CHAPTER 6: CONTACT DERMATITIS AND DRUG ERUPTION Flashcards
(94 cards)
1
Q
Inflammatory reaction of the skin from exposure to a substance that causes eruptions No previous exposure necessary
A
Irritant contact dermatitis
2
Q
Acquired sensitivity to various substances that produce inflammatory reactions only in persons who have been previously sensitized
A
Allergic contact dermatitis
3
Q
Pain and burning more common in this type of contact dermatitis
A
Irritant
4
Q
Alkalis penetrate and destroy deeply because they:
A
Dissolve keratin
5
Q
Principal compounds in alkalis
A
Sodium, Potassium, Ammonium, Ca hydroxide
6
Q
Powerful acids are _______________ whereas weaker acids are ________________
A. Astringent B. Corrosive
A
B A
7
Q
What type of acid produces a brownish charring of the skin, beneath which is an ulceration that heals slowly
A
Sulfuric acid
8
Q
This acid is used more widely than any other acid in industry
A
Sulfuric acid
9
Q
This acid causes deep burns Tissue is stained yellow
A
Nitric acid
10
Q
One of the strongest inorganic acids, capable of dissolving glass
A
Hydrofluoric acid
11
Q
___ may produce paresthesia of the fingertips, with ing agents when possible, and protection, most often by
cyanosis and gangrene. The nails become discolored yellow
A
OXALIC ACID
12
Q
This acid is used in the manufacturing of pigments
A
Titanium hydrochloride
13
Q
What to do if you come in contact with titanium hydrochloride
A
Application of water to the Alkalis
exposed part will produce severe burns. Therefore, treatment
consists only of wiping away the noxious substance.
14
Q
is a protoplasmic poison that pro- cleaners, and toilet bowl and oven cleansers. Alkalis penetrate
duces a white eschar on the surface of the skin.
A
Phenol (carbolic acid)
. . .
readily neutralized
with 65% ethyl or isopropyl alcohol.
15
Q
Acid in tear gas (lacrimators) that can cause dermatitis
A
Chloroacetophenone
16
Q
Petrolatum dermatitis from impure petroleum jelly or lubricating oil manifests as
A
Verrucous thickening of skin
17
Q
What type of hypersensitivity Allergic contact dermatitis
A
it is caused by a spe- cific acquired hypersensitivity of the delayed type, also known as :
cell-mediated (type IV) hypersensitivity.
18
Q
Application of substances suspected to be the cause to intact uninflamed skin usually on upper back
A
Patch test
19
Q
Patches in patch test are removed after_____ and reevaluated after ______
A
48 hours ;Day 4 or 5
20
Q
In photopatch test, a standard patch test is applied for 48h then exposed to ______ J/m2 of UVA and read after another 48 hours
A
5-15
21
Q
Most frequent site for nail polish dermatitis
A
Eyelids
22
Q
Earlobe dermatitis is indicative of sensitivity from ______
A
Nickel
23
Q
Deodorant and clothing dye can cause dermatitis in the axillary area. Which part of the axilla is involved in what substance?
A
Deodorant-axillary vault Clothing dye- axillary fold
24
Q
Most common cause of allergic contact dermatitis in florists
A
Peruvian lily
25
Difference between dermatitis and fungal infection on the foot
Toe webs involved in fungal infections
26
Dermatitis from metals is usually due to
Nickel and chromates
27
Most common cause of allergic contact dermatitis in children and adults
Nickel
28
Leading cause of allergic contact dermatitis associated with cosmetics
Fragrance
29
Chemical in hair dye that can cause dermatitis
Phenylenediamine
30
Hair bleaches contain ________ that can cause dermatitis
Ammonium persulfate
31
Chemical found in most so called natural products that is an allergen
Propolis
32
Most common sunscreen allergen
Oxybenzone
33
Least irritating antiperspirant
Aluminum chlorhydrate
34
Which drug induces the highest rate of allergic reactions
Clonidine
35
Produce sensitization of skin when applied topically, when ingested, an acute flare at site of contact dermatitis may occur
Anamnestic (recalled) eruption
36
Most common topical local anesthetic that can cause dermatitis
Benzocaine
37
Antibiotics that most commonly cause dermatitis
Neomycin Bacitracin
38
Wheal and flare reaction occurring when a substance is applied to the intact skin
Contact urticaria
39
two types of dermatitis caused by substances coming in contact with the skin
irritant dermatitis and allergic contact dermatitis
40
nflammatory reaction in the skin resulting from exposure to a substance that causes an eruption in most people who come in contact with it
Irritant dermatitis
41
an acquired sensitivity to various substances that produce inflammatory reactions only in those persons who have been previously sensitized to the allergen.
