P.K.’s family and medical history are classic for atopic dermatitis. His family
history is significant for asthma, allergic rhinitis, and atopic dermatitis. He had his
initial outbreak at the age of 1 month and then experienced seasonal allergic rhinitis
after his dermatitis went into remission. His skin examination reveals findings of both
acute and chronic atopic dermatitis, with typical lesion location and description.
on pertinent biopharmaceutic considerations, why is this prescription appropriate for P.K.?
Results from P.K.’s treatment regimen might be improved by providing more
frequent (twice daily) application or a more potent preparation to control inflamed
lesions. Once any weeping is stopped, a less potent preparation in the ointment form
should be used for maintenance and the number of applications may be reduced.
Because of the reservoir effect, control can be maintained in many cases with
intermittent regimens such as once daily, every other day, or every third day use of
topical corticosteroids. In addition, intermittent regimens can involve alternating
corticosteroids and agents such as topical pimecrolimus or tacrolimus to maintain
control and minimize adverse effects of either agent.
Because the calcineurin inhibitors are as potent as mid-potency topical
corticosteroids without causing atrophy, telangiectasias, or striae, many
dermatologists would use either tacrolimus or pimecrolimus on the face in preference
Topical Antibiotics with Corticosteroids
together? What are the risks associated with topical antibiotics?
It is determined that P.K. has impetigo superimposed on his atopic dermatitis.
Because impetigo can be treated with topical antibiotics such as mupirocin,
combination therapy with a corticosteroid–antibiotic preparation would appear to be
a logical choice. Although mupirocin may be an appropriate alternative for some
topical dermatologic infections, the current over-the-counter topical antibiotics
(bacitracin, neomycin, and polymyxin) are ineffective for most dermatologic
infections and are indicated only for the prophylaxis of skin infections. In addition,
because staphylococcal toxins act as superantigens, eliciting the production of IgE,
cephalexin, in combination with topical corticosteroids for the atopic dermatitis.
Oral antibiotics reduce the bacterial counts faster and have a lower incidence of
recurrent impetigo compared with topical agents. In areas in which community
methicillin-resistant Staphylococcus aureus rates are high, more effective antibiotic
therapy might be indicated as an alternative. P.K. would most likely benefit from a
treatment course of an oral antibiotic plus a topical corticosteroid preparation.
P.K. is prone to repeated infections and atopic dermatitis flares because his skin is
colonized with staphylococci. Many dermatologists upon clearance of the impetigo
would initiate dilute bleach baths. These consist of 5- to 10-minute baths twice a
week, made by adding 120 cc (1/2 cup) of household bleach (6%) to a full bathtub
(approximately 40 gallons) to create a 0.005% solution. Because of the variety of tub
sizes, the amount of bleach should be adjusted to the size of the bathtub and the
could you recommend for relief of pruritus?
As previously noted, pruritus (itching) is the most common cutaneous symptom in
21 Scratching, which can damage or fatigue receptor nerve endings,
is the most common method of relieving pruritus. Topically applied local anesthetics
or antihistamines could also be effective in dulling the sensation. However, this
approach is often disappointing, probably because the intact epidermis poorly
absorbs the salt forms of these drugs. In addition, low concentrations are used in
many over-the-counter preparations. If adequate concentrations of local anesthetics
are used (lidocaine 3%–4%), pruritus or pain may be reduced for up to 45 minutes.
These agents are most useful for relieving pruritus or pain for short periods (e.g.,
when trying to go to sleep at night).
21 A serious drawback to the use of topical
benzocaine and antihistamine preparations is their propensity to induce allergic
P.K. could also try cold water or ice cubes, which effectively relieve pruritus via
vasoconstriction, as do products containing aluminum acetate (Burow solution),
tannic acid, or calamine. A cool bath may be useful for the relief of pruritus from
dermatologic lesions if they are widespread.
Moisturizing mixtures such as Eucerin, Nivea, Lubriderm, or even simply mineral
or baby oil are useful in the treatment of pruritus caused by dry skin in patients with
atopic dermatitis. Bathing should be restricted to avoid washing away normal body
oils, the drying effect of water, the irritant effect of alkaline soaps, and the trauma of
Topical corticosteroid applications can be very effective if dermatologic lesions
exist. They reduce inflammation, which helps soothe the affected area.
