Vitiligo :: Efficacy of Homoeopathic Drugs in cases of Leucoderma – Vitiligo

Six hundred and ninety five (695) patients suffering from leucoderma were registered for treatment at Gaurang Clinic & Centre for Homoeopathic Research, Lucknow from April 1996 to March 2001 out of which a total of five hundred and sixty (560) patients were available for proper follow up of treatment and analysis to assess the percent response by treatment with homoeopathic drugs.

The treatment of leucoderma with homoeopathic drugs, based on totality of symptoms, showed significant improvement in three hundred and twenty eight (328) patients (58.57%), out of which four (4) patients (0.71%) were cured, seventeen (17) patients (3.04%) showed more than 90% improvement, three hundred and seven (307) patients (54.82%) are improving; while two hundred (200) patients (35.72%) maintained status quo and thirty two (32) patients (5.71%) did not improve at all.

OBJECTIVE

This pilot study was conducted to scientifically establish the efficacy of homoeopathic drugs in cases of Leucoderma as well as to establish the predisposing and causative factors, age group more prone to it and fungal species associated with Leucoderma.

INTRODUCTION

The skin colour of an individual depends on the thickness of the horny layer, on the circulation and the volume of reduced and oxyhaemoglobin in the superficial vessels and on the presence of other pigments in the skin and subcutaneous tissues. The most important of which are melanin and the melanoid. Racial and constitutional differences in skin pigmentation depend on the quantity of melanin. Leucoderma is characterised by localised or generalised hypomelanosis (less synthesis of melanin) which occasionally may become so extensive that it covers the whole body. Although the exact aetiology is still unknown there are various predisposing factors that could lead to leucoderma. Out of various hypotheses viz. auto-immune, self-destruction and neural hypotheses; auto – immune hypothesis is universally accepted. However, the hypothesis “destruction of melanocyte” is still in existence (Srivastava and Gupta 1999). Most of the leucoderma patients are healthy but prone to other infections due to the absence of melanin.

Other associated conditions may be the sunburn, fungal or bacterial infections (Gupta, Srivastava,
Chandra, Gupta 1997; Gupta, Srivastava, Gupta 1997). Worldwide prevalence is 1 % affecting both sexes equally. No age is exception but children and young adults are most commonly affected. Genetic predisposition, autosomal dominant trait with variable penetrance and family history is present in about 1/5th of the patients. Lesions may remain stationary, self – healing or progressive. Prognosis is better in young patients, early lesions and hairy areas. Repigmentation is spontaneous or therapy induced and is caused by repopulation of depigmented skin with melanocytes from the hair follicles or the adjoining normal skin (Bhutani 1993).

Histopathological examination reveals decrease or absence of melanocytes and upper dermal lympho – histiocytic infiltrate with preponderance of CD4 positive cells on Immunohistochemical staining (Bhutani 1993). Skin scraping and culture from the leucodermic lesions showed the presence of various fungi. The role of these isolated fungi from leucodermic lesions in the development of disease could not be established, however, it could be super-added infection in previously leucodermic lesions. Characteristic distribution patterns of leucoderma involves extensor surfaces and bony prominence (elbow, knee, small joints in the hand) and the area around eyes and mouth. The lower back, axilla, wrist, genitals, palms and soles and mucus membrane are often affected.

Leucoderma can be classified into two major groups:

A. Congenital:

Albinism: It is a congenital condition. It may be partial with single or multiple areas devoid of pigment, or complete with no melanin in the skin, hair, or its appendages, or in the iris.

B. Acquired: It is extremely common and may present as macules of varied configuration viz. irregular, oval, circular, linear or punctate, discrete or confluent. It may start as hypopigmented macules on an otherwise normal skin and become depigmented. Acquired variety of Leucoderma can be classified into following different types:

1. Vitiligo / Classical Leucoderma: Symmetrical depigmented patches can develop on any part of the body, which may become sore on exposure to sunlight but disability is mainly cosmetic. The course is variable with partial temporary remissions and occasional spontaneous cure. Morphoea and Lichen sclerosus also have white patches but the texture is abnormal, scar like in former and soft and wrinkled in latter (Savill 1909).

2. Secondary and symptomatic Leucoderma: Some inflammatory disorders such as Psoriasis and Lichen simplex may be followed by temporary depigmentation. It very rarely develops in secondary syphilis and in anaesthetic lesions of leprosy, however, scars may be depigmented in Lupus erythematosus (Savill 1909).

3. Occupational Leucoderma: Catechols and phenolic compounds are often responsible for Chemical hypomelanosis. Leucoderma develops in the hands and forearms in Negroes wearing gloves made of rubber containing monobenzyl ether of hydroquinone (MBH) as an antioxidant or if the same is used for the treatment of melasma (Savill 1909).

4. Contact Leucoderma: Depigmentation is caused due to contact with articles containing MBH or other depigmenting chemicals. Rubber footwear, adhesive coated ‘Bindi’ (worn on the forehead by Indian women), rubber gloves and possibly some condoms (Bhutani 1993).