Allergic contact dermatitis
42
Irritant dermatitis is often produced by alkalis such as soaps, cement, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, and toilet bowl and oven cleansers (Fig. 6.1). Alkalis penetrate and destroy deeply because they dissolve keratin. Strong solutions are corrosive, and immediate application of a weak acid such as vinegar, lemon juice, or 0.5% hydrochloric acid solution will lessen their effects.
Fig. 6.1 Cement burns. (Courtesy Steven Binnick, MD.)
ALKALIS
| The principal compounds are sodium, potassium, ammonium, and calcium hyd
43
Management of acid burns
Treatment of acid burns consists of immediate rinsing with copious amounts of water and alkalization with sodium bicarbonate, calcium hydroxide (limewater), or soap solutions. Phosphorus burns should be rinsed off with water, followed by application of copper sulfate to produce a precipitate.
44
Airbag Dermatitis
Airbags are deployed as a safety feature on cars when rapid deceleration occurs. Activation of a sodium azide and cupric oxide propellant cartridge releases nitrogen gas, which expands the bag at speeds exceeding 160 km/hour (96 miles/hour). Talcum powder, sodium hydroxide, and sodium carbonate are released into the bag. Abrasions, thermal, friction, and chemical burns and an irritant contact dermatitis may result. Superficial erythema may respond well to topical steroids, but full-thickness burns may occur and require debridement and grafting.
45
Lacrimators such as chloroacetophenone in concentrated form may cause dermatitis, with a delayed appearance about 24–72 hours after exposure. Irritation or sensitization, with erythema and severe vesiculation, may result. Treatment consists of lavage of the affected skin with sodium bicarbonate solution and instillation of boric acid solution into the eyes. Contaminated clothing should be removed.
Tear Gas Dermatitis
Fig. 6.3 Mustard gas burn
46
Pathophysiology of allergic contact dermatitis
Allergic contact dermatitis results when an allergen comes into contact with previously sensitized skin. It is caused by a specific acquired hypersensitivity of the delayed type, also known as cell-mediated (type IV) hypersensitivity. These sensitizers do not cause demonstrable skin changes on initial contact.
47
used to detect hypersensitivity to a substance that is in contact with the skin so that the allergen may be determined and corrective measures taken
| Patch Test.
Fig. 6.5 Positive patch test reaction.
48
test that may be used to screen products used by the patient
Provocative Use Test
| Products that are made to stay on the skin once applied (as opposed to s
49
test used to evaluate for contact photoallergy to such substances as sulfonamides, phenothiazines, p-aminobenzoic acid, oxybenzone, 6-methyl coumarin, musk ambrette, and tetrachlorosalicylanilide
Photopatch Test
50
Black or greenish staining under rings, metal wristbands, bracelets, and clasps is caused by the abrasive effect of cosmetics or other powders containing zinc or titanium oxide on gold jewelry.
Black dermatographism
51
Exanthems (Morbilliform or Maculopapular Reactions)
Fig. 6.21 Morbilliform (exanthematous) drug eruption caused by exposure to an antibiotic.
Exanthems are the most common form of adverse cutaneous drug eruption. They are characterized by erythema, often with small papules throughout. Exanthems tend to occur within the first 2 weeks of treatment but may appear later, or even up to 10 days after the medication has been stopped. Lesions tend to appear first proximally, especially in the groin and axilla, generalizing within 1 or 2 days. The face may be spared. Pru- ritus is usually prominent, helping to distinguish a drug erup- tion from a viral exanthem. Antibiotics, especially semisynthetic penicillins and TMP-SMX, are the most common causes of this reaction pattern (Fig. 6-20). Ampicillin-amoxicillin given during EBV infection causes an exanthem in 29–69% of adults and 100% of children. TMP-SMX given to AIDS patients causes exanthems in about 40%. Certain quinolones (e.g., gemifloxa- cin) cause exanthems at a high rate: 4% overall and 30% in young women.
