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Several types of lice, bacteria, and fungi can invade the scalp and cause numerous problems. These infectious agents of the scalp and other regions of hair are collectively called \"dermatophytes\". Different dermatophytes are common in different parts of the world and at different times in history. The same clinical diagnosis today may be caused by something very different than the same clinical diagnosis fifty years ago. For example the most common cause of tinea capitis in Europe and the USA in 1955 was Microsporum audouini. Today the most common cause of tinea capitis may be due to other infectious agents such as Trichophyton tonsurans and Microsporum canis in Europe. Scalp infections and infestations are still very common today, even in the developed Western world. Because the diseases are due to bacteria, fungi, viruses, and microscopic animals, they can easily be transmitted from one individual to another. Transmission usually occurs between those living in close proximity to each other where there may be physical contact. However, it is also possible to transmit infectious scalp agents through using contaminated towels, from contact with infected animals including pets, or even from contact with contaminated soil or water. “Hot Tub” Folliculitis is a condition caused by the pathogen Pseudomonas Aeruginosa, and is often seen where spa and public bath sanitation is at fault. Public hot tubs are a particularly common source of infection, as they are nice and warm, but often not very clean, so the bacteria can survive and as so many people use them cross infection is easy. Vitiligo
and its homoeopathic managements Conducted By Dr. Rajeev Singh,
B.Sc., B.H.M.S., Gold Medallist; Introduction: Vitiligo is a disease process
that results in depigmented areas in the skin. It usually begins after birth
and, although it can develop in childhood, the average age at onset is about
20years. Most commonly, vitiligo produces symmetrical depigmented areas of skin
that otherwise appears normal. A less common type is the segmental form in
which asymmetrical, one-sided depigmentation develops. There is increasing
evidence to support the view that vitiligo is an autoimmune disease and that it
shows a familial trait in about 18% of cases. An important aspect of vitiligo
is the psychological effect of the disease. Vitiligo is often immediately
visible to others and those with the condition may suffer social and emotional
consequences including low self-esteem, social anxiety, depression,
stigmatization and, in extreme cases, rejection by those around them. In people
with a pale white skin colour, vitiligo may cause little concern. Clinical features: Vitiligo vulgaris/nonsegmental
vitiligo is an acquired chronic depigmentation disorder characterized by white
patches. These are often symmetrical and usually increase in size with time.
This corresponds with a substantial loss of functioning epidermal and,
sometimes, hair follicle melanocytes. Segmental vitiligo is a variant of
vitiligo confined to one unilateral segment. One unique segment is involved in
most patients but two or more segments on the same or opposite sides may be
involved or depigmentation may follow a dermatome distribution or Blaschko's lines.
In symmetrical vitiligo, the commonest sites to be affected are the fingers and
wrists, the axillae and groins and the body orifices such as the mouth, eyes
and genitalia. As the pigment cells are destroyed, sometimes a 'trichrome'
appearance of a white centre with an intermediate, pale area around it is
found. In vitiligo skin there is no surface change and usually no redness. Very
occasionally, inflammation is seen at the advancing edge of a vitiligo macule.
Vitiligo can affect melanocytes in the hair roots, resulting in white eyelashes
and white hair within the pale skin patches. Depigmentation can affect mucosal
areas such as in the mouth. Differential diagnosis: These are: Halo naevus Hypopigmented naevus Idiopathic guttate hypomelanosis Leprosy Lichen sclerosus (for genital vitiligo) Melanoma-associated leucoderma Melasma Mycosis fungoides-associated depigmentation Naevus anaemicus Naevus of Ito Piebaldism Pityriasis alba Pityriasis versicolor Postinflammatory depigmentation, e.g. scleroderma,
psoriasis, atopic eczema Post-traumatic depigmentation Topical or drug-induced depigmentation Tuberous sclerosis The three main diseases that
can be mistaken for vitiligo are tinea (pityriasis) versicolor, piebaldism and
guttate hypomelanosis. Tinea versicolor is a superficial yeast infection that
can cause loss of pigment in darker skinned individuals. It presents as pale
macules typically on the upper trunk and chest, with a fine dry surface scale.
