Download Dr. CHETHANA. SG

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE,
KARNATAKA.
ANNEXURE – II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1.
Name of the Candidate and Dr. CHETHANA. S.G.
D/O Dr. GURUMURTY,
Address
# 542, 8TH MAIN, 4TH BLOCK,
(in block letters)
KORAMANGALA,
BANGALORE – 560034,
KARNATAKA.
2.
Name of the Institution
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577004.
KARNATAKA.
3.
Course of Study and Subject
POST GRADUATE DEGREE- M.D.
DERMATOLOGY, VENEREOLOGY AND
LEPROLOGY
4.
Date of admission to Course
31st May 2007
5.
Title of the Topic
“CLINICOPATHOLOGICAL STUDY OF
ACQUIRED HYPERPIGMENTATION”
6.
Brief resume of the intended work
6.1 Need for the study:
Cutaneous hyperpigmentation may be diffuse due to various etiological
factors like systemic medications, metabolic, nutritional diseases, systemic illness,
sunlight exposure, topical therapy or may be localized or circumscribed in many
other conditions.
Though acquired hyperpigmentation is a very common dermatological
condition, the subject is not much explored. Hence an attempt is made to know the
various etiological factors responsible for the causation of the same.
6.2 Review of Literature :
Cutaneous hyperpigmentation is a disorder due to increased melanin
production by existing melanocytes (melanocytic hyperpigmentation) or by
increased proliferation of active melanocytes (melanocytotic hyperpigmentation).1
Epidermal hyperpigmentation refers to brown hyperpigmentation that is
generally caused by increased melanin production by existing melanocytes
(melanotic hyperpigmentation) and less often by increased proliferation of active
melanocytes (melanocytotic hyperpigmentation).2
Dermal hyperpigmentation may result from melanin in the dermis attributed to :
1) Dermal melanotic hyperpigmentation, due to melanin formed in the
epidermis by epidermal melanocytes and transferred to the dermis.
2) Dermal melanocytotic hyperpigmentation, due to melanin formed in
dermal melanocytes.
3) Non melanin dermal pigmentation, attributed to pigment other than
melanin deposited in the dermis.2
Melasma is a common acquired pigmentary disorder, usually seen in women
of child bearing age. Its association with pregnancy and oral contraceptives is well
known. The lesions are predominantly distributed over photoexposed areas and
are usually bilateral and symmetrical.3
Beta-carotene in nanothalospheres appears to be effective drug added to the
armamentarium to fight against melasma with minimal side effects.4
Amyloidosis is an end result of many divergent disorders in which a
characteristic fibrillar protein is deposited within one or more tissues.5 It has
characteristic
physiochemical
properties
like,
congophillia
and
green
birefringence under polarized light.6 Primary localized cutaneous amyloidosis
(PLCA) occurs when amyloid deposits occur in previous apparently normal skin.
They are of various types.
1) Lichenoid or papular type
2) Macular type
3) Nodular, bullous, vitiliginous or icthyosiform (rarely).5
The familial association of hereditary cutaneous lichen amyloidosis and
MEN IIa and macular amyloidosis and hypothyroidism have been described.7
The treatment of primary cutaneous amyloidosis is often disappointing.
Milder
cases
respond
Dimethylsulphoxide
to
potent
(DMSO),
topical
Etretinate,
corticosteroids,
oral
topical
10%
cyclophosphamide
and
colchicines.6
As long back as 1938, Ota reported an unusual syndrome, consisting of
greyish blue macular discolouration affecting the sclera of one eye and ipsilateral
facial skin in the distribution of corresponding trigeminal nerve, under the title,
‘Nevus fuscocaeruleus opthalmomaxillaries. But the term nevus of ota is used all
over the world.8
Ephelides or freckles are pale-brown, macular lesions usually less than 3mm
in diameter with a poorly defined lateral margin which appears and darkens on
light exposed skin sites during periods of UV exposure. They are common in
children and individuals of all ages who are red or fair haired and fair skinned. 9
Becker’s nevus or pigmented hairy epidermal nevus was first reported by
Becker in late 1940s, who described two young men developing localized
hypermelanosis and hypertrichosis. It is not an uncommon condition and is been
reported in 0.5% of young men.10
6.3 Objectives of the study:
1. To know the incidence of acquired localized and diffuse hyperpigmentation
due to various etiological factors.
2. To study the various clinical forms and pattern of distribution of acquired
hyperpigmentation.
3. To study the various treatment modalities of acquired hyperpigmentation.
7.