Morbilliform eruptions may rarely be restricted to a previ- ously sunburned site, the so-called “UV recall–like” phenom- enon. It occurs with various antibiotics. The sunburn may have occurred 1–7 months before the drug eruption. This pattern of eruption must be distinguished from a true UV recall caused by antimetabolites (see later section, “Adverse reactions to chemotherapeutic agents”).
52
severe cutaneous eruption with associated systemic involvement, where host genetic factors, medication exposure, plus frequent viral reactivation, lead to activated T cells and create a multiorgan inflammatory reaction
Drug-induced hypersensitivity syndrome or drug reaction with eosinophilia and systemic symptoms
53
Characteristic features of Drug-Induced Hypersensitivity Syndrome or Drug Reaction With Eosinophilia and Systemic Symptoms (DIHS/DRESS)
All patients with DIHS share the characteristic features of fever, rash, and internal organ involvement. Characteristic features include the following:
* Rash developing late (>3 weeks) after the inciting medication is started; often occurs with the first exposure to the medication
* Long-lasting symptoms (>2 weeks) after discontinuation of the causative drug
* Fever (>38°C)
* Multiorgan involvement
* Eosinophilia (>1500 absolute eosinophilia); less common
with dapsone (criteria vary, with some groups citing counts greater than 1500/μl and others more than 700/μl or above 10% if the leukocyte count is lower than 4000/μl)
* Lymphocyte activation (lymphocytosis, atypical lymphocytosis, lymphadenopathy)
* Frequent reactivation of HHV-6, HHV-7, EBV, and CMV
54
is currently the most common anticon- vulsant causing DRESS, because it is also used to treat neuropathic pain, bipolar disorder, and schizophrenia
Carbamazepine
55
typically occurs in patients with preexisting renal failure. Often, affected patients are treated unnecessarily for asymptomatic hyperuricemia, with clear indications for therapy present in only about one third of these patients. They are often given a dose not adjusted for their coexisting renal disease and are frequently taking a thiazide diuretic.
Allopurinol hypersensitivity syndrome
56
is similar to that seen with the anticonvulsants, including the characteristic facial and periorbital edema. It typically begins 3 weeks after starting the medication but may occur as soon as 1 week. The skin eruption is usually morbilliform or an erythroderma.
Sulfonamide hypersensitivity syndrome
57
ccurs in young adults, usually in the context of acne therapy. Deficiency of glutathione S-transferases is common in affected individuals and is more common in persons of African Caribbean descent.
Minocycline hypersensitivity syndrome
58
It usually begins 4 weeks or more after starting drug
Hemolytic anemia and methemo- globinemia may be present. A morbilliform eruption that heals with desquamation is most characteristic. Icterus and lymph- adenopathy occur in 80% of patients. Eosinophilia is typically not present. Liver involvement is a mixture of hepatocellular and cholestatic. The bilirubin is elevated in 85%, partly attrib- utable to the hemolysis, and hypoalbuminemia is characteris- tic. Liver involvement is often severe and may be fatal. As with the hypersensitivity syndromes previously discussed, cortico- steroids are the mainstay of treatment.
Dapsone hypersensitivity syndrome
59
defined as <10 % epideramal detachment
Stevens-Johnson Syndrome
60
defined as >30 % epidermal detachment
Toxic Epidermal Necrolysis
61
Differentiate SJS, SJS/TEN overlap, and TEN
the exact definitions of SJS and TEN remain arbitrary, and some consider these syndromes to be parts of a disease spectrum, based on the following:
* Both SJS and TEN are most frequently induced by the same medications.
* Patients initially presenting with SJS may progress to extensive skin loss resembling TEN.
* The histologic findings of TEN and SJS are indistinguishable.
* Both are increased by the same magnitude in HIV infection.
62
Manifestations of SJS/TEN
Fig. 6.24 Bullous drug reaction.