Piebaldism is an autosomal dominant disease in which there is absence of
melanocytes from the affected areas of the skin. It usually presents at birth
with depigmented areas that are usually near the mid-line on the front,
including a forelock of white hair. In idiopathic guttate hypomelanosis,
multiple small, white macules are noted, mostly on the trunk or on sun-exposed
parts of the limbs. When vitiligo affects only the genital areas, it can be
difficult to exclude lichen sclerosus, which sometimes can coexist with
vitiligo. N.B.: Patients with vitiligo often
develop autoimmune thyroid disease or other autoimmune diseases and a history
of autoimmune disease in a family member is obtained in 32% of patients. In one
series of 41 adults, a history of autoimmune thyroid disease was found in 14 (34%),
suggesting that screening for abnormal thyroid function or the presence of
autoantibodies to thyroid antigens may be helpful in the management of adults
with vitiligo. Homoeopathic treatments and Managements: As per homoeopathic point of
view it is a case of syphilitic miasm. It can easily be controlled and cured by
homoeopathy. As per my experience it can easily be cured in primary stage. It
can also be arrested in it's secondary stage. The prognosis becomes poor when
there is substantial loss of huge amounts of melanocytes. The main drugs are; Alumina, Arsenic sulph flavum, Calcaria
carb, Merc sol, Sepia, Silicea are good drugs for. I also have seen very good result of Ami visnaga Q, Psorelia
Q and Sepia Q in outer/ external applications. Psoriasis
and Homoeopathy Conducted by: Dr. Rajeev
Singh, B.Sc., B. H. M. S., Gold Medallist; Psoriasis Definition:
Psoriasis is a common, genetically determined, inflammatory skin disorder of
unknown cause, which, in its most usual form, is characterized by
well-demarcated, raised, red scaling patches that preferentially localize to
the extensor surfaces. Clinical features: The lesions: Typical lesions are red,
raised, and scaly and have well-demarcated margins. They often start out
discoid, but end up polycyclic as several lesions coalesce. Site affected: Psoriasis affects the extensor
aspects of the trunk and limbs preferentially. The knees, elbow, and scalp are
frequently affected, although the mucosae seem to be spared. The nails are often affected
and may show the so- called thimble pitting, separation of the nail plate from
the nail bed (onycholysis), sublingual debris, brownish- black discolorations,
and deformities of the nail plate. Flexural lesions, which occur
in some patients, are most often seen in the major body folds in the elderly,
especially in those who are overweight. The groins and genitalia, axillae,
inframammary folds in women and the skin of abdominal folds and the umbilicus
in either sex are affected. The moistness of the flexural areas decreases the
scaling and produces a moist and glazed appearance. Psoriasis sometimes appears at
the site of a minor injury such as scratch or a graze. This reaction is known
as isomorphic response or the Koebner phenomenon mostly occurs when the
psoriasis is in active spreading phase. Natural History and Epidemiology: Disorder is less common in
African and Asian groups. The disease is more common in men than in women.
There are two main peaks of incidence, the first of which is in the second half
of the second decade of life. Psoriasis may also occur for the first time in
the seventh decade. In general, the younger the age of onset, the worse the
outlook as far as frequency, severity, and persistence of the disease are
concerned. Genetics: Psoriasis is often familial,
but does not appear to be inherited in any regular dominant, sex- linked or
recessive way. With one parent affected, there is an approximately 30% chance
of a child being affected. With both parents suffering, the risk rises up to
60%. Psoriasis is associated with
HLA groups HLA-B13, HLA-B17, and HLA-B37 as well as with the class II
antigen DR7. Differential Diagnosis: Any red, scaling disorder can
be mistaken for psoriasis, and vice versa. On the scalp, most frequently seen
disorder to be mistaken for psoriasis is seborrhoeic dermatitis, although this
usually affects the scalp diffusely rather than in distinct plaques. Lichen
simplex chronicus of scalp typically presents with a red, scaling patch on the
occiput, which can look very psoriasis- like. The intense itching and
lichenified surface should serve to distinguish the two disorders. Multiple patches of ringworm
may appear very like psoriasis, but the lesions are often more ring- like and
can be distinguished by microscopical examination of KOH-treated skin scraping.
On the legs, raised, round,
red, scaling psoriasiform patch often turn out to be the Bowen’s disease in the
elderly, or Discoid Eczema. Superficial basal cell
carcinoma lesions sometimes several centimeters in diameters and quite
psoriasiform in appearance, but have a fine, raised, “hair- like” margin. Differential diagnosis of red, scaling rashes: Psoriasis:
Nails changes, family history, multiple patches on extensor surfaces Discoid Eczema:
Round, scaly patches on arms and legs. Lichen simplex chronicus: Itchy, lichenified, persistent patches Bowen’s disease:
Plaques tend to be smaller and more limited in no., biopsy decides. Superficial Basal- Cell Carcinoma: Thin slightly raised edge; biopsy decides. Mycosis fungoides:
Multiple psoriasiform patches, but irregularly thickened; biopsy. Ringworm:
Often annular, spreads peripherally; microscopic and culture of scale Clinical variants: Guttate psoriasis: It
is mainly seen in children aged 7-14 yrs. Often, it develops some 2-4 weeks
after an episode of tonsillitis or pharyngitis, mostly due to beta-hemolytic
streptococci. It behaves like an exanthema, as the characteristically ‘drop’-
sized lesions develop suddenly and at the same time. The lesions do not usually
last longer than 8-10 weeks. Napkin Psoriasis:
Infantile napkin dermatitis sometimes takes on a very psoriasis-like appearance
and typical psoriatic lesions develop on the scalp and trunk. Erythrodermic psoriasis:
Psoriasis sometimes progresses to generalized skin involvement. Typical plaque
like, lesions disappear, the skin is universally red and scaly and the
condition is known as Erythrodermic psoriasis. Patient who are seriously ill,
suffer from: 1. Heat loss, and are in danger of hypothermia. 2. Water loss, leading to dehydration because of the disturbed
barrier function of the stratum corneum 3. A hyperdynamic circulation, because effectively there is a vascular
shunt in the skin; when the patient’s myocardium is already compromised because
of other factors, there is a danger of high output failure. 4. Loss of protein, electrolytes and metabolites via the shed
scales and exudates; patient may develop deficiency state. Pustular psoriasis: It
seems probable that Pustular psoriasis is indeed a type of psoriasis, with
exaggeration of one particular component of the disease. There are two main
types: 1.