MATERIALS AND METHODS:
7.1 Source of data:
The study group will consists of persons attending the out patient and
inpatient, Department of Dermatology, Venereology and Leprology at Chigateri
General Hospital and Bapuji Hospital, attached to J.J.M Medical College,
Davangere, over a period of 2 years.
7.2 Method of collection of data :( including sampling procedure if any)
Detailed clinical history, general, physical, cutaneous and systemic
examination will be done. In all cases necessary investigations will be done and
skin biopsy for histopathological study with patients consent will be done.
Sampling size :
-
Atleast hundred patients will be included in the study that fulfills the
inclusion criteria.
Inclusion criteria:
-
Patients presenting with acquired hyperpigmentation (localized or diffuse).
-
Patients who are able to understand the value of skin biopsy and confirmation of
diagnosis, and are ready to give consent.
Exclusion criteria:
-
Patients presenting with hyperpigmented lesions since birth.
-
Patients with both hyper and hypopigmented lesions co-existing together.
-
Patients who are not willing for investigations and consent for relavent
treatment.
7.3 Does the study require any investigations or interventions to be conducted
on patients or other humans or animals? If so, please describe briefly:
Yes
Investigations to be conducted include :
 Blood : Hb%, TC, DC, ESR, PS.
 Urine – sugar, Albumin, Microscopy.
 Examination with magnifying hand lens (7-10X)
 Microscopic examination with 10% KOH preparation.
 Skin biopsy for histopathological examination with haemotoxylin and
eosin stain.
7.4 Has ethical clearance been obtained from your institution in case of 7.3?
Yes
8.
LIST OF REFERENCES:
1. Trout CR, Levine N, Chang MW. Disorders of Hyperpigmentation. In:
Textbook of dermatology, Jean B, Jorizzo J, Pradini R, Thomas DH, Josem
M, Antony MJ et al. edt., Chapter 67, vol.1, Mosby London, 2003;p.975.
2. Grichnik JM, Rhodes AR, Sober AJ. Benign hyperplasias and Neoplasias of
Melanocytes. In: Fitz Patricks Dermatology in General Medicine. Freedberg
IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI edt., Chapter
91, 6th Edn, McGraw Hill 2003;p.863,872.
3. Goutam D, Sandipan D, Amrinder KJ. Unilateral Melasma. Ind J Dermatol
Venerol Leprol 1994;60(6):372.
4. Kar HK. Efficacy of beta carotene topical application in melasma – An open
clinical trail. Ind J Dermatol Venereol Leprol 2003;69(2):92-94.
5. Das J, Gogoi RK. Treatment of primary localized cutaneous amyloidosis
with cyclophosphamide. Ind J Dermatol Venereol Leprol 2003;69(2):163164.
6. Bela P, Umesh K, Bel S. Primary cutaneous amyloidosis. Ind J Dermatol
Venereol Leprol 1997;63(2):105-106.
7. Adarsh C, Komal P, Dimple C. Macular amyloidasis and hypothyroidism.
Ind J Dermatol Venereol Leprol 1999;65(2):79-80.
8. Bhatia KK, Surinder G, Ramesh NK, Satish K. Unusual presentation of
nevus of Ota. Ind J Dermatol Venereol Leprol 1985;33(4):255-257.
9. MacKie RM. Disorders of Cutaneous Melanocytes. In : Rook’s textbook of
dermatology. Tony B, Stephen B, Neil C, Christopher G edt., Chapter 38,
Vol. 2, Bhackwell Science 2004;38:p.1.
10. Amladi ST, Jerajani HR. Nevi and other Developmental Defects. In:
IADVL text book and Atlas of Dermatology. Ed Valia RG, Valia AR edt.,
Chapter 10, Vol. 1, Bhalani Publishing house, Bombay, p.148.
9.
Signature of the Candidate
10. Remarks of the Guide
Recommended and forwarded to study
11. Name & Designation of
(In block letters)
11.1 Guide
Dr. NADIGA RAJASHEKHAR M.D.,D.V.D.,
PROFESSOR,
DEPARTMENT OF DERMATOLOGY,
VENEREOLOGY AND LEPROSY
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577 004.
11.2 Signature
11.3 Co-Guide (if any)
11.4 Signature
11.5 Head of the Department
11.6 Signature
12. 12.1 Remarks of the Chairman
& The Principal
12. 2 Signature
Dr. P. MADAVA MURTHY MD., D.VD.,
PROFESSOR AND HEAD OF
DEPARTMENT,
DEPARTMENT OF DERMATOLOGY,
VENEREOLOGY AD LEPROSY,
J.J.M. MEDICAL COLLEGE,
DAVANGERE-577 004.