Fever and influenza-like symptoms often precede the erup- tion by a few days. Skin lesions appear on the face and trunk and rapidly spread, usually within 4 days, to their maximum extent. Initial lesions are macular and may remain so, followed by desquamation, or may form atypical targets with purpuric centers that coalesce, form bullae, then slough. Patients with purpuric atypical targets may evolve more slowly, and usually the skin lesions are clinically inflammatory. In SJS, virtually always, two or more mucosal surfaces are also eroded, with the oral mucosa and conjunctiva most frequently affected. The patient may have photophobia, difficulty with swallowing, rectal erosions, painful urination, and cough, indicative of ocular, alimentary, urinary, and respiratory tract involvement, respectively. Over time, more than 10% of the skin surface may be sloughed, leading to SJS/TEN overlap; if more than 30% of the skin is lost, a case is classified as TEN.
63
Management of SJS/TEN
Management of SJS/TEN patients is similar to those with an extensive burn. They have fluid and electrolyte imbalances, bacteremia from loss of the protective skin barrier, hyperca- tabolism, and sometimes acute respiratory distress syndrome (ARDS).
IVIG
cyclosporine
high dose steroids
etanercept
64
If phenytoin is given prophylactically in neurosurgical patients who are receiving whole-brain radiation therapy and systemic steroids, an unusual reaction occurs. As the dose of steroids is being reduced, erythema and edema initially appear on the head in the radiation ports. This evolves over 1 or 2 days to lesions with the clinical appearance and histology of SJS or even TEN. The eruption spreads caudad, and mucosal involve- ment may occur (Fig. 6-24). A similar syndrome has been reported with the use of amifostine, phenobarbital, or leveti- racetam during radiation for head and neck cancers. This EM syndrome can rarely be seen with radiation therapy alone. If amifostine is used to reduce acute and chronic, radiation- associated head and neck xerostomia, there is a significant risk of SJS/TEN.
Radiation-Induced Epidermal Necrolysis
65
a nonnucleoside reverse transcriptase inhibitor, has been associated with a high rate of severe drug eruptions, including SJS/TEN.
Nevirapine
66
toxic pustuloderma and pustular drug erup- tion, AGEP is an uncommon reaction with an incidence of 1–5 cases per million per year.
Causes:
Drugs - most common
mercury exposure.
viral and bacterial infections
Loxosceles spider (e.g., brown recluse) bites
The eruption is of sudden onset, within 1 day in many cases associated with antibiotics, and averaging 11 days in other cases. The rash is accompanied by fever in most patients. Facial edema may be present. Initially, there is a scarlatiniform erythema. The eruption evolves and disseminates rapidly, consisting usually of more than 100 nonfollicular pustules less than 5 mm in diameter (Fig. 6-26). Nikolsky’s sign may be positive. Mucous membrane involvement is common but usually affects only one surface and is nonerosive. Laboratory abnormalities typically include a leukocytosis with neutro- philia (90%) and at times an eosinophilia (30%). Typically, the entire self-limited episode lasts up to 15 days. Characteristi- cally, widespread superficial desquamation occurs as the eruption clears. AGEP can recur with a second exposure to the medication.
Fig. 6.28 Acute Generalized Exanthematous Pustulosis
67
most common drug-induced pseu- dolymphoma is one resembling _____
clinically and histologically.
utaneous T-cell lymphoma (CTCL)
## Footnote
Lymphadenopathy and circulating Sézary cells may also be present. CD30+ cells may be present in the infiltrate. Usually, other features (e.g., keratinocyte necrosis, dermal edema) help to distinguish these reactions from true lymphoma. Importantly, T-cell receptor gene rearrangements in the skin and blood may be positive (or show pseudoclones) in these drug-induced cases, representing a potential pitfall for the unwary physician. Pseudolymphoma resolves with discontinuation of the medication. The medication groups primarily responsible are anticonvulsants, sulfa drugs (including thiazide diuretics), dapsone, and antidepressants. Vaccinations and herbal supplements can also induce pseudolymphoma.
68
________are the most common causes of nonim- munologic urticarial reactions. They alter prostaglandin metab- olism, enhancing degranulation of mast cells. They may therefore also exacerbate chronic urticaria of other causes.