5. Pseudo – Leucoderma: It develops when diseased patches of skin fail to develop pigment on exposure to sunlight, as conspicuously as surrounding normal skin, and so appears white. The dry scaly patches on the face of children (Pityriasis alba and Pityriasis versicolor) are common examples (Savill 1909).

Depending upon the appearance and distribution Vitiligo can be classified as Acrofacial Vitiligo, Vitiligo vulgaris, Dermatomal Vitiligo, Generalised Vitiligo and Halo naevus / Sutton’s naevus (Bhutani 1993):

1. Acrofacial Vitiligo: The distribution of lesion is symmetrical, confined to mucocutaneous junctions or acral parts of the body viz. face, hands, feet, and both lips.
2. Vitiligo vulgaris: Lesions are randomly distributed in various parts of the body.
3. Dermatomal Vitiligo: Lesions are often unilateral.
4. Generalised Vitiligo: Lesions are present all over the body symmetrically or asymmetrically, particularly affecting the skin overlying bony prominences.
5. Halo naevus / Sutton’s naevus: It is characterised by oval or circular, sharply defined hypo or depigmented halo around a pigmented mole.

MATERIALS AND METHODS
1. Patients: A total of six hundred and ninety five (695) well diagnosed cases of Leucoderma were registered for treatment at Gaurang Clinic and Centre for Homoeopathic Research (GCCHR) from April 1996 to March 2001. Out of which a total of five hundred and sixty (560) cases were available for proper follow up of treatment and analysis to assess and explore percent response by treatment with homoeopathic drugs.

2. Skin Scraping: All the patients, suffering from leucoderma, who approached GCCHR for the treatment of their disease were recommended for skin scraping and culture for pathogenic fungi from the lesions by following the method of Rona M. Mackie 1997 and Richardson 1993 to ascertain the presence of super-added fungal infection, if any. Skin scales were scraped with the help of sterilised surgical blade from the affected area of skin until reasonable numbers of silvery scales were obtained. Bleeding by scraping or vigorous scraping were avoided. Part of scraping from leucodermic lesions were examined directly in KOH (10%) slide mount for presence of mycelia and spores. For isolation of pathogenic fungi, remaining part of scraping was inoculated in petridish poured with Sabouraud’s dextrose agar and incubated at 37 ? 1 ?C for fifteen days. Colonies appeared were identified. Scraping from healthy skin were kept as control done in Mycology Lab. of GCCHR.

3. Repertorisation: All chronic, clinically non responding and longstanding cases of Leucoderma along with the cases with prolonged treatment in other pathies with no significant response were repertorised considering the totality of symptoms keeping in view the constitution of the patient giving much emphasis to mental, physical and general symptoms through computer by using Hompath Classic Software.

4. Software: An indigenous software for the research and analysis to assess the percent response in the patients with Leucoderma by treatment with of Homoeopathic drugs was developed at GCCHR by computer programmer.

5. Homoeopathic Drugs: Homoeopathic drugs prescribed after repertorisation are discussed with individual cases.

 

?

 

TABLE
? 1

 

PERCENT
DISTRIBUTION OF LEUCODERMIC LESIONS IN THE BODY OF PATIENTS

 

(Total
Patients: 695)

 

?

 

S.N.

 

Patients

 

Number

 

Percentage

 

?

 

1.

 

?

 

2.

 

?

 

Lesions
distributed all over body

 

?

 

Localised
Lesions

 

?

 

484

 

?

 

211

 

?

 

69.64

 

?

 

30.36

 

?

 

?

 

TABLE
? 2

 

DIVISION
OF CASES OF LEUCODERMA ACCORDING TO AGE

 

(Total
Patients: 695)

 

?

 

S.N.

 

Age
of Patient

 

Number

 

Percentage

 

?

 

1.

 

?

 

2.

 

?

 

3.

 

?

 

Below
15 years

 

?

 

Between
15 ? 45 years

 

?

 

Above
45 years

 

?

 

146

 

?

 

427

 

?

 

122

 

?

 

21.01

 

?

 

61.44

 

?

 

17.55

 

?

 

?

 

TABLE
? 3

 

DIVISION
OF CASES OF LEUCODERMA ACCORDING TO SEX

 

(Total
Patients: 695)

 

?

 

S.N.

 

Sex

 

Number

 

Percentage

 

?

 

1.

 

?

 

2.

 

?

 

Male

 

?

 

Female

 

?

 

352

 

?

 

343

 

?

 

50.65

 

?

 

49.35

 

?

 

?

 

TABLE
? 4

 

CLINICAL
STATUS OF LEUCODERMA PATIENTS AFTER TREATMENT WITH HOMOEOPATHIC DRUGS

 

(Total
Patients: 560)

 

?

 

S.N.

 

Patients

 

Number

 

Percentage

 

?

 

1.

 

?

 

1(a).