Systemic antihistamines are effective antipruritic agents, although their major
beneficial effect may be attributable to sedation. The newer, nonsedating
antihistamines are notably ineffective at relieving itch, with the exception of
25 There is disagreement over which antihistamine or antiserotonin agents
are most effective for treatment of pruritus.
21,25,26 Oral hydroxyzine is a commonly
used antihistamine; doses of 10 to 25 mg 3 to 4 times a day are commonly used. Oral
cyproheptadine is another option. There is little evidence that antihistamines are
effective in treating non–histamine-mediated pruritus, except that their inherent
sedative effect may be somewhat beneficial in all pruritic conditions. Doxepin, a
tricyclic antidepressant with potent H1
worse at night, as is typical with atopic dermatitis, the use of any of the three H1
blockers mentioned at bedtime would be appropriate.
Nondrug Recommendations for Atopic Dermatitis
by mouth at bedtime as needed), what nondrug interventions should be suggested for P.K.?
The general goals of therapy for atopic dermatitis are to decrease pruritus,
suppress inflammation, and moisturize the skin. The nondrug recommendations shown
in Table 39-10 are useful adjuncts and mainstays for use between disease flares for
patients such as P.K. with atopic dermatitis or any other irritant dermatitis. Often
careful attention to nonpharmacologic measures can markedly reduce the incidence of
disease flare. Because even nonlesional skin in patients with atopic dermatitis has
reduced moisture, the use of emollients should include all skin surfaces.
Nondrug Recommendations for Patients with Atopic Dermatitis or Other
and low in humidity (30%–50%). Rapid changes in ambient temperature should be avoided.
(e.g., Basis soap). A colloid bath or the use of appropriate amounts of bath oil may be useful.
Primary irritants such as paints, cleansers, solvents, and chemicalsprays should be avoided.
P.K. should be warned to avoid people with active herpes simplex infections
because severe disseminated infections can occur.
Tachyphylaxis and Calcineurin Inhibitors
Clinicians commonly misdiagnose tachyphylaxis due to corticosteroids. Failure of
topical corticosteroids to clear difficult atopic dermatitis after an initial improvement
may give the false impression of tachyphylaxis, when the actual problem is a primary
29 This could be caused by either inappropriate application
technique by the patient or the choice of a product with inadequate potency.
Tachyphylaxis can occur within 1 week of therapy, but generally takes several weeks
29 To treat this problem, patients should discontinue the
corticosteroid for a week and restart at an appropriate dose. Alternatively, patients
may be switched to topical tacrolimus or pimecrolimus.
inhibitory effect on cytokine production, calcineurin inhibitors result in decreased
immunologic response to antigens. Transient burning, erythema, and pruritus are the
most common adverse effects. Neither pimecrolimus nor tacrolimus causes skin
atrophy, making them attractive alternatives for patients with lesions on the face and
the neck. Issues regarding the long-term safety of these products have led the U.S.
Food and Drug Administration to place a black-box warning in the manufacturer’s
literature regarding a potential increased cancer risk.
ALLERGIC CONTACT DERMATITIS: POISON
IVY, POISON OAK, OR POISON SUMAC
Contact dermatitis is an inflammation of the skin that occurs when a substance comes
in direct contact with the epidermal surface. The most common form is irritant
contact dermatitis caused solvents or other chemicals that irritate the skin resulting
red, painful lesions, for example, dish pan hands, diaper dermatitis. Allergic contact
Poison ivy (Rhus) dermatitis is a major cause of allergic contact dermatitis in the
United States, exceeding all other causes combined. Other allergens include latex,
leather, nickel, and laundry detergents. It is estimated that 50% to 95% of the
population is sensitive to the plants to some degree. The severity of the condition
varies from mild discomfort to an extremely painful, debilitating condition. Rhus
dermatitis is caused by sensitization to an allergic substance in the leaves, stems, and
roots of poison ivy, poison oak, and poison sumac plants. All three plants contain the
same sensitizing oleoresin, urushiol oil, which contains pentadecacatechol, the actual
sensitizing agent. Therefore, the dermatitis caused by the three different plants is
Direct contact with the plant is unnecessary for the rash to occur. Highly sensitive
persons may develop severe dermatitis merely from exposure to Rhus oleoresin
carried by pollen or by smoke from burning leaves. The oleoresin may remain active
for months on clothing, shoes, tools, and sporting equipment. Once the toxic
substance is exposed to the skin, it can be spread by the hands to other areas of the
body (e.g., genitals or eyes) or to people who may come into close contact with the
exposed person. Although washing with soap and water may not prevent the
dermatitis, even if it is done within 15 minutes of exposure, it will prevent spread of
the oleoresin to other parts of the body.
