold selectivity for inhibition of COX-2 over COX-1 at the defined therapeutic doses.

It is generally safe for patient with a pseudoallergic NSAID reaction to take a highly selective COX-2 inhibitor, such as celecoxib. Some allergists prefer to give an initial dose in a medically supervised setting (eg, a clinic), although there are no reported cases of pseudoallergic reactions who subsequently reacted to celecoxib.

Management of allergic reactions

Type 5 and 6 reactions are presumed IgE-mediated reactions to single NSAIDs. Patients with these types of reactions should avoid the causative agent.

Patients with types 5 and 6 reactions may require diagnostic challenge with aspirin to confirm that they are not sensitive to all COX-1 inhibitors (ie, exclude pseudoallergy), if the history is not sufficient to determine this. Confirmed cases of anaphylaxis to aspirin have not been reported.

Patients with types 5 or 6 reactions may safely take NSAIDS that are structurally dissimilar to the drug that caused the initial reaction.

However, selective COX-2 inhibitors may be unsafe in subjects with urticaria and/or angioedema caused by hypersensitivity reactions to NSAIDs with cross-intolerance if they are intolerant to paracetamol. Allergy, 2011.

References

Practical approach to management of hypersensitivity to NSAIDs - 2013 EAACI position paper http://buff.ly/GNVDCa
Patient with Arthritis and Hypersensitivity to Nonsteroidal Antiinflammatory Drugs (NSAIDs)
UpToDate, 2010.
The Kounis-Zavras syndrome with the Samter-Beer triad http://goo.gl/g7qGh
NSAIDs are responsible for 21-25% of reported adverse drug events http://goo.gl/m6vMK
Selective COX-2 inhibitors may be unsafe in subjects with urticaria and/or angioedema caused by hypersensitivity reactions to NSAIDs with cross-intolerance if they are intolerant to paracetamol. Allergy, 2011.
How Can We Better Classify NSAID Hypersensitivity Reactions – Validation from a Large Database  http://goo.gl/sal36

Published: 07/27/2010
Updated: 07/27/2012

Omalizumab can serve as a bridge to immunotherapy in severe asthma

Author: M. Sandhu, M.D.; V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport) Department of Allergy and Immunology

A 14-year-old African American male is referred to the allergy clinic with a severe persistent asthma that is poorly controlled on maximum dose inhaled corticosteroids and a long acting beta-agonist. The patient required oral steroids on 4 separate occasions in the past 2 years.

Past medical history (PMH)

Severe persistent asthma, allergic rhinitis.

Medications

Advair 500/50 one inhalation BID, Singulair 10 mg po daily, albuterol prn, Rhinocort daily, loratidine 10 mg po daily.

Physical examination

VSS.
Skin: no rashes, keratosis, excoriations, or lichenifications.
HEENT: pale boggy turbinates (B).
Chest: slightly decreased air entry (B).
CVS: Clear S1S2.
Abdomen: Soft, NT, ND, +BS.
Extremities: no c/c/e.

What diagnostic tests would you suggest?

His FEV1 values ranged widely from as low as 55% to as high as 89% predicted with the higher FEV1 measurements representing recent oral steroid administration. The average FEV1 excluding those values due to oral steroid administration was 68% predicted. The average ACT score was 21.6

What happened?

Our patient was started on omalizumab and his condition stabilized. Allergen immunotherapy was added 5 months later. The patient was initially built up on immunotherapy followed by monthly maintenance doses. The total overlap period of immunotherapy and omalizumab was 19 months.

The average FEV1 during the 19 month overlap phase was 86% predicted and average ACT score was 23.8. During this time the patient had no ER visits, oral steroid doses or adverse reactions to immunotherapy.

What happened next?

Omalizumab was discontinued after 2 years. The patient has been maintained on immunotherapy alone since that time and has maintained this benefit with an average FEV1 of 103%. His average ACT score has been 23.5, with no oral steroid use. Because of overall improvement, his ICS were tapered from high to medium dose. Currently, the patient’s regimen consists of a medium dose inhaled steroid with a long acting beta- agonist, montelukast, and monthly maintenance immunotherapy.

Final diagnosis

Use of Omalizumab as a bridge to immunotherapy in severe asthma.

Summary

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (JACI, 2011). Allergen immunotherapy was introduced by Leonard Noon 100 years ago and is the only disease-modifying treatment for allergic individuals (Allergy, 2012).

