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0% found this document useful (0 votes)
69 views3 pagesSunscreen
Uploaded by
Lazar CrinaCopyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF or read online on Scribd
Grrrrie ae
Piaminacological ©
~ LAURENCE BRUNTON
4 BRUCE CHABNER « BJORN KNOLLMAN
Scanned with CamScanner js, tuberculosis), including leading to hospitalization
‘death, Patients should be screened for latent tubercu-
josis infection before beginning treatment and closely
nonitored during and after drug therapy.
pfliximab. Infliximab (REMICADE) is a mouse-human
chimeric IgG, monoclonal antibody that binds to solu:
te and membrane-bound TNF-c (Krueger and Callis,
2004). Infliximab is a complement-fixing antibody that
induces complement-dependent and cell-mediated lysis
sshen bound to cell-surface-bound TNF-a. Neutralizing
sniibodies to infliximab may develop against its chimeric
sinucture. Concomitant administration of methotrexate
cglucocorticoids may suppress this antibody formation
Adolimumab. Adalimumab (HUMIRA) is a human IeG,
‘monoclonal antibody that binds soluble and membrane=
found TNF-a. Like infliximab, it can mediate comple-
sment-induced cytolysis on cells expressing TNF. Unlike
infliximab, however, itis fully human, which reduces the
sk for development of neutralizing antibodies.
{Cutaneous T-cell Lymphoma
Denileukin diftitox. Denileukin diftitox or DAB,.=-IL-2
(oxtak) is a fusion protein composed of diphtheria tox
fragments A and B and the receptor-binding portion of
IL-2. DAB,,,-IL-2 is indicated for advanced cutaneous
Teell lymphoma in patients with >20% of T cells
expressing the surface marker CD25. Specificity is
derived from the presence of IL-2 receptor (IL-2R) on
malignant and activated T cells but not resting B and T
cells. Following binding to the IL-2R, DAB IL-2
intemalized by endocytosis. The active fragment of diph-
theria toxin then is released into the cytosol, where it
inhibits protein synthesis through ADP ribosylation,
leading to cell deat. Clinical trials have shown an over-
allresponse rate of 30% and a complete response rate of
10% in cutaneous T-cell lymphoma, Adverse effects
include pain, fevers, chills, nausea, vomiting, and diar-
(hypotension,
of patients;
back pain, dyspnea,
and capillary leak
a
all of which are e
amounts of IgA, soluble CD4, CD8, HLA molecules,
and cytokines. Although the mechanism of action of
IVIG is not understood fully, proposed mechanisms
include suppression of IgG production, accelerated
catabolism of IgG, neutralization of complement-
mediated reactions, neutralization of pathogenic at
bodies, downregulation of inflammatory cytokines, inhi-
bition of autoreactive T lymphocytes, inhibition of
immune cell trafficking, and blockage of Fas-ligand/
Fas-receptor interactions (S
In dermatology, IVIG is used off label as an adjuvant oF res
cue therapy for multiple diseases. These include auto-immune bul-
Tous diseases, toxic epidermal necrolysis, connective tissue diseases,
vasculitis, urticaria, atopic dermatitis, and graft-versus-host disease
Prospective controlled studies are lacking forthe efficacy in these
diseases and likely vary based on the [VIG product u
IVIG is relatively contraindicated in patients with severe
selective IgA deficiency (IgA <0.05 g/L). These patients may pos-
‘sess ant-[gA antibodies that place them at risk for severe aniaphylac-
tic reactions, Other relative contraindications include congestive
‘heart failure and renal failure due to the risk of fluid overload.
Patients with rheumatoid arthritis or eryoglobulinemia are at an
increased risk of renal failure (Thomas eta, 2007).
SUNSCREENS
Photoprotection from the acute and chronic effects of sun
exposure is readily available with sunscreens. The major
active ingredients of available sunscreens include chem-
ical agents that absorb incident solar radiation in the
UVB and/or UVA ranges and physical agents that
contain particulate materials that can block or reflect
incident energy and reduce its transmission to the skin.
‘Many ofthe sunscreens available are mixtures of organic
chemical absorbers and particulate physical substances.
[deal sunscreens provide a broad spectrum of protection
and are formulations that are photostable and remain
{ntact for sustained periods on the skin. They also should
| benon-irtating, invisible, and nonstining o clothing.
em No sing ‘single sunscreen ingredient possesses all these desir-
able properties, but many are quite effective nonetheless.
lle UVA filters inthe US.
include 1 avobenzone, also known a Paso 1789; 2) oxybenzone;
43) titanium dioxide; 4) zine oxide; and 5) ecamsule (MEXoRY1. Sx).
Additional UVA sunscreens, including bemotrizinol (risosoRs s)
and bisoctrizole (TmNSoRB M), are availabe in Europe and elsewhere,
‘out notin the US.
We Sunscreen Agents, Tere are numerous UYB fiers, incluing 1)
‘paminobenzoic acid (PABA) esters (eg. padimate 0), 2) cinnamates
(e.g., octinoxate), 3) octocrylene, and 4) salicylates (¢.g., octisalate).
‘The major measurement of sunscreen photoprotection is the
sun protection factor (SPF), which defines a ratio of the minimal dose
of incident sunlight that will produce erythema or redness (sunburn)
on skin wth the sunsreen in place (protected) andthe dose that
Scanned with CamScanner
1827
A90102VWUVHd T2190 T01vWUaa 1830
XI NOLLI3S
| X90103VWUVHd SW3ISAS TVID3dS
Finasteride is approved for use only in men. Pregnant women
should not be exposed to the drug because of the potential for
inducing genital abnormalities in male fetuses. Adverse effects of|
astride include decreased libido, erectile dysfunction, ejacula-
tion disorder, and decreased ejaculate volume. Each of these
‘occurs in <2% of patients (Leyden et a, 1999), Like minoxidil,
treatment with finasteride must be continued, or any new hi
growth will be lost
TREATMENT OF HYPERPIGMENTATION
‘The agents mentioned in this section are most effective
on hormonally or light-induced pigmentation within the
epidermis. They have limited efficacy on post-inflamma-
tory pigmentation within the dermis.
Hydroquinone. Hydroquinone(1.4-dinydrobenzene: TR/-LUMA) is
te first-line agent in medical therapy of byperpigmentation. It
