aznil jurnal 1
TRANSCRIPT
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By:Aznil Fajri
Supervisor:
dr. Nanda Earlia, Sp. KK
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bstract
The etiopathogenesis of perioraldermatitis (PD) is still unknown andconsequently, medical treatment is
difficult,.
neurogenic inflammation could playa role in the pathogenesis of PD, as
many cutaneous diseases.
PD seems to be mainly related to themercury contained in dental fillings
and/or its organic compounds formedby oral/gut bacteria.
the possible role of thesesubstances as causes of PD,
providing new information on thepossible cross-talk between
neuroimmunodermatology andpotential triggers of PD.
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Introduction
Perioral dermatitis (PD) is classically
characterized by perioral papules and
pustules sparing a narrow zone around
the lips.
Clinically polymorphic presentations,
including papulovesicles and erythematous-
eczcematous and scaling eruption, are
frequently reported.
Many exogenous and endogenous factors
have been proposed as possible causative
agents, but the etiopathogenesis is still
unknown.
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Case Report
erythematous-eczematous, nonitching, perioral
lesions, which appeared 6 weeks earlier
filling of three molars performed 2 months earlier, hadcaused mild pain and local inflammation in the filling
sites
redness and edema surrounding the aforementionedteeth, and a localized pain in the filling sites
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Case Report
Use of topical or systemic drugs in the last 3 months,
as well as recent prolonged UV exposure, use of
cosmetics, or use of toothpaste were denied
Routine blood exams, thyroid and sex hormones were
normal, Lesional microbial and fungal flora were quali-
quantitatively normal
Patch test (Tabel 1) : a single sensitization (++) to
thiomersal (sodium ethylmercury thiosalicylate)
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TABLE 1 Haptens Used for First (A) and Second (B) Patch Test in our Patient.
(A) First Patch Test
Thiuram mix 1% Neomycin sulfate 20%
Nickel sulfate 5% Colophony 20%
Phenol-formaldehyde resin 5% Ethylenediamine 1%
Balsam of Peru 25% Fragrance mix 8%
Lanolin alcohols 30% Potassium dichromate 0.5%
p-Phenylenediamine 1% Mercaptobenzothiazole 2%
Epoxy resin 1% Disperse blue 1%
Disperse yellow 1% Disperse red 1%
Disperse orange 1% Paraben mix 15%
Kathon CG 0.01% (in water) Formaldehyde 1% (in water)
Benzocaine 5% Cobalt chloride 1%Thiomersal 0.1% Diaminodiphenylmethane 0.5%
Carba mix 3% Mercaptobenzothiazole mix (MBT mix) 2%
Quaternium-15 1% Mercury ammonium chloride 1%
Quinoline mix 6% Imidazolidinyl urea 1%
Phenylisopropylparaphenylenediamine 0.1% p-Toluenediamine 1%
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Hydrocortisone-17-butyrate 1% (in
ethanol) Budesonide 0.1%
Ketoprofen 10% Latex 0.1% (in water)
Tegobetaine 1% (in water) Euxyl K 400 1.5%
Compositae mix 5% Propylene glycol 10% (in water)
Diphenylguanidine 1% Hexamethylenetetramine 1%
Hydroquinone-monobenzylether 1% Palladium chloride 1%
Eugenol 5% Hydroquinone 1%Mercury 0.5% Ethylene glycol dimethacrylate 2%
Methyl methacrylate 5% Bisphenol A dimethacrylate 2%
Propolis 20% Sorbic acid 5%
Butylated hydroxyanisole 2% Alpha-tocopherol 20%
(B) Second Patch Test
Tin 2.5% Colloidal silver 0.1%
Tin chloride 1% Zinc 2.5%
Copper sulfate 1% (in water) Zinc chloride 2%
Silver nitrate 1% (in water) Zinc sulfate 2%
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Case Report
lesions overlapped with the facial areas innervated by
infraorbitary nerves and right mental nerve
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Case Report
these nerves also innervate the dental half arcs that
contained the amalgam-filled molars
new lesions in the facial area innervated by the left
mental nerve
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Discussion
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This case appears as a good model ofneuroinflammation: the distribution oflesions supports the idea of
neuroinflammation involving trigeminalbranches that innervate teeth and
perioral skin.