Both allergen immunotherapy (IT) and omalizumab (anti-IgE antibody) are used to treat persistent perennial allergic asthma. Allergen immunotherapy can lead to long lasting improvement with a typical regimen lasting a set time period of 3-5 years. More severe asthmatic patients are at greater risk for serious and potentially life threatening reactions with allergen immunotherapy. Omalizumab treats perennial allergic asthma, acts synergistically with allergen immunotherapy and reduces anaphylactic reactions associated with immunotherapy. Allergic asthma improvements associated with omalizumab are generally present only while on therapy, and thus therapy may continue indefinitely. Our use of omalizumab is as a bridge to immunotherapy making immunotherapy more effective and safer in high risk severe asthmatics.



Severe asthma - differential diagnosis and management (click to enlarge the image).

References

Response to omalizumab after 16 weeks is a predictor of continuing persistent response to omalizumab in asthmatics. Allergy 2011.
Immunotherapy can reduce asthma symptoms and it is possibly as effective as inhaled steroids - Cochrane, 2010.

Published: 03/19/2010
Updated: 01/19/2012

Immunosuppressive drugs: Azathioprine

Author: V. Dimov, M.D., Allergist/Immunologist at Cleveland Clinic
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport) Department of Allergy and Immunology

(This article is based in large part on Wikipedia articles that were reviewed for accuracy, please see the reference links).

Azathioprine is an immunosuppressant pro-drug, converted in the body to the active metabolites 6-mercaptopurine and 6-thioinosinic acid. It is a purine synthesis inhibitor. Azathioprine is available in oral form.


Azathioprine. Image source: Wikipedia, public domain.

For many years, dual therapy with azathioprine and steroids was the standard anti-rejection regimen, until cyclosporine was introduced into clinical practice in 1978.

Azathioprine is a purine synthesis inhibitor, inhibiting the proliferation of cells, especially leukocytes. Azathioprine suppresses the bone marrow and CBC should be monitored. Caution should be exercised when it is used in conjunction with purine analogues such as allopurinol.


Metabolic pathway for azathioprine. Image source: Wikipedia, GNU Free Documentation License.

Azathioprine may be used in severe atopic dermatitis. It has a slow onset of action and needs a trial for several months to see an improvement.

Mycophenolate (CellCept) - an alternative to azathioprine


Mycophenolic acid. Image source: Wikipedia, public domain.

Mycophenolate mofetil is increasingly being used in place of azathioprine in organ transplantation, as it is associated with less bone marrow suppression, fewer opportunistic infections, and a lower incidence of acute rejection.

Mycophenolic acid is commonly marketed under the trade names CellCept (mycophenolate mofetil; Roche) and Myfortic (mycophenolate sodium; Novartis).

Mycophenolate is derived from the fungus Penicillium stoloniferum.

Mycophenolate blocks lymphocyte proliferation by inhibiting guanine nucleotide synthesis in lymphocytes.

What is the molecule that tacrolimus binds to in order to exert its therapeutic effect?

(A) NFkB
(B) calcium
(C) ipraimmunophilin
(D) NFAT
(E) calcineurin
(F) calmodulin
(G) AP-1

Answer: E.

References

Immunosuppressive drugs. Wikipedia.
Abbas' Immunology, edition 6, 2009.
Azathioprine. Wikipedia.
Mycophenolic acid. Wikipedia.

Published: 05/20/2009
Updated: 08/20/2014

Commonly Used Medications in Allergy and Immunology

Author: V. Dimov, M.D., Allergist/Immunologist, Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist, Assistant Professor at NSU

Inhaled Medications

Pulmicort (budesonide) Flexhaler DPI 90 mcg, 180 mcg INH BID, max dose 1440 mcg/day. More info at PulmicortFlexhaler.com

Pulmicort (budesonide) Respules 0.25 mg/0.5 mg/1 mg in 2 ml NEB BID (prior steroid - max dose 1 mg/day, no prior steroid - max dose 0.5 mg/day). More info at Epocrates and PulmicortRespules.com

Asmanex (Mometasone) Twisthaler 110 mcg, 220 mcg DPI, dose 220-440mcg/day qd/bid. If 4-11 yrs, dose 110 mcg/day, if older than 12, dose 220-440 mcg/day qd/bid. More info at Asmanex.com. Momethasone is also in Dulera (ICS/LABA)

Advair (fluticasone/salmetrol) Diskus 100/50, 250/50, 500/50 one puff bid, 4-11 yrs, dose 100/50 bid, if older than 12yrs, dose 100/50 – 250/50 1 puff bid

Advair HFA 45/21, 115/21, 230/21 two puff bid, if older than 12 yrs, dose 90/42 – 460/42

Symbicort (budesonide/formoterol) 80/4.5 mcg, 160/4.5 mcg/spray MDI 2puffs bid, if older than 12yrs 2 puffs bid. More info at SymbicortTouchpoints.com

Dulera (momethasone/formoterol) 100 mcg/5 mcg, 200 mcg/5 mcg/spray MDI, 2 INH BID. More info at Dulera.com

Flovent (fluticasone) HFA 44, 110, 220, 4-11 yrs 88 mcg bid, if older than 12 yrs 88-440 bid, 440-880 if prior oral steroid use. Flovent is available as Diskus, 100 mcg and 250 mcg, more info at Epocrates

Azmacort (triamcinolone) 75 mcg/spray MDI, 300mcg bid, tid or qid - max dose 1200/day, 6-12 yrs, dose 150-300mcg bid, if older than 12 yrs, dose 300mcg bid - max dose 1200/day

Relative binding affinity for glucocorticoid receptor (GR): mometasone > fluticasone > budesonide > triamcinolone.

