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Cicafiricial alopecia

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Cicafiricial alopecia Powered By Docstoc
					                              Cicatricial Alopecia
Dr. Sahni BS                               Website: http://www.homoeopathyclinic.com
DHMS Hons, PGRT (BOM), FF Hom              Email: drsahnibs@vsnl.com
                                                   health_homoeo@yahoo.com
Deputy Chief Medical Officer (H),
ONGC Hospital Panvel-410221,
Navi Mumbai, INDIA

Introduction
       Cicatricial alopecia is the generic term applied to alopecia which accompanies or
       follows the destruction of hair follicles, whether by a disease affecting the
       follicles themselves or by some process external to them. The follicles may be
       absent as the result of a developmental defect or may be irretrievably injured by
       trauma, as in burns or radio dermatitis, They may be destroyed by a specific and
       identifiable infection - favus, tuberculosis or syphilis, for example - or by the
       encroachment of a benign or malignant tumor, In other cases, their destruction can
       be reliably attributed to a named, though still mysterious, disease process such as
       lichen planus or lupus erythematosus or sarcoidosis. When all the clinically and
       histologically acceptable causes have been eliminated, two named syndromes of
       cutaneous origin remain, pseudopelade and the less well-defined folliculitis
       decalvans. Once these too have been excluded, there still remain cases in which
       any greater precision of diagnosis than 'cicatricial alopecia' may be unwarranted.
       Once the preliminary diagnosis of cicatricial alopecia has been made, the scalp
       should be searched for other changes - folliculitis, follicular plugging or broken
       hairs - and hairs, even if grossly normal in appearance, should be extracted from
       the edge of the bald area for microscopy and culture. If no firm diagnosis is
       achieved, then general skin examination and systemic studies should be carried
       out where appropriate, if the decision is made to take a biopsy, its site must be
       carefully selected and an early lesion should be preferred. Several punch biopsies
       are preferable to a single elliptical biopsy - in this way the biopsies can be
       orientated along follicles and different stages of the 10-disease process can be
       investigated.

Classification
The causes of cicatricial alopecia are classified here into broad groups:
   1. Developmental defects and hereditary disorders
       Aplasia cutis
       Facial hemiatrophy (Romberg's syndrome)
       Epidermal naevi
       Hair follicle hamartomas
       Incontinentia pigmenti
       Focal dermal hypoplasia of Goltz
       Porokeratosis of Mibelli
       Scarring follicular keratosis
       Ichthyosis
       Darier's disease
       Epidermolysis bullosa
    Polyostotic fibrous dysplasia
    Conradi s syndrome (chondrodystrophia calcificans)
2. Physical injuries
    Mechanical trauma
    Scalp necrosis after embolization surgery
    AIDS - secondary infections (various)
    Burns
    Radiodermatitis
3. Medicaments
4. Fungal infections
    Kerion
    Trichophyton violaceum
    T. sulphureum
    Favus
5. Bacterial infections
    Tuberculosis
    Syphilis
6. Pyogenic infections
    Carbuncle
    Furuncle
    Folliculitis
    Acne necrotica
7. Protozoal infections
    Leishmaniasis
8. Virus infections
    Herpes zoster.
    Varicella
9. Tumours
    Basal cell epithelioma
    Squamous cell epithelioma
    Syringoma
    Metastatic tumours
    Lymphomas
    Adnexal tumours
10. Dermatoses of uncertain aetiology
    Lichen planus
    Graham-Little syndrome
    Tufted folliculitis
    Dermatomyositis
    Lupus erythematosus
    Scleroderma morphoea
    Necrobiosis lipoidica
    Pyoderma gangrenosum
    Lichen sclerosus
    Mastocytosis
    Sarcoidosis
       Cicatricial pemphigoid
       Follicular mucinosis
       Temporal arteritis
       Erosive pustular dermatosis
       Eosinophilic cellulitis
   11. Clinical syndromes
       Dissecting cellulitis of the scalp
       Pseudopelade
       Folliculitis decalvans
       Alopecia parvimacularis

Homoeopathic Treatment:
      It is very difficult to treat this syndrome. Constitutional remedies along with
      symptomatic remedies may help to overcome this syndrome. Following
      homoeopathic remedies are indicated as per the classification given above:
Hereditary Disorders:
              • Aplasia cutis: Graphites, Natrum mur
              • Facial hemiatrophy (Romberg's syndrome): Causticum, Rhus Tox
              • Epidermal naevi: Thuja, Acid Flouric, Syphlinum
              • Hair follicle hamartomas: Hammamelis, Phosphorus, Arnica Mont
              • Incontinentia pigmenti: Phosphorus, Sulphur
              • Focal dermal hypoplasia of Goltz: Phosphorus, Phytollacca, Ars Iod
              • Porokeratosis of Mibelli: Syphlinum
              • Scarring follicular keratosis: Silicea, phytolacca, Acid Flouric
              • Ichthyosis: Phosphorus, Hydrocotyle, Ars iod, Ars Alb
              • Darier's disease: Not Known
              • Epidermolysis bullosa: Acid Nitric, Cal Carb
              • Polyostotic fibrous dysplasia: Thuja
              • Conradi s syndrome (chondrodystrophia calcificans): Calcarea Flour

