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Presented by : Mais Al- Joulany Alaa Sherif

DERMATOLOGY. VITILIGO. SUPERVISOR : DR. SAMI …. Presented by : Mais Al- Joulany Alaa Sherif. Case study.

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Presented by : Mais Al- Joulany Alaa Sherif

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  1. DERMATOLOGY VITILIGO SUPERVISOR: DR. SAMI … Presented by :Mais Al-JoulanyAlaaSherif

  2. Case study A 26 year old young man presented with depigmentedpatches on face (below the eyes) and neck 2 yrs. Along with this, he also complainedof eructation which was worse after food, incontinence of urine with sudden urging and sticky watery dischargefrom ears since 5 yrs which was worse after head bath. Lesions first appeared on forehead which disappeared of its own and then gradually appeared below eyes, on lips and on neck. The lesions were of progressing type. The patient did not receive any treatment for the above complaints prior to this visit. There was no family history of vitiligo. Childhood history was uneventful. He discontinued studies due to his lack of interest. He started working in a cloth shop from 15 yrs of age.

  3. Case study Patient had desire for sweets and fried food and cold climate; was intolerant to warm weather with profuse perspiration from soles. There was sudden urging for urination. He was mild, gentle and had a clear conception. He was dark and moderately built, weigh 60 kg. and height 160 cm; bloodpressure maintained at 120/80 mm of Hg, Pulse rate of 75/minute and Respiratory rate 20/minute. On examination tenderness of left hypochondria on palpation, no other systemic abnormality was detected.

  4. Case summery • hot patient • Desires sweets • Profuse perspiration from soles • Sudden urging to urinate • White discoloration of skin •Eructations <after eating. •Sticky watery discharge from ear <head bath.

  5. Differential Diagnosis -Leukodermaassociated with melanoma -Postinflammatoryleukoderma -Mycosis fungoides -Pityriasis alba -Pityriasisversicolor alba - Chemical leukoderma - Leprosy - Nevus depigmentosus -Hypomelanosis of Ito - Nevus anemicus

  6. Introduction Hypomelanosis is a decrease of melanin in the epidermis. This reflects mainly two types of changes: ▪ No decrease of melanocytes but a decrease of the production of melanin only that is called melanopenichypomelanosis (an example is albinism). ▪ A decrease in the number or absence of melanocytesin the epidermis producing no or decreased levels of melanin. This is called melanocytopenichypomelanosis (an example is vitiligo)

  7. Introduction Sex :Equal in both sexes Incidence: Common, worldwide. Affects up to 1% of the population. Age of Onset:begin at any age, but in 50% of cases it begins between the ages of 10 and 30 years. Race:All races, most common in India, Mexico, Japan, Egypt and other tropical countries. of vitiligo casesInheritance:in about 30 % there is a positive family history.

  8. Introduction Vitiligois a chronic ,acquired ,idiopathic depigmentary condition :causes The cause of vitiligois not yet fully understood. Three principal theories have been presented about the mechanism of destruction of melanocytes in vitiligo -Autoimmune (activated Lymphocytes destroy melanocytes ) -neurogenic hypothesis - self-destruct hypothesis (destruction of melanocytes by a toxic subestance produced by normal melanocytes) onset of vitiligo - physical trauma (Koebnerphenomenon) - Illness - emotional stress - Sunburn

  9. Clinical Presentation The disease appears symmetrically, usually in the face, but also on the nape of neck, axillae, elbows, hands, knees and genitals. Vitiligo usually occurs in a localized or generalized pattern The “ lip-tip ” pattern involves the skin around the mouth as well as on distal fingers and toes; lips, nipples, genitalia and anus may be involved.

  10. Clinical Presentation Skin Lesions - Macules, 5 mm to 5 cm - “Chalk” or pale white - sharply marginated - Margins are convex Trichromevitiligo (three colors: white, light brown, dark brown) Inflammatory vitiligo has an elevated erythematous margin and may be pruritic.

  11. Vitiligo: face Extensive depigmentation of the central face. Involved vitiliginous skin has convex

  12. Vitiligo: knees Depigmented, sharply demarcated macules on the knees.

  13. Distribution The focal type : is characterized by one or several maculesin a single site Segmental Vitiligo: usually develops in one unilateral region; usually does not extend beyond that initial onesidedregion Mucosal Vitiligo: depigmentation of only the mucous membranes Generalized vitiligo: is more common and is characterized by widespread distribution of depigmentedmacules, often in a remarkable symmetry AcrofacialVitiligo: fingers and periorificial areas vitiligouniversalis: extensive generalized vitiligo may leave only a few normally pigmented areas of skin

  14. Universal vitiligoVitiliginousmacules have coalesced to involve all skin sites with complete

  15. Examination General Examination : Associated with thyroid disease: (Hashimoto thyroiditis, Graves disease) diabetes mellitus pernicious anemia Addison disease Multiple endocrinopathysyndrome Ophthalmologic examination healed chorioretinitis or iritis Vision is unaffected The Vogt-Koyanagi-Harada syndrome: is vitiligo + poliosis + uveitis + dysacusis+ alopecia areata.

  16. Laboratory Examination - Wood Lamp Examination - Dermatopathology - Electron Microscopy - Laboratory Studies • Thyroxine(T 4 ) • TSH • FBG • CBC • ACTH stimulation test

  17. Diagnosis Normally, diagnosis of vitiligo can be made readily on clinical examination of a patient with progressive, acquired, chalk-white, bilateral (usually symmetric), sharply defined macules in typical sites.

  18. Management Sunscreens : -protection from acute sunburn reaction - limitation of tanning of normally pigmented skin. Cosmetic Coverup : (called self-tanning agents, which contain Dihydroxyacetone) The objective is to hide the white macules so that the vitiligois not apparent Repigmentation : The objective is the permanent return of normal melanin pigmentation. • Topical glucocorticoids • Topical calcineurininhibitors • Topical photochemotherapy • Systemic photochemotherapy • Narrow-band UVB • Excimer laser (308 nm)

  19. Management Minigrafting: may be a useful technique for refractory and stable segmental vitiligomacules.- PUVA may be required after the procedure to unify the color between the graft sites Depigmentation: The objective of depigmentation is “one” skin color in patients with: -extensive vitiligo- failed PUVA- who cannot use PUVA - who reject the PUVA option.• Bleaching of normally pigmented skin with monobenzyletherof hydroquinone 20% (MEH) cream is a permanent, irreversible process. note that the depigmentation achieved is permanent !!

  20. Before After Vitiligo: therapy-induced repigmentation This 20-year-old Indian female is being treated with photochemotherapy (PUVA).

  21. Conclusion In the above case of Vitiligo, initially a medicine was selected (Merc.sol.) basing upon the totality of symptoms and analyzing the case but the patient did not show any improvement after taking that medicine. The patient discontinued treatment thereafter and again came back after one year with depigmented patches but this time it was found intensified although he did not use any other medicine and medication during this period. The case was re-analysed taking the presenting totality and Sulphur was the medicine selected. Sulphur in 30C potency, single dose was prescribed. The patient improved markedly with this remedy withvery few repetitions (2 doses of Sulphur 30) followed by placebo in a very short period. The depigmented spots on his face were almost completely disappeared and regimentation marked on the neck. The patient has been continuing Placebo till date with steady improvement

  22. THANK YOU !! ^_^

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