Albuterol NEB 0.63 mg, 1.25 mg, and 2.5 mg/3 ml, TID/QID PRN

Atrovent NEB one vial 300 mcg tid/qid

Xopenex NEB 0.31, 0.63, 1.25mg/3ml, 6-11 yrs, dose 0.31 mg tid, if older than 11 yrs, 0.63mg tid

Xolair (Omalizumab) 150-375 mg q2-4 weeks ( older than 12yrs, severe refractory asthma, IgE 30-700, evidence of sensitization to at least one perennial aeroallergen)

Nose Sprays and Eye Drops (see Rhinitis Action Plan)

Nasonex (mometasone) 50 mcg/spray, Age 2-12 y, Dose: 1 spray/nostril qd. Age older 12 yo, Dose: 2 sprays/nostril qd.

Atrovent nasal, if older than 6yr, dose 0.03, 0.06% 2 spray/nostril bid

Astelin (Azelastine), 5-11 yrs, dose 1 spray/nostril bid, if older than 12 yrs, dose 1-2 spray/nostril bid

Patanase (Olopatadine), if older than 12 years, dose 2 sprays/nostril b.i.d.

Nasalcrom (Cromolyn Na), if older than 2 yrs, dose 1 spray/nostril q4-6 hrs

Patanol (Olopatadine) 0.1%, if older than 3 years, 1 gtt. in eyes b.i.d.

Ketotifen (Zaditor), if older than 3 yrs, 1 gtt in eyes bid/tid. Over-the counter options include Zaditor/Zaditen, Alaway, Zyrtec Itchy-Eye Drops, and Claritin Eye. A generic version of ketotifen fumarate ophthalmic solution, 0.025%, is available as store brands.

Lotemax/Alrex (Loteprednol), adults, 1-2 gtt in eyes qid

Optivar (Azelastine), if older than 3 yrs, 1 gtt in eyes bid

Oral Antihistamines

Fexofenadine (Allegra), 2-11 yrs, dose 30 mg bid, older than 12 yr, dose 180 mg. Children’s Allegra Oral Suspension, Fexofenadine HCl 30 mg/5 ml, adults and children 12 years of age and over take 2 teaspoonfuls (10 mL) every 12 hours, children 2 to under 12 years of age take 1 teaspoonful (5 mL) every 12 hours.

Zyrtec (cetirizine) 5mg/5ml, 2 – 6 yrs, dose 2.5- 5mg qd, 6 and above, dose 5-10mg qd

Xyzal (levocetirizine), 6 months – 5 yrs, dose 1.25 mg qd, 6 – 11 yrs, dose 2.5 mg qd, if older than 12 yrs, dose 2.5 – 5 mg qd

Hydroxyzine, younger than 6 yrs, dose 2mg/kg/day, 6 – 12 yrs, dose 12.5 – 25 mg q6hrs, older than 12 yrs, dose 25-100 mg q 6 hrs

Cyproheptadine (4; 2 mg/5ml), 2 – 6 yrs, dose start 0.25mg/kg/day - increase to 2mg q 8-12 hrs (max 12 mg/day), 7 – 14 yrs, start 0.25mg/kg/day - increase to 4 mg q 8-12hrs (max 16mg/day)

Leukotriene antagonist (LTRA)

Singulair (montelukast), Dosage forms: 10; 4,5 CH; 4 mg granule pkt. Age 12-24 mo, Dose: 4 mg PO qpm, use granules. Age 2-5 yo, Dose: 4 mg PO qpm; use chew tabs or granules, Age 6-14 yo, Dose: 5 mg PO qpm; Age older than 15 yo, Dose: 10 mg PO qpm.

Antibiotics

Bactrim (Trimethoprim), older than 2months, dose 15-20 mg/kg/day, prophylaxis 2-4 mg/kg/day

Augmentin 125/31.25/5ml, 200/28.5/5ml, 250/62.5/5ml, 400/57/5ml - if more than 40 kg, use adult dose, younger than 3 months, 30 mg/kg/day bid, older than 3 mo, less than 40 kg, 25-45 mg/kg/day bid

Augmentin ES-600 (amoxicillin/ clavulanate), 600/42.9/5 mL, for acute otitis media, dose: 90 mg/kg/day PO div q 12 hr x10 days.