Aspirin and NSAIDs
| Other agents causing nonimmunologic urticaria include radiocontrast mate
69
Immunologic urticaria is most often associated with _____and related ____________.
penicil- lin and related β-lactam antibiotics
70
caused by intravenous infusion of vancomycin.
At any time during the infusion, a macular eruption appears initially on the back of the neck, sometimes spreading to the upper trunk, face, and arms. Angioedema has been described. There is associated pruritus and “heat,” as well as hypotension that may be severe enough to cause cardiac arrest.
Red man syndrome
| The red man reaction is caused by elevated blood histamine. Red man synd
71
Fig. 6.30 Amiodarone hyperpigmentation.
Amiodarone photosensitivity develops in up to 75% of treated patients and occurs after a cumulative dose of 40 g.
A reduced minimal erythema dose (MED) to UVA, but not UVB, occurs, and gradually returns to normal between 12 and 24 months after stopping the medication. Stinging and burning may occur as soon as 30 min after sun exposure.
Less fre- quently, a dusky, blue-red erythema of the face and dorsa of the hands occurs (Fig. 6-28). At times, papular reactions are also seen. Desquamation, as seen after sunburn, is not observed following amiodarone photosensitivity reactions. This reaction may be dose dependent, and acute burning may be relieved by dose reduction. Narrow-band UVB may desen- sitize patients with persistent phototoxicity after stopping amiodarone.
72
piroxicam photosensitivity
The NSAIDs, especially piroxicam, are frequently associated with photosensitivity (Fig. 6-29). The characteristic reaction is a vesicular eruption of the dorsa of the hands, sometimes asso- ciated with a dyshidrosiform pattern on the lateral aspects of the hands and fingers. In severe cases, even the palms may be involved. Histologically, this reaction pattern shows intraepi- dermal spongiosis, exocytosis, and perivascular inflammatory cells—a pattern typical of photoallergy. However, this reaction may occur on the initial exposure to the medication, but pho- totoxicity tests in animals and humans have been negative. Patients with photosensitivity to piroxicam may also react to thiosalicylic acid, a common sensitizer in thimerosal. Half of patients having a positive patch test to thimerosal with no prior exposure to piroxicam test positive to piroxicam. This suggests that piroxicam reactions seen on initial exposure to the medica- tion may be related to sensitization during prior thimerosal exposure.
73
Anticoagulant-Induced Skin Necrosis
Fig. 6.33 Warfarin-induced necrosis. (Courtesy Steven Binnick, MD.)
Warfarin-induced skin necrosis (WISN) usually occurs 3–5 days after therapy is begun, and a high initial dose increases the risk. Patients with a much more delayed onset (up to 15 years) are ascribed to noncompliance, drug-drug interactions, or liver dysfunction. WISN occurs in 1:1000 to 1:10,000 patients treated with warfarin. Lesions begin as red, painful plaques that develop petechiae, then form a large bulla. Necro- sis follows (Fig. 6-31). Priapism can complicate warfarin necrosis. Hereditary or acquired deficiency of protein C, and less often protein S, antithrombin III, or factor V Leiden, and lupus anticoagulant syndrome are associated with warfarin necrosis. A less common variant seen in patients with a deep venous thrombosis (DVT) of an extremity is necrosis of a distal extremity, usually the one with the DVT. Warfarin-induced venous limb necrosis is most often seen in cancer patients, but also in the setting of heparin-induced thrombocytopenia and antiphospholipid syndrome.
74
as been suggested for prevention
of warfarin-induced skin necrosis in the patient with protein
C deficiency.
Dabigatran extexilate
75
Cowboy and gunbelt andholsterpattern: plaques in the hip tend to progress around
the waist and down the thigh
Vitamin K allergy
76
In Europe, a second pattern of vitamin K reaction has been
reported. Subcutaneous sclerosis with or without fasciitis appears at the injection site many months after vitamin K
treatment. There may have been a preceding acute reaction as
previously described. Peripheral eosinophilia may be found.