Sensitive individuals should be instructed to avoid contact with the offending
plant. If contact is inevitable, every effort should be made to shield exposed areas of
the skin with appropriate clothing.
Exposed individuals should bathe or shower as soon as they come in from
outdoors and should wash their clothes. Nonprescription topical cleansers (Tecnu,
Zanfel, Mean Green Hand Scrub) claim to remove urushiol oil embedded in the skin
through the action of microfine scrubbing beads and surfactants, thus possibly
preventing the rash or limiting spread. They are applied to exposed areas of the skin,
followed by vigorous scrubbing, and rinsed off after application.
After an initial incubation period of 5 to 21 days, a patient would be expected to
react to the oleoresin in 12 to 48 hours after re-exposure. A mild exposure to these
plants in a sensitized person results in a typical erythematous, vesicular, linear, and
sometimes, oozing rash after 2 to 3 days; complete clearing occurs in 1 to 3 weeks.
If a large area is exposed, lesions appear within 6 to 12 hours and may appear
blistered and eroded; in some cases, ulcers may appear. Healing occurs more slowly,
often requiring 2 to 3 weeks for complete resolution. The following factors
contribute to the development of poison ivy, poison oak, or poison sumac dermatitis:
the concentration of the oleoresin to which the skin is exposed, area of exposure (i.e.,
the thickness of the stratum corneum), duration of exposure, site of exposure, genetic
factors, and immune tolerance. It is important to determine the areas of the body that
are affected. If the eyes, genital areas, mouth, respiratory tract, or more than 15% of
the body is affected, the patient should receive a course of systemic corticosteroids.
if the condition becomes more severe?
Weeping lesions should be treated with aqueous vehicles (e.g., Burow solution or
saline) as outlined in the beginning of this chapter. Lesions that are not wet or
weeping should be treated with calamine lotion applied 2 to 4 times daily. The zinc
oxide in calamine lotion may act as a mild astringent, although some people find this
preparation to be unacceptable because of its pink color, which can stain clothes.
Alternatively, a topical corticosteroid appropriate for the body part affected could be
used. If K.P.’s poison oak reaction becomes more severe, additional treatment with
prednisone 1 mg/kg/day for at least 2 or 3 weeks will be required; such therapy
should be withdrawn slowly (1–2 weeks) to prevent recurrence of the lesions.
his clothes thoroughly. How should he be treated?
The fact that Z.T.’s facial rash is not linear (as one would expect if he had just
contacted the plant) suggests that he may have contacted the smoke of a burning
poison ivy plant. This can be quite serious because the oleoresin can be carried in
smoke and, if inhaled, can cause vesiculation of lung tissue leading to severe
respiratory problems. Z.T. should be observed for signs of respiratory difficulties
and should be treated with a course of systemic corticosteroids.
time. Why is he experiencing a relapse?
Two weeks is the minimum course of treatment when systemic corticosteroids are
used for severe cases of poison ivy, poison oak, or poison sumac. The oleoresin
remains fixed in the skin, and if the systemic corticosteroid is withdrawn too soon,
the lesions return. This is probably the most common reason for treatment failure
with systemic corticosteroids. Alternatively, systemic corticosteroids can be
discontinued before 2 weeks of treatment and a moderate-potency topical
corticosteroid preparation can be started 24 hours before discontinuation of systemic
corticosteroids and continued for 7 to 10 days to prevent relapse.
Clinically recognizable adverse drug reactions are manifested on the skin more often
than any other organ or organ system.
30–33 An estimated 1% to 5% of hospitalized
patients experience a drug eruption.
31 Outpatient statistics are more difficult to
obtain, but are probably within the same range.
Many of the common dermatologic reactions that can be induced by drugs have
other causes as well, so a complete workup must include other nondrug etiologies.
Viral, fungal, and bacterial infections, as well as certain systemic diseases and
foods, have been identified as causes for common reactions such as urticaria,
erythema multiforme, and erythema nodosum. The diagnosis of drug eruptions is best
made by identifying the type of lesions observed and associating the lesions with
specific drug therapy. The most important diagnostic criterion is an accurate
assessment of the skin lesions. With this critical information, the clinician can then
refer to a drug information source to associate any current or past drug therapy with
the specific lesions observed (see Chapter 32, Drug Hypersensitivity Reactions).