Clindamycin, 75 mg,150 mg, 300 mg tabs; 75/5 mL. Infants/children, 10 – 20 mg/kg/day (tid dosing), Adolescent, 150-300 mg q6hrs.

Omnicef (Cefdinir), 6 mo-12 yrs, 14 mg/kg/day qd-bid for 10 days, older than 13 yrs, 300 mg bid

Azithromycin 100 mg/5ml, 200mg/5ml. Pediatric dose: 10 mg/kg qd x 1, and then 5 mg/kg qd x 4 days.

Cephalexin (Keflex), 50,500; 125,250/5 mL. Children: infections, bacterial, [25-50 mg/kg/day PO div q6-12h]. Max: 4000 mg/24h. Adults: 1000-4000 mg/day PO div q6-12h. Max: 4000 mg/24h.

Oral steroids

Dose: 1-2 mg/kg/day PO divided qd-bid; Max: 60 mg/day.

Prelone/Orapred (prednisolone) 15/5ml

Veripred 20 (prednisolone) 20/5ml

Prednisone

Dexamethasone, dosage forms:  0.25,0.5,0.75,1,1.5,4,6; 0.5/5 mL; 1/mL. Croup: 0.6 mg/kg PO x1. Max: 10 mg/dose; Alt: 0.15 mg/kg PO x1; Info: higher dose regimen may also be divided into 4 doses given q6h.


Topical creams and ointments for atopic dermatitis

Triamcinolone cream/ointment 0.025, 0.1, (15, 80, jar 453.6gm) 0.5% (15gm), lot .025, 0.1% (60ml)

Cutivate (Fluticasone) 0.05% crm/oint (15, 30, 60gm). lotion 0.05% 120ml

Desonide crm/oint 0.05% (15, 60gm), lotion (59, 118ml)

Protopic (Tacrolimus), 2-15 yrs, only use 0.03 oint (30, 60gm), for adults, 0.1% oint (30, 60, 100gm)

Elidel (Pimecrolimus) 1% crm, older than 2 yrs (30, 60, 100gm)

Cough medications

Expectorants

Mucinex ER (guaifenesin), 600 mg tablets, dose for older than 12 years, 1-2 tables BID. More info at Mucinex.com

Mucinex Children's (guaifenesin), 4-6 yrs, 5 ml q 4 hr; 6-12 yrs, 10 ml q 4 hr; older than 12 years, use adult Muciner ER. More info at Mucinex.com and Epocrates

Cough suppressants

Delsym (dextromethorphan) syrup, Dose: 4-6 years, 2.5 mL every 12 hours; 6-12 years, 5 mL; adults and children 12 years of age and over, 10 mL every 12 hours. More info at Delsym.com

Mucinex Cough for Kids (dextromethorphan/guaifenesin), 4-5 yo, Dose: 2.5-5 mL PO q4h prn; Max: 30 mL/24h; Info: give w/ plenty of water; 6-11 yo, Dose: 5-10 mL PO q4h prn; Max: 60 mL/24h; Info: give w/ plenty of water. More info at Mucinex.com and Epocrates

Mucinex DM (dextromethorphan/guaifenesin), oral ER tablet, Older than 12 yo, Dose: 1-2 tabs PO q12h prn; Max: 4 tabs/24h; Info: do not cut/crush/chew; give w/ plenty of water. More info at Mucinex.com and Epocrates

Anaphylaxis

EpiPen Jr, [15-30 kg], Dose: 0.15 mg SC/IM once; Info: may repeat dose.

EpiPen, [0.3 mg SC/IM once]; Info: may repeat dose.

Epinephrine (adrenaline) is the first-line the treatment of anaphylaxis. Adult intramuscular dose is 0.3 to 0.5 ml of 1:1,000 concentration. This should be given in the lateral aspect of the thigh by intramuscular injection. The dose can be repeated every 5 to 15 minutes, depending upon the response, for 3-4 doses. The same is true for children except the dose is 0.01 mg per kg (AAAAI Ask the Expert, 2012).

Disclaimer

Information provided here is for medical education only. It is not intended as and does not substitute for medical advice. If you are a patient, please see your doctor for evaluation of your individual case. Under no circumstances will the authors be liable to you for any direct or indirect damages arising in connection with use of this website.

The appearance of external hyperlinks to other websites does not constitute endorsement. We do not verify, endorse, or take responsibility for the accuracy, currency, completeness or quality of the content contained in these sites.

Published: 02/21/2010
Updated: 04/27/2014