RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA



RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

BANGALORE

ANNEXURE - II

PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION

|1. |Name of the Candidate & Address |: |Dr.TAMBOLKAR UMA DEVIDAS |

| |(In block letters) | |C/o Dr.MALLIKARJUN BHANDAR |

| | | |H.No. 1-1166/4, AIWAN-E-SHAHI ROAD, |

| | | |GULBARGA-585 102. |

|2. |Name of the Institution |: |H.K.E. SOCIETY’S |

| | | |MAHADEVAPPA RAMPURE MEDICAL COLLEGE, GULBARGA – 585 105. |

|3. |Course of Study and Subject |: |M.D. (DERMATOLOGY, VENEROLOGY AND LEPROLOGY) |

|4. |Date of Admission to Course |: |31.05.2011 |

|5. |Title of the Topic |: |CLINICAL, EPIDEMIOLOGICAL STUDY AND EFFICACY OF DIFFERENT TREATMENT |

| | | |MODALITIES IN KELOID |

|6. |Brief resume of the intended work |

| |6.1 |Need for the study: |

| | |Keloid is one of the common skin lesions encountered in patients attending dermatology out patient department. It is of |

| | |cosmetic concern and has high recurrence rate. |

| | |So it is necessary to evaluate the clinico-epidemiological study and efficacy of different treatment modalities for keloid|

| | |and to reduce the recurrence rate of keloid study is required, hence the present study. |

| |6.2 |Review of Literature: |

| | |Definition: Keloid is an area of overgrowth of fibrous tissue that usually develops after healing of injury and extends |

| | |beyond the borders of original wound, does not regress spontaneously and tends to recur after excision. |

| | |Predisposing factors: |

| | |Damage to deep dermis |

| | |Physical: Burn, scalds, ear lobe piercing, surgery |

| | |Pathological: Acne |

| | |Post: Vaccination1 |

| | |Infected lesions |

| | |Haematoma |

| | |Increased skin tension |

| | |Presence of foreign material (suture material, embedded hair)2 |

| | |Predisposed sites: Most commonly shoulder, chest, ear, lobe, upper arm, cheek also flexor surfaces, joints, abdomen3. |

| | |Pathophysiology: Increased collagen (mainly type-I) is produced than degraded during wound healing due to imbalance |

| | |between anabolic and catabolic phases. |

| |1. |Increased TGF(, TGF(2, actinin and decreased IFN(, INF-r leads to increased collagen and fibronectin4. |

| |2. |Increased plasminogen activator-I and decreased urokinase leads to decrease collagen removal. |

| |3. |IL-6 pro-inflammatory cytokine5. |

| |4. |Derranged FAB induced apoptosis6. |

| | |Clinical features: |

| | |Either symptomless or may present with pruritus, pain, burning, tenderness. Pale erythematous or brownish, oval or oblong|

| | |lesions with regular or claw like irregular margin, soft to rubbery usually devoid of hair follicle7. |

| | |Differential diagnosis |

| |1. |Hypertrophic scar |

| |2. |Blastomycosis |

| |3. |Lobomycosis |

| |4. |Acne keloidalis |

| |5. |Dermatofibrosarcoma |

| |6. |Sclerotic BCC |

| |7. |Scar sarcoid |

| |8. |Malignancy |

| | |Complications: |

| | |Chronicity, secondary infection, contracture, hyper-pigmentation, Lichenification, disability and discomfort in acute |

| | |stage with secondary infection, superimposed allergy to topical medicaments, malignant changes. |

| | |Treatment: |

| |a) |Topical applications |

| | |Retinoic acid |

| | |Steroids |

| | |5FU – 1%, 5% |

| | |Imiquimod |

| | |Tacrolimus |

| | |Silicon cream |

| | |Heparin |

| | |Cepa extract |

| | |Colchicine |

| |b) |Intra-lesional |

| | |Triamcinoloe – 10 mg/ ml, 40 mg/ ml |

| | |5-fluorouracil 10 mg/ ml |

| | |Bleomycine8 |

| | |IFN-(2 (9 |

| | |TNF-(3 |

| | |verapamil – antiarrhytmic |

| | |Lathrogens ((-aminopropionitrile) |

| |c) |Radiation – Grenz rays, X-rays |

| |d) |Laser – Pulsed dye laser (585 nm), Nd-YAG, Flash lamp, CD2 laser |

| |e) |Cryotherapy10 |

| |f) |Pressure bandage |

| |g) |Silicon gel sheet |

| |h) |Surgical |

| |6.3 |Objectives of the Study |

| |1. |To know the age and sex distribution of keloid |

| |2. |To know various etiologies and precipitating factors |

| |3. |To find out and ascertain different clinical presentations. |

| |4. |To find out commonest and rarest variant of keloid. |

| |5. |To know efficacy of various treatment modalities. |

| |6. |To know about the recurrence rate. |

|7 |MATERIAL AND METHODS |

| |7.1 |Source of Data: |

| | |Patients attending skin OPD at Basaveshwar Teaching & General Hospital and Sangameshwar Hospital, Gulbarga |