 

?

 

1(b).

 

?

 

1(c).

 

?

 

2.

 

?

 

3.

 

?

 

Positive
response

 

?

 

????????
Cured

 

?

 

????????
Improvement
above 90 %

 

?

 

????????
Significant
Improvement

 

?

 

Status
Quo (as such)

 

?

 

Not
Improving

 

?

 

328

 

?

 

????????
004

 

?

 

????????
017

 

?

 

????????
307

 

?

 

200

 

?

 

032

 

?

 

58.57

 

?

 

????????
00.71

 

?

 

????????
03.04

 

?

 

????????
54.82

 

?

 

35.72

 

?

 

05.71

 

Reports Of A Few Model Cases – Leucoderma
–Please see “Homeopathy Cases”–


RESULTS AND DISCUSSIONS

1. Treatment of Leucoderma with homoeopathic drugs showed significant improvement in 328 patients (58.57%), out of which 4 patients (0.71%) were cured, 17 patients (3.04%) showed more than 90% improvement, 307 patients (54.82%) are improving; while 200 patients (35.72%) maintained status quo and 32 patients (5.71%) did not improve at all (Table IV).

2. Patients with Leucoderma all over the body contributed 69.64 % (484 patients) while only 30.36 % (211 patients) had localised lesions (Table I).

3. Both sexes are equally affected by Leucoderma. Males contributing 50.65 % (352 patients) while in females the percentage is 49.35 % (343 patients) (Table III). No age is bar, however, young and adults of both the sexes are predominantly affected. Total 427 patients (61.44 %) were between 15 – 45 years of age (Table II).

4. The social stigma attached with this disease that it spreads by contact, runs in families and is not easily curable (causing mental trauma to patient and family members) turned out to be only a myth.


CONCLUSION

1.The results of the present study are highly encouraging.

2. The results are better in children and young adults. Facial lesions respond much quickly as compared to lesions in other parts of the body while lesions on joints have relatively poor response.

3. Homoeopathic drugs are cost effective and easy to use with no side effects while treatment with Psoralen compounds, Placental extracts, Steroids (topical or systemic) may result in side effects.

4. The recurrence rate after homoeopathic treatment is nil or very less as compared to treatment in other pathies.

5. It is also inferred from this study that Leucoderma patients are highly prone to fungal infections.


REFERENCES

1. Gupta, G., Srivastava, A. K., Chandra, B., Gupta, N., (1997), Cutaneous Candidiasis: Therapeutic potential of Homoeopathic drugs, Asian Homoeopathic Journal, 7 (2): pp. 8 – 32.
2. Gupta, G., Srivastava, A.K., Gupta, N., (1997) Mycoses: An update over clinical cure with Homoeopathic drugs, Asian Homoeopathic Journal, 7 (4): pp. 67 -96.
3. Mackie Rona, M., (1997), Clinical dermatology, Oxford Medical publication, New York, pp. 324.
4. Richardson, M.D., Wornock, D.W., (1993), Fungal infection: Diagnosis and Management. Oxford Blackwell Scientific Publication, London, pp. 205.
5. Rippon, J.W., (1988), Medical Mycology – The pathogenic fungi and the pathogenic Actinomycetes, W. B. Saunders Company, Philadelphia, pp. 797.
6. Srivastava, A. K., Singh, K. P., Ray P. K., (1997), Protein A induced protection against experimental candidiasis in mice Mycopathologia (accepted).
7. Srivastava, O. P., Srivastava, A. K., Shukla, P. K., (1997), Advances in Medical Mycology, Vol. 2 Council for Advances in Bioresearch and Evoker Research Perfecting Co. pp. 188.
8. Srivastava, A.K., (1999) Candidiasis – An Alarming Increase Among Lucknowites. The fungus factor. Jigyasa, 3, 1 – 2, An in-house newsletter of GCCHR, Lucknow.
9. Srivastava, A.K., Gupta, G.,(1999). The Leucoderma story. Jigyasa 3 (5), An in-house newsletter of GCCHR, Lucknow.

10. Bhutani, L. K., (1993), Disorders of skin pigmentation, Color atlas of Dermatology, 4th Edition: pp. 147 – 152.

11. Savill, T. D., (1909), Pigmentary and vascular changes, Savill’s System of Clinical Medicine, 14th edition (1964) pp. 1012 – 1013.

By

Dr. Girish Gupta, B. Sc., G.H.M.S., Chief Consultant
Dr. Naveen Gupta, B.H.M.S., Additional Physician (Research and Publication)
Dr. Vijay Singh, B. Sc., B.H.M.S., Assistant Physician (Repertorisation)

*This paper was presented in the National Homoeopathic Conference (Kent Memorial Lectures) organised by South Delhi Homoeopathic Association held in New Delhi on September 15′ 2001.

* The first author is member of the Scientific Advisory Committee of Central Council for Research in Homoeopathy, Ministry of Health and Family Welfare, Government of India.



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