Physical injuries:
              • Mechanical trauma: Hypericum, Arnica, Calendula
              • Scalp      necrosis after    embolization     surgery:  Staphisgaria,
                   Thiosinaminum
              • AIDS - secondary infections (various): Aids, Carcinocin
              • Burns: Cantharis, Causticum, Kali Bich
              • Radiodermatitis: X-Ray, Cadmium Sulph

Fungal infections: Sepia, Thuja, Psorinum, Tuberculinum
Bacterial infections:
               • Tuberculosis: Phosphorus, Ars Iod, Tuberculinum, Cal Carb
               • Syphilis: Kali Iod, Syphlinum
Pyogenic infections:
              • Carbuncle: Anthracinum, Hep Sulph, Silicea, Lachesis, Sulphur,
                  Petroleum
              • Furuncle: Hep Sulph, Silicea, Gun Powder
              • Folliculitis: Vinca Minor, Mezerium, Silicea
              • Acne necrotica: Acid Flour, Carbo Ani, Custicum, Petroleum, Nat
                  Mur, Graphites, Echinacea
Protozoal infections:
              • Leishmaniasis: Psorinum, Vinca Minor
Virus infections:
              • Herpes zoster: Mezerium, Rhus Tox, Variolinum, Lycopodium,Thuja,
                  Psorinum, Petrol
              • Varicella: Mezerium, Rhus Tox, Variolinum, Ant tart
Tumours:
              • Basal cell epithelioma: Carcinocin, Ars Alb, Kali sulph, sepia
              • Squamous cell epithelioma: Ars Alb, Thuja, Hydrastis
              • Syringoma: Cal Carb, Lycopodium
              • Metastatic tumours: Ars Alb, Carcinocin, Cal Carb,
              • Lymphomas: Conium, Phytolacca, Silicea, phosphorus, Carb Ani,
                  Bromium, Tuberculium
              • Adnexal tumours: Cal Carb, Carcinocin
Dermatoses of uncertain aetiology:
              • Lichen planus: Kali Ars, Juglan R, Calotropis G, Rumex, Ars Alb,
                  Sulphur, Cortisone & Tuberculinum
              • Graham-Little syndrome: Same as Lichen Planus
              • Tufted folliculitis: Mezerium, Vinca Minor, Thuja, Cal Sulph
              • Dermatomyositis: Mezerium, Rhus tox
              • Lupus erythematosus: Cal Carb, Lyco
              • Scleroderma morphoea: Arnica, Baryta Carb
              • Necrobiosis lipoidica: Mezerium, Ars Iod, Vinca Minor
              • Pyoderma gangrenosum: Phosphorus, silicea, Acid Flouric
              • Lichen sclerosus: Sulphur, Ars Iod, Phosphorus, Conium
              • Mastocytosis: Apis Mel, Lyco, Rhus Tox, Thuja, Ars Alb
              • Sarcoidosis: Tuberculinium, Cortisone, Phosphorus
              • Cicatricial pemphigoid: Apis Mel, Cantharis, Echinacea
              • Follicular mucinosis: Merc Sol, Petroleum, Graphites, Natrum mur,
                  Sulphur
              • Temporal arteritis: Hamamelis, Pulsatilla
              • Erosive pustular dermatosis: Mezerium, Vinca minor, Olender
              • Eosinophilic cellulites: Ars Alb, Hydrocotyle As, Ars Iod, Sulphur
Clinical syndromes:
              • Dissecting cellulitis of the scalp: Calendula, Hypericum, Staphisgaria
Pseudopelade
    The term pseudopelade is used here to designate a slowly progressive cicatricial
    alopecia, without clinically evident folliculitis and no marked inflammation.
    There is no doubt that lichen planus can produce a very similar clinical picture
    and there are some authorities that maintain on the basis of associated skin lesions
    and histopathological findings that 90% of cases of 'pseudopelade' are caused by
    lichen planus. At a later stage lupus erythematosus also can cause similar changes.
    However, some patients with pseudopelade never show any clinical or
    histological evidence of lichen planus. Pseudopelade is therefore generally
    regarded as a clinical syndrome, which may be the end result of any one of a
    number of different pathological processes (known and unknown) though a
    specific clinically uninflamed type has always been recognized.