Acneiform eruptions appear very much like common acne. They may be distinguished
from acne by their sudden occurrence, the absence of comedones, uniform
appearance (i.e., all at the same stage of development), and the fact that they may
drug-induced acne should be suspected when the lesions appear in persons outside
the typical age bracket for acne. Drugs implicated include adrenocorticotropic
hormone, anabolic steroids, azathioprine, danazol, glucocorticoids, iodides,
bromides, lithium, gefitinib, erlotinib. lapatinib, and oral contraceptives. For patients
with acne vulgaris, these drugs may worsen existing lesions (see Chapter 40, Acne).
Photosensitivity eruptions require the presence of both a drug (or chemical) and a
light source of appropriate wavelength. These eruptions are divided into two
increased sensitivity to sunburn. The ultraviolet A (UVA) light source alters the drug
to a toxic form, resulting in tissue damage independent of any allergic response, and
occurs in everyone who gets high enough skin levels of the offending drug. This
eruption can occur on first exposure to a drug, is dose-related, and will continue as
long as the skin concentration of the drug exceeds the threshold level for the reaction
to occur. Photoallergic reactions, which are very uncommon, may appear as a variety
of lesions, including urticaria, bullae, and eczema. UVA light alters the drug so it
becomes an antigen or acts as a hapten. Photoallergic eruptions require previous
contact with the offending drug, are not dose related, exhibit cross-sensitivity with
chemically related compounds, and are secondary to the use of topical agents.
Unfortunately, outside light through a window and fluorescent lighting permit passage
of or can emit UVA light. In addition, until recently there were inadequate topical
preparations that provide protection against UVA light. Avobenzone, although
covering much of the UVA spectrum, is photolabile, losing 60% of its effectiveness
in less than 1 hour. However, many products now solve that problem by adding
agents such as octocrylene, which stabilize avobenzone’s photolability, and are
usually labeled “stabilized UVA protection.” New products containing ecamsule
appear to offer an advance in protection against lower spectrum UVA rays. Most
phototoxic and photoallergic reactions occur fairly soon after exposure to light.
Implicated drugs are numerous, including among others, antibiotics (tetracyclines,
fluoroquinolones, and sulfonamides), antidepressants (tricyclics), antihypertensives
oral contraceptives, and antipsychotics (phenothiazines) (see Chapter 42,
Photosensitivity, Photoaging, and Burns Injuries).
Topical administration of a sensitizing agent produces localized papulovesicular
lesions. These lesions are limited only to areas that are exposed to the topical
product. Neomycin, benzocaine, and diphenhydramine are well-known topical
34–36 Systemic administration of a drug to a patient
previously sensitized to the drug by topical application can provoke widespread
dermatitis. Implicated systemically or topically administered drugs that reactivate
allergic contact dermatitis include procaine or benzocaine, radiographic contrast
media or iodine, and streptomycin and gentamicin or neomycin, among others.
As the name implies, erythema multiforme (EM) eruptions take on a varied spectrum
of morphologic forms, ranging from the mildest with tiny maculovesicular lesions to
more severe forms such as SJS and toxic epidermal necrolysis syndrome (TENS)
with extensive bullous lesions and routine involvement of mucous membranes.
Although all forms have been reported to have oral lesions, they are much more
severe in SJS and TENS, in which genital, nasal, and ocular mucosae can also be
involved. Target lesions are usually present in all forms of the disorder, which
characteristically are erythematous, iris-shaped papules, and vesiculobullous lesions
typically involving the extremities, especially the palms and soles in EM and the
torso in SJS and TENS. The lesions take on the appearance of a circular target with a
bull’s-eye in the middle, thus the term target lesion. Questions have recently been
raised about the shared pathologic nature of these forms of EM.
forms, EM minor and EM major, is more common in children and young adults, and
is self-limited in nature with only transient hypopigmentation or hyperpigmentation as
complications. Sometimes malaise, a low-grade fever, and itching or burning may
accompany this type of eruption. Etiologic factors associated with EM include drugs,
mycoplasma and herpes infections, radiation therapy, foods, and sometimes
neoplasms. Allopurinol, barbiturates, phenothiazine, and sulfonamides are the drugs
most often implicated in EM eruptions.