These pseudosclerodermatous reactions have been termed
Texier disease
77
3 types of hyperpigmentation induced by minocycline
Type I is a blue-black discoloration appearing in areas of prior
inflammation, often acne or surgical scars (Fig. 6-33). This may
be the most common type seen by dermatologists.
. . .
The second type (type II) is the appearance of
a similar-colored pigmentation on the normal skin of the anterior shins, analogous to that seen in antimalarial-induced
hyperpigmentation. It is initially mistaken for ecchymoses but
does not fade quickly.
. . .
can confirm the presence of minocycline in the granules. The least common type (type III) is
generalized, muddy-brown hyperpigmentation, accentuated
in sun-exposed areas
78
treatment is reproducibly complicated by the
appearance of a pink discoloration that gradually becomes
reddish blue or brown and is concentrated in the lesions of
patients with Hansen’s disease.
. . .
This pigmentation may be
disfiguring and is a major cause of noncompliance with this
drug in the treatment of Hansen’s disease.
. . .
Histologically, a
PAS-positive, brown, granular pigment is variably seen within
foamy macrophages in the dermis. This has been called “druginduced lipofuscinosis.”
Clofazimine
79
causes a blue or brown hyperpigmentation that
is most frequently observed in the nails. The lunula may be
blue, or the whole nail plate may become dark brown. Diffuse
hyperpigmentation of the skin, pigmentation of the lateral
tongue, and increased tanning are less common. It occurs in
darkly pigmented persons, is dose dependent, and clears after discontinued.
zidovudine
80
by far the most common form of heavy
metal–induced pigmentation seen by dermatologists.
Silver
81
typically follows
the topical use of silver sulfadiazine or silver-containing dressings (Acticoat). Blue-gray pigmentation occurs at the site of
application. Implantation into the skin by needles or pierced
jewelry may lead to focal areas of argyria
Local argyria
82
can also arise from topical application to the skin (in burn and
epidermolysis bullosa patients), by inhalation, by mucosal
application (nose drops or eyedrops), or by ingestion. Patients
may purchase or build devices that allow them to make colloidal silver solutions, which they then ingest in the belief that
it will improve their health. After several months of such exposure, the skin becomes slate-gray or blue-gray, primarily in
areas of sun exposure.
. . .
Histologically, granules of silver are
found in basement membranes around adnexal (especially
eccrine) and vascular structures. Sun exposure leads to the
silver binding to either sulfur or selenium in the skin, increasing deposition. The deposited silver activates tyrosinase,
increasing pigmentation.
Systemic argyria
83
also presents as blue-gray pigmentation, usually after a cumulative dose of 8 g of gold, usually after the treatment of rheumatoid arthritis
Cutaneous chrysias
84
can cause a
severe photodistributed hyperpigmentation. This is most
common in African American or Hispanic women and occurs
about 1 year after starting therapy. The lesions are slate-gray
or gray-blue macules and patches on the face, neck, and forearms. Perifollicular accentuation is noted.
. . .
Histology shows a
sparse lichenoid dermatitis with prominent dermal melanophages. The action spectrum of the drug appears to be in
the UVB range, but hyperpigmentation is induced by UVA
irradiation.
. . .
The mechanism appears to be postinflammatory
hyperpigmentation from a photosensitive lichenoid eruption
rather than drug or drug metabolite deposition.
. . .
Treatment is
broad-spectrum sunscreens, stopping the agent, and
bleaching creams if needed.
calcium channel blocker (CCB) diltiazem
85
refer to adverse reactions that
have similar symptoms to serum sickness, but in which
immune complexes are not found. This reaction was particularly common with cefaclor. Patients present with fever, an
urticarial rash, and arthralgias 1–3 weeks after starting the
medication (Fig. 6-35). Minocycline, bupropion, and rituximab
have been reported to cause serum sickness like reactions.
serum sickness- like reaction
86
Numerous macular and papular eruptions have been
described with chemotherapeutic agents as well. Many occur
at the earliest recovery of the bone marrow, as lymphocytes
return to the peripheral circulation. They are associated with
fever. This phenomenon has been called “_______.” Histologically, these reactions demonstrate a nonspecific, superficial perivascular mononuclear
cell infiltrate, composed primarily of T lymphocytes. Treatment is not required, and the eruption spontaneously resolves.
cutaneous eruptions
of lymphocyte recovery
87
_______induces characteristic flagellate erythematous
urticarial wheals associated with pruritus within hours or
days of infusion (Fig. 6-37). Lesions continue to appear for
days to weeks. Although investigators have not always been
able to induce lesions, the pattern strongly suggests scratching
is the cause of the erythematous lesions. A similar characteristic pattern of flagellate hyperpigmentation occurs after bleomycin treatment, possibly preceded by the erythematous
reaction or simply pruritus.