    Pathology: If clinically normal scalp at the edge of a plaque of pseudopelade is
    examined, numerous lymphocytes are seen around the upper two-thirds of the
    follicles. Later, the follicles are destroyed and the epidermis becomes thin and
    atrophic, and the dermis densely sclerotic. Follicular ‘ghosts’ without
    inflammatory changes are seen.

    Clinical features: Although both sexes may be
    affected, and the condition has occurred in
    childhood, the patient is usually a woman and
    over 40 years of, age. She may complain of
    slight irritation at first, but more often a small
    bald patch or patches (See Fig.) discovered by
    chance by the patient or by her hairdresser, is the
    first evidence of the disease. The initial patch is
    most often on the vertex, but may occur anywhere on the scalp. The course
    thereafter is extremely variable, In a majority of cases extension of the process
    takes place only very slowly; indeed after 15 or 20 years the patient may still be
    able to arrange her hair to conceal the patches effectively. In some cases extension
    occurs more rapidly, and exceptionally there may be almost total baldness after 2
    or 3 years.

    On examination the affected patches are smooth,
    soft and slightly depressed. At an early stage in
    the development of any individual patch there
    may be some erythema. The patches tend to be
    small and round or oval, but irregular bald
    patches may be formed by confluence of many
    lesions (See Fig.). The hair in uninvolved scalp
    is normal, but if the process is active the hairs at
    the edges of each patch are very easily extracted. Detailed studies by Braun-Falco
    and coworkers strongly support the idea that pseudopelade is a distinct entity with
    the diagnostic criteria as follows:
      Clinical criteria
              Irregularly defined and confluent patches of alopecia
              Moderate atrophy (late stage)
              Mild perifollicular erythema (early stage)
              Female:male = 3:1
              Long course (more than 2 years)
              Slow progression with spontaneous termination possible
      Direct immunofluorescence
              Negative or at least only IgM
      Histological criteria
              Absence of marked inflammation
              Absence of widespread scarring
              Absence of significant follicular plugging.
              Absence, or at least decrease, of sebaceous glands
              Presence of normal epidermis (only occasionally atrophy)
              Fibrotic streams into subcutis.

      Treatment. Homoeopathic Remedies like Kali Ars, Juglan R, Calotropis G,
      Rumex, Ars Alb, Sulphur & Tuberculinum can be given as per their symptoms.

      The intradermal injection of corticosteroids does not seem to influence the
      extension of the disease process in cases of unknown origin.

Folliculitis decalvans
      Under the general term folliculitis decalvans, we group together the various
      syndromes in which clinically evident chronic folliculitis leads to progressive
      scarring. This is probably a heterogenous group.

      Aetiology. The cause of folliculitis decalvans is still uncertain. Some authors have
      emphasized the possible role of the seborrhoeic state and some use the term
      ‘cicatrizing seborrhoeic eczema’ but folliculitis decalvans is rare and the
      seborrhoeic state is common, so the association probably has no special
      significance.

      Shitara and co-workers reported severe folliculitis decalvans in two siblings who
      also had chronic candidiasis; defective cell-mediated immunity was demonstrated.
      It seems probable that a local failure in the immune response or in leucocyte
      function may be the essential abnormality in most cases. Folliculitis decalvans of
      the scalp occurs in both sexes. It typically affects women aged 30-60 years and
      men from adolescence onwards.

      Pathology. Scarring directly succeeds follicular abscesses with a
      polymorphonuclear infiltrate, or there may be a prolonged intermediate stage of
      granulomatous folliculitis with numerous lymphocytes, and some plasma cells
      and giant cells.
     Clinical features. Any or all hairy regions may be involved, and in the syndrome
     sometimes referred to as 'atrophic folliculitis in seborrhoeic dermatitis', the beard,
     pubes, axillae and inner thighs may be involved, and less often the scalp as well.
     The severity of the inflammatory changes fluctuates, but the course is prolonged.

     The scalp alone may be involved or the scalp
     together with pubes and axillae. There are
     multiple rounded or oval patches, each
     surrounded by crops of follicular pustules (See
     Fig.). There may be no other changes, but
     successive crops of pustules; each followed by
     destruction of the affected follicles, produce
     slow extension of the alopecia.

     Tufted folliculitis may be a variant of this entity - an upper follicular acute
     inflammatory polymorphonuclear infiltrate is associated clinically with close
     grouping or 'tufting' of hairs.

     Treatment. All patients should be investigated for underlying defects of immune
     response and of leukocyte function, as a possible guide to effective treatment.
     Homoeopathic Remedies like Tuberculinum, Staphylocoocus, Mezerium, Vinca
     minor can be given according to their respective symptoms.