Ammonia Soaps, chemicals, hair dyes
Antihistamines Topical anti-itch creams and ointments
Benzyl alcohol Medications, cosmetics
“Caine” anesthetics Medications (e.g., over-the-counter benzocaine
Ethylenediamine Stabilizer in topical products (e.g., aminophylline)
Formaldehyde Shoes, clothing, soaps, insulations
Neomycin Topical medications (e.g., Neosporin)
Nickelsulfate Jewelry, fasteners
Paraben Preservative in many topical products
Paraphenylenediamine Hair dyes, leather
Potassium dichromate Shoes, leather
Thiomersal Preservatives, contact lens products
Wool alcohols Lanolin-containing products, clothes
SJS is probably the most common type of severe drug eruption. The syndrome is
usually a moderate mucocutaneous and systemic reaction. Blisters and atypical target
lesions involve less than 10% of body surface area, with some epidermal
detachment, which can cause scarring in some cases.
With more extensive involvement, clinical findings are almost indistinguishable
from TENS. The skin can become hemorrhagic, and pneumonia and joint pains may
occur. Serious ocular involvement is common and can culminate in partial or
complete blindness. Besides drugs, this syndrome has been associated with
infections, pregnancy, foods, deep radiographic therapy, and neoplasms. Mortality is
estimated to be in the range of 5% to 18%. The duration of the syndrome is usually 4
to 6 weeks. The long-acting sulfonamides are most often implicated. Allopurinol,
carbamazepine, fluoroquinolones, hydantoin, phenylbutazone, piroxicam, and other
sulfa derivatives such as sulfonylureas are also possible causative agents.
Toxic Epidermal Necrolysis Syndrome
Epidermal necrolysis, a severe, life-threatening mucocutaneous and systemic
reaction, may be preceded by a prodrome characterized by malaise, lethargy, fever,
and occasionally throat or mucous membrane soreness. Epidermal changes follow
and consist of erythema and massive bullae formations that easily rupture and peel,
giving the skin a scalded appearance.
Hairy parts of the body are usually not affected, but mucous membrane
involvement is common. Blisters cover more than 30% of body surface area, with
extensive epidermal detachment that can result in scarring. Mortality in TENS
patients is roughly 30%, often within 8 days after bullae appear. The usual cause of
death is infection complicated by massive fluid and electrolyte loss, similar to
patients with extensive burns. Although the skin takes on a grave appearance, healing
occurs within 2 weeks in approximately 70% of patients, with some potential for
scarring. In addition to drugs, certain bacterial infections and foods are believed to
cause this type of eruption. Most causes of TENS in children are owing to infection
(e.g., S. aureus). A higher incidence of this type of drug eruption appears to occur in
HIV-positive patients. Drugs most frequently implicated include allopurinol,
aminopenicillins, carbamazepine, hydantoin, phenylbutazone, piroxicam, and sulfa
Erythema nodosum eruptions appear as red, indurated, inflammatory nodules on the
In addition to the unusual distribution, the lesions are tender when palpated.
Occasionally, these lesions are accompanied by mild constitutional symptoms, but
there is usually no mucous membrane involvement. Etiologic factors associated with
the development of erythema nodosum include drugs, female sex, rheumatic fever,
sarcoidosis, leprosy, certain bacterial infections (e.g., tuberculosis), and systemic
fungal infections such as coccidioidomycosis. Usually, the lesions heal slowly over
the course of several weeks after the offending agent is removed. Oral contraceptives
are the most frequently implicated drug with this type of eruption. Other implicated
drugs include sulfonamides and penicillin.
Drug Hypersensitivity Syndrome
This severe systemic reaction is also known as anticonvulsant hypersensitivity
syndrome and as a drug reaction with eosinophilia and systemic symptoms (DRESS).
Symptoms begin with a high fever followed by widespread maculopapular–pustular
rash on the trunk, arms, and legs that may lead to exfoliative dermatitis with large
areas of skin sloughing. Hair and nails are sometimes lost. Eosinophilia occurs in
greater than 50% of cases, 30% have abnormal lymphocytosis, and 20% have
lymphadenopathy. Internal organ damage appears late in the syndrome with
elevations of liver function or renal function laboratory values. These may be
accompanied by other general systemic symptoms such as headache and malaise.