87
_______induces characteristic flagellate erythematous
urticarial wheals associated with pruritus within hours or
days of infusion (Fig. 6-37). Lesions continue to appear for
days to weeks. Although investigators have not always been
able to induce lesions, the pattern strongly suggests scratching
is the cause of the erythematous lesions.
Bleomycin
88
Patients may present with linear erythematous wheals 1–2
days after eating raw or cooked shiitake mushrooms (Fig.
6-38). This so-called_______, is thought to be caused by a toxic reaction to lentinan, a
polysaccharide component of the mushrooms.
. . .
It is self-limited
and resolves within days to weeks of its appearance, but can
be treated with topical corticosteroids to relieve the associated
pruritus some patients experience.
Other associations with
flagellate eruptions include adult-onset Still’s disease, dermatomyositis, and docetaxel therapy
toxicodermia, or shiitake flagellate dermatitis
89
is a recombinant human keratinocyte growth factor
used to reduce the severity and duration of mucositis in
patients undergoing preparative regimens for hematopoietic
stem cell transplantation. An intertriginous erythema accompanied by oral white confluent plaques and small lichenoid
papules developed in one patient receiving palifermin therapy.
The papules resembled flat warts clinically and histologically
but were human papillomavirus (HPV) negative by in situ
hybridization studies. A direct hyperproliferative effect of the
keratinocyte growth factor is the proposed mechanism.
Palifermin
90
Drug that is associated with ulceration of striae distensae
Bevacizumab
91
Mercury may induce multiple cutaneous syndromes. The
classic syndrome is______, also known as calomel disease,
pink disease, and erythrodermic polyneuropathy.It
is caused by mercury poisoning, usually in infancy. The skin
changes are characteristic and almost pathognomonic: painful
swelling of the hands and feet, sometimes associated with
considerable itching of these parts. The hands and feet are also
cold, clammy, and pink or dusky red. The erythema is usually
blotchy but may be diffuse. Hemorrhagic puncta are frequently evident. Over the trunk, a blotchy macular or papular
erythema is usually present. Stomatitis and loss of teeth may
occur. Constitutional symptoms consist of moderate fever, irritability, marked photophobia, increased perspiration, and a
tendency to cry most of the time. There is always moderate
upper respiratory inflammation with throat soreness. The
infant may have hypertension, hypotonia, muscle weakness,
anorexia, and insomnia. Albuminuria and hematuria are
usually present. The diagnosis is made by finding mercury in
the urine.
Acrodynia
92
Treatment of crodynia
Treatment with a seafood-free diet
and chelation with succimer led to resolution of the eruption
in some patients. Nummular dermatitis improved in
two mercury patch test–positive patients when their dental
amalgam was removed.
93
Iodides may cause a wide variety of skin eruptions. The most
common sources of exposure are oral and IV contrast materials
and when iodides are used to treat thyroid disease. Application
of povidone-iodine to the skin, mucosa, or as a tub soak has
produced iododerma. The most common type is the acneiform
eruption with numerous acutely inflamed follicular pustules,
each surrounded by a ring of hyperemia (Fig. 6-43). Dermal
bullous lesions are also common and may become ulcerated
and crusted, resembling pyoderma gangrenosum or Sweet
syndrome. The eruption may involve the face, upper extremities, trunk, and even the buccal mucosa. Acne vulgaris and
rosacea are unfavorably affected by iodides. Acute reactions
may follow IV radiocontrast studies in patients with renal
failure. The lesions may be associated with severe leukocytoclastic vasculitis, intraepidermal spongiform pustules, and
suppurative folliculitis. The lesions respond to prednison
Iododerma