Alopecia parvimacularis
     Dreuw reported an outbreak of alopecia affecting 60 of the 85 boys in two
     schools. The patches of alopecia were small, irregularly round or angular, and
     appeared atrophic, but in 90% of cases the hair re-grew satisfactorily. Permanent
     scarring alopecia developed in the remaining 10% of cases. There were no
     inflammatory changes and no fungus or other organisms could be discovered.

     Pathology. Non-specific inflammatory changes are seen involving some follicles,
     whilst sparing others. The degree of scarring depends on the number of
     contiguous follicles destroyed. In some cases the pathological changes eventually
     resemble those of pseudopelade.

     Clinical features. All reported cases have been children. The patches of alopecia
     are of rapid onset, quickly reaching their greatest extent, and are usually
     numerous. They seldom exceed 1-2 cm in diameter, and are characteristically
     irregularly angular in shape. Over the course of a few weeks, the hair re-grows in
     most cases to leave no clinically evident alopecia, but in some patient’s cicatricial
     alopecia results.

     Diagnosis. Mycotic infection must be excluded by microscopy and by culture.
     The multiple bites of insects, scratched and secondarily infected, can give rise to
     small patches of alopecia, but the history should exclude this diagnosis, as well as
     secondary syphilis.
       Homoeopathic remedies most indicated in this are: Acid flour, Bacillinum &
       Phosphorus.


Dermatoses Of Uncertain Aetiology
Lichen planus
      Aetiology. Lichen planus is a disease or, more probably, a ‘reaction pattern’, of
      unknown origin but belonging to the autoimmune groups of conditions. It occurs
      throughout the world, but there are marked regional variations in its incidence and
      in its clinical manifestations. These variations probably result from relative
      differences in the importance of various aetiological agents.

       Pathology. The initial abnormality is in the epidermis: fibrillar changes in the
       basal cells lead to the formation of colloid bodies and at an early stage these, and
       macrophages containing pigment, may be seen in the dermis. By
       immunofluorescence, fibrin and IgM may be detected in the upper dermis, and
       various components of complement in the basement membrane zone. The
       wounded basal cells are continually replaced by the migration of cells from
       neighbouring normal epidermis. In the established lesion, the horny layer and
       granular layer are thickened and there is irregular acanthosis. Flattening of the
       rete pegs gives rise to a saw-tooth configuration. There is liquefaction
       degeneration of the basal cells Close up against the epidermis is a dense infiltrate
       of lymphocytes and some histiocytes. In many sections, some colloid bodies can
       be seen. If the process involves hair follicles, the infiltrate extends around them
       and keratin plugs replace the hairs. The follicles may ultimately be totally
       destroyed.

       Clinical features. Lichen planus occurs at any age, but in over 80% of cases the
       onset is between 30 and 70 years. Significant involvement of the scalp is
       relatively infrequent - only 10 of 807 patients in one series - but the incidence is
       probably rather higher than such figures suggest, since they tend to exclude those
       patients in whom alopecia, classified as pseudopelade, was the only manifestation
       of the disease. Scalp involvement occurs in over 40% of patients with either of
       two unusual variants of lichen planus: the bullous or erosive form and lichen
       planopilaris. Most patients seen with scalp lesions are middle-aged women, but a
       girl aged 13 with scarring has been reported.

       Recent scalp lesions may show violaceous papules, erythema and scaling, but
       before long, follicular plugs become conspicuous and scarring replaces all other
       changes. Eventually, the plugs are shed from the scarred area, which remains
       white and smooth. If the patch is extending, horny plugs may still be present in
       follicles around its margins.
More often, the scalp lesions are well established by the time the patient attends
hospital and the irregular white patches are not clinically diagnostic and indeed
may not show any distinctive histological features. This is the clinical picture
known as pseudopelade. The diagnosis of lichen planus can be made only in the
presence of unquestionable lesions elsewhere and lichen planus histology. These
may take the form of bullous lichen planus with shedding of nails, of bullous
lesions associated with typical lichen planus of the skin and mucous membranes,
or of lichen planus of very limited extent involving, for example, the nails only.

Prognosis. In some patients, the course of lichen planus of the scalp is slow and
only a few inconspicuous patches are present after many years. However,
particularly if the skin lesions are of bullous or planopilaris type, they may rapidly
result in extensive and permanent baldness. The rare childhood cicatricial lichen
planus has a very poor prognosis.

Homoeopathic Treatment: The most common remedies used for this problem
are Kali Ars, Juglan R, Calotropis G, Rumex, Ars Alb, Sulphur, Cortisone and
Tuberculinum.

				
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