Secondary bacterial infections can occur. Approximately 10% of patients die, many
because of infection. If exfoliative dermatitis occurs, it can take weeks or months to
resolve, even after withdrawal of the offending agent. The most commonly implicated
drugs are sulfonamides, antimalarials, anticonvulsants, and penicillin. Although
rarely reported in the literature, its broad range of symptoms, confusing
nomenclature, and symptom overlap with other drug-related adverse effects may lead
to underdiagnosis and reporting.
Maculopapular eruptions are subdivided into two groups: scarlatiniform and
morbilliform. Most drug eruptions fall within one of these two groups. Scarlatiniform
eruptions are erythematous and usually involve extensive areas of the body. They are
differentiated from streptococcal-induced scarlet fever by the lack of other diagnostic
signs and laboratory studies. Morbilliform eruptions usually begin as discrete,
reddish-brown maculae that may coalesce to form a diffuse rash. These eruptions are
differentiated from measles by the lack of fever and other typical clinical signs. In
either type of maculopapular eruption, pruritus may or may not be present. Generally,
this type of eruption appears within 1 week after the causative drug (2 or more weeks
with penicillins) has been started and completely clears within 7 to 14 days after
stopping it. Morbilliform eruptions commonly are caused by ampicillin, amoxicillin,
Urticarial eruptions are immediate hypersensitivity reactions (IgE-mediated) and
usually appear as sharply circumscribed (raised), edematous, and erythematous
lesions (wheals) with an abrupt onset.
In most cases, individual lesions disappear within 24 hours. These are replaced
with new lesions elsewhere until the offending allergen is cleared from the body.
Urticarial lesions are associated with an intense itching, stinging, or prickling
sensation. Commonly called hives, urticarial eruptions are frequently associated with
certain drugs, foods, psychic upsets, and serum sickness. The most frequently
implicated drugs with this type of reaction are aspirin, penicillin, and blood
products. Patients who exhibit urticaria attributable to a drug are at increased risk of
anaphylaxis if re-exposed to the same medication in the future.
Angioneurotic edema (also called angioedema) is a more severe form of urticaria in
which giant hives penetrate more deeply into surrounding tissues.
Lips, mouth, tongue, and eyelids are common locations. Extensive involvement of
the tongue, throat, or larynx can be fatal.
Angiotensin-converting enzyme inhibitors (ACEIs) are the most common drug
cause of angioedema. Patients taking ACEIs should be warned to look out for any
unusual swelling in the facial or oral area and, if present, should go immediately to
the nearest emergency room for treatment. Although it usually occurs within the first
several months of treatment, cases have been reported up to as long as 3 years after
initiation of ACEI therapy (see Chapter 14, Heart Failure and Chapter 32, Drug
QUESTION 1: D.Z., a 42-year-old man with a chronic seizure disorder and long-standing anxiety, was
onset for a drug-induced dermatologic reaction? How should the drug eruption in D.Z. be managed?
Although most drug eruptions occur within 1 to 2 weeks after starting therapy, it
may take 3 to 4 weeks after an initial exposure to a medication for the reaction to
occur. Repeated exposure to the same offending agent can reduce the time of onset of
the reaction to a few days or even within hours of ingestion. Because D.Z. has been
taking clonazepam and carbamazepine chronically and penicillin for only 8 days, the
temporal relationship would logically lead to the conclusion that penicillin is a
highly probable cause. Almost all cases of urticaria are associated with extensive
eosinophilia; however, it is not specific for any particular antigen. However, before
labeling penicillin as the cause of his drug eruption, a thorough history to rule out
other common nondrug causes should be taken.
For D.Z., a different antibiotic (macrolide) should be substituted for penicillin (to
complete the 10-day course of therapy). The individual lesions should begin to clear
in 24 hours of eruption (if the penicillin is the cause of the urticaria). If the urticaria
does not begin to clear in a few days, another cause should be investigated.
Treatment is primarily supportive, and use of an oral antihistamine (e.g.,
diphenhydramine 25–50 mg 4 times daily) for several days would be recommended.
If the reaction is severe, a 1- to 2-week course of prednisone 40 to 60 mg/day will
control most symptoms within 48 hours.
A full list of references for this chapter can be found at
http://thepoint.lww.com/AT11e. Below are the key references and websites for this
chapter, with the corresponding reference number in this chapter found in parentheses
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