| | |Referred patients from other departments of both the above mentioned hospitals. |

| |7.2 |Methods of collection of data (including sampling procedure) |

| | |Inclusion criteria: |

| |1. |Patients attending Skin OPD with features suggestive of keloid |

| |2. |All age groups |

| |3. |Both sexes |

| |4. |No. of cases to be studied – minimum of 100 |

| |5. |Duration of study – September 2011 to August 2013 |

| | |Exclusion Criteria |

| |1. |Patients with keloid already on treatment. |

| |2. |Hypertrophic scar. |

| |7.3 |Does the study require any investigation or intervention to be conducted on patients or other humans or animals? If so |

| | |please describe briefly. |

| | |Skin biopsy |

| |7.4 |Has ethical clearance been obtained from your institution in case of 7.3? |

| | |Yes, ethical clearance has been obtained from “Ethical Clearance Committee of the Institution”. |

|8. |List of References: |

| | |Mandy Harting, M.John Hicks, Moise L, Levy. Chapter-64: Dermal hypertrophies from Fitzpatrick’s Dermatology in General |

| | |Medicine, Vol. 1, 7th edition, 2008; p. |

| | |Tony Burns, Stephen Breathnach, Neilcon Christopher Griffiths, Chapter-45: Disorders of Connective Tissue: Keloids from |

| | |“Rooks Textbook of Dermatology”, Vol. 3, 8th edition, 2010: p. 45, 54. |

| | |Valia RG, Ameet R Valia, Chapter-33 Disorders of Connective Tissue from IADVL Textbook of Dermatology, 3rd edition 2010, |

| | |Vol. 2, P. 1179-1181. |

| | |Mukhopadhyay A, Chan SY, Lim IJ, Philliphs DJ, Phan TT. The role of the activin system in keloid pathogenesis. Am J |

| | |Physiol Cell Physiol. 2007; 292: C 1331-8. |

| | |Ghazizadeh, Nippon J. essential role of IL-6 signaling pathway in keloid pathogenesis. Med Sch 2007; 74: 11-22. |

| | |Lu F, Gao J, Ogawa R, Hyakusoku H, Ou G. Fas-mediated apoptotic signal transduction in keloid and hypertrophic scar. |

| | |Plast Reconstr Surg. 2007; 119: 1714-21. |

| | |Verman B, Perez OA. Keloid and hypertrophic scar. Available at: . derm/ topic 205.htm. |

| | |Espana A, Solano T, Quintanilla E. Bleomycin in treatment of keloids and hypertrophic scars. Dermatol Surg. 2001; 27: |

| | |23-7. |

| | |Berman B, Dunan MR. Short-term keloid treatment in vivo with human interferon (2( results in selective and persistent |

| | |normalization of keloid fibroblast collagen, glycosaminoglyca and collagenase production in vitro. J Am Acad Dermatol. |

| | |1989; 21: 694-702. |

| | |Rusciani L, Rossi G, Bono R. Use of Cryotherapy in treatment of keloids. J Dermatol Surg Oncol. 1993; 19: 329-34. |

|9. |Signature of Candidate |: | |

| | | | |

|10. |Remarks of the Guide |: |Study of keloid including the management with multiple treatment options is a|

| | | |good topic. It helps to know the effect of each treatment options including |

| | | |intervention therapy. |

|11. |Name & Designation of (in block letters) | | |

| |11.1 |Guide | |Dr.S.K.PATIL, |

| | | | |M.D. |

| | | | |PROFESSOR & HEAD, |

| | | | |DEPARTMENT OF DERMATOLOGY, |

| | | | |MAHADEVAPPA RAMPURE MEDICAL COLLEGE, GULBARGA |

| |11.2 |Signature | | |

| |11.3 |Co-guide | | |

| |11.4 |Signature | | |

| |11.5 |Head of the Department | |Dr.S.K.PATIL, |

| | | | |M.D. |

| | | | |PROFESSOR & HEAD, |

| | | | |DEPARTMENT OF DERMATOLOGY, |

| | | | |MAHADEVAPPA RAMPURE MEDICAL COLLEGE, GULBARGA |

| |11.6 |Signature | | |

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|12. |12.1 |Remarks of the Chairman & Principal | | |

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| |12.2 |Signature | | |

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