Palmoplantar pustulosis:
Patient with Palmoplantar pustulosis develop yellowish white, sterile pustules
on the central parts of the palms and soles. Older lesions take a brownish
appearance and are later shed in a scale at the surface. 2.
Generalized Pustular psoriasis: This
is also known eponymously as Von Zumbusch disease, and is one of the most
serious disorders dealt with by dermatologists. In its classical form, attacks
occur suddenly and are characterized by severe systemic upset, as swinging
pyrexia, arthralgia, and a high polymorphonuclear leucocytosis. The skin first become
Erythrodermic and then develops sheets of sterile pustules over the trunk and
limbs. Sometimes, the pustules become
confluent so that ‘lakes of pus’ develop just beneath the skin surface. 3. Other
form of Pustular psoriasis: (a) Acrodermatitis
continua, in which there is a
recalcitrant Pustular erosive disorder on the fingers and toes around the
nails. (b) Pustular
bacterid, in which sterile pustules
suddenly appear on the palms, soles, and distal parts of the limbs after an infection
Arthropathic psoriasis:
There is a high prevalence of a rheumatoid- like arthritis with symmetric
involvement of the small joints of the hands and feet, wrist and ankles in
patients with psoriasis (5-6%). This ‘rheumatoid arthritis- like’ disorder
differs in one important respect from ordinary rheumatoid arthritis – there is
no circulating rheumatoid factor. In this ‘psoriatic
arthropathy’, the distal interphalengeal joints, the posterior zygohypophysial,
the temporomandibular, and the sacroiliac joints are particularly affected. The
disorder is more destructive than rheumatoid disease. Bony erosion and
destruction take place, leading to ‘collapse’ of affected digits, justifying
the term for this dreadful disease- Arthritis mutilans. Pathology and pathogenesis: The histopathological
appearance of psoriasis is distinctive but not specific. The main features may
be subdivided into (1) the epithelial thickening, (2) the inflammatory
components, and (3) the vascular component.
The epidermal thickening:
The epidermis shows marked exaggeration of the rete pattern and elongation of
the epidermal down growths with bulbous, club like enlargement of their ends.
The average thickness is increased from 3- 4 cells in to normal skin to
approximately 12-15 cells in the psoriatic lesion. The turnover time of
psoriatic epidermis and stratum corneum is consequently very much shortened.
Normally it takes some 28 days for new cells to ascend from the basal layer,
travel through the epidermis and the stratum corneum, and reach the surface. In
psoriasis, it takes some 4days. Epidermal nuclei are retained in the
inefficient horny layer that results parakeratosis. The inflammatory component: Interspersed between the ‘parakeratotic’ horn cells are
collections of desiccated polymorphonuclear leucocytes known as Munro
microabscesses. The epidermis is oedematous and infiltrated by inflammatory
cells. The dermis immediately below the epidermis also contains many
inflammatory cells, mostly lymphocytes. The vascular component:
The papillary capillaries are greatly dilated and tortuous to a degree not seen
in other skin disorders. There are larger gaps than usual between the
endothelial cells. Aetiology: One
obvious abnormality in psoriasis is the hyperplasic epidermis with increased
mitotic activity, and one line of intense investigation was directed at the
control of intense investigation was directed at the control of epidermal cell
production in this disease. Currently psoriasis is thought of as a
‘lymphocyte-driven’ disease. Infection has been considered
as a cause and in recent yrs, the involvement of retrovirus has been suggested.
Homoeopathic treatment and management: A hypertrophy of the papillae of the
corium, not contagious or itching:
Alumina, Amb., Amm. carb., Ars., Arsenic iod, Aurum, Berbaris aqua, Bryonia,
Borex (recent case), Calcaria carb, Carbolic acid, Clematis, Coral,
Chrysophanic acid., Dulcamara, Graphites, Iris, Iod, Kali br, Ledum, Lyco,
Mangnum, Magnesia carb, Merc sol, Nitric acid, Nuphar, Phos, Psor, Ranun., Rhus
tox, Sarraca., Sepia, Sulph, Tellu, Teucrium, Psoriasis diffusa: Ars iod, Borex, Calc carb, Cicuta, Clematis, Dulc,
Graphites, Lyco, Merc proto iod, Psoriasis inveterata: Calc, Clem, Kali ars, Merc, Petr, Rhus, Sepia, N.B. Phosphorus may help
after the failure of Arsenic alb or Arsenic iod, and Kali sulph is found
efficacious in psoriasis palmaris and plantaris. |
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