The amalgam seems the mostprobable trigger, through two possiblemechanisms, not mutually exclusive
(see top panel fig. 3)
Direct effect of mercury released by theamalgam (and/or methylmercury,
synthesized from inorganic mercury by
oral bacteria) on neuronalfunction/excitability and/or cholinergicreceptors/pathways— Several papersindicate the possible involvement of thecholinergic system during intoxicationby mercury and/or organomercurials.
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FIGURE 3. Schematicre presentationof possible pathogenic mechanisms
involving the cholinergic system in
neurogenic inflammation.
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Methylmercury, synthetized from amalgam-derived inorganic
mercury by oral and gut bacteria, could have elicited type IVhypersensitivity reactions in our patient, leading to release of
mediators causing/worsening neuroinflammation.
Nerve stimulation could cause perioral skin neuroinflammation
through antidromic signal conduction on a specially branching set
of nociceptors connecting the alveolar cavity and the face(classic axon reflex), and/or through an indirect mechanism
related to central processing of the trigeminal signal followed by
involvement of autonomic parasympathetic fibers.
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Conclution
the role of neuroinflammation in PD is worthy of
investigation. Apart from the present case,
neuroinflammation could play a role, more in general,
in the pathogenesis of perioral dermatoses and,
possibly, oral lichenoid reactions in patients allergic todental filling metals. The cholinergic system seems
crucial in the communication between oral mucosa,
nerves, and the immune system in skin diseases.
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Thanks......Thank you
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Telaah Kritis Diagnosis Dini
1. Apakah jika prosedur diagnosis dini dilaksanakan
akan dapat memperbaiki hasil akhir dari pada
perjalanan klinik penderita?
Ya
b) Tidak
c) Tak iketahui
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2. Jika hasil pemeriksaan dini positif, apakah kita
dapat meluangkan waktu tambahan yang
diperlukan untuk konfirmasi diagnosis pasti
maupun jika diperlukan perawatan jangka lama?
Ya
b) Tidak
c) Tak iketahui
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3. Apakah penderita dengan hasil test diagnisis dini
yang positif dapat mengikuti program pengobatan
yang akan diberikan sesuai dengan penyakit
tersebut?
a) Ya
Tidak
c) Tak iketahui
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4. Apakal telah ada bukti pemeriksaan kesehatan
berkala dengan menggunakan test tunggal lebih
baik dibandingkan dengan menggunakan
beberapa test?
a) Ya
Tidak
c) Tak iketahui
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5. Apakah ada kecacatan yang tersembunyi akibat
penyakit tersebut membutuhkan tindakan medik
yang nyata?
Ya
b) Tidak
c) Tak iketahui
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6. Apakah test screening yang akan digunakan
cukup adekuat dalam segi biaya, akurasi, dan
aseptabilitasnya?
a) Ya
Tidak
c) Tak iketahui
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Telaah Kritis Screening Test
1. Apakah metode penelitian suatu randomized
trial?
a) Ya
Tidakc) Tak iketahui
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2. Apakah ada pengobatan yang efektif untuk
kelainan tersebut?
Ya
b) Tidakc) Tak iketahui
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3. Apakah ada sesuatu hal tersembnyi pada penyakit
tersebut yang memerlukan screening?
a) Ya
Tidak
c) Tak diketahui
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4. Apakah screening test mempunyai angka
sensitifitas dan spesifisitas yang tinggi?
Ya
b) Tidakc) Tak iketahui
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5. Dapatkah sistem kesehatan (skala nasional atau
profesi) selaras dengan program test yang akan
dilaksanakan?
Ya
b) Tidak
c) Tak iketahui
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6. Apakah hasil test yang positif memerlukan
tindakan lanjutan berupa tindakan intervensi, atau
pemeriksaan lanjutan?
Ya
b) Tidak
c) Tak iketahui