July 2004

Acne
Dr.Sahni's Homoeopathy Clinic & Research Center Pvt. Ltd

Introduction
Definition: Acne is a chronic inflammatory disease of the pilosebaceous units. It is characterized
by the formation of comedones, erythematous papules and pustules, less frequently nodules
or cysts and, in some cases, scarring. Four major factors are involved in the pathogenesis:
increased sebum production, an abnormality of the microbial flora, cornification of the
pilosebaceous duct and the production of inflammation.
Natural history: The condition usually starts in adolescence and resolves by the mid-twenties.
Acne develops earlier in females than in males, which may reflect the earlier onset of
puberty. Some subjects show small non-inflamed lesions by the age of 89 years. A peak
in incidence and severity occurs between 1417 years in women, when 40% are affected, and
1619 years in men, when 35% are affected. Thereafter, the acne resolves slowly, but some
patients still have problems worthy of treatment up to the age of 35 years or more. At the age
of 40 years, significant lesions are still present in 1% of males and 5% of females. It is not
known why acne resolves or why it is more persistent in females.
Genetic factors: Several studies have shown that genetic factors influence susceptibility to
acne, A survey in Germany, showed that acne had been present in one or both parents of
45% of schoolboys with acne, but in only 8% of parents of boys without acne, Similar findings were recorded in a later survey of both girls and boys.
Racial studies provide an insight into genetic and environmental factors. Acne in black
Americans is less evident than in white Americans, who also have more severe acne than
Japanese. The incidence of acne is said to be low in Eskimoes eating a diet rich in fish,
but increases markedly when they change to a 'Western' (Canadian) diet with more saturated
fats. Similar changes have been noted in Japanese who emigrate to Hawaii and consume an
American-style diet.
Figure 1: The correlation
between sebum excretion and
acne in males and females
between 15 and 25 years of
age.

Etiology
Increased sebum production. Active sebaceous glands are a prerequisite for the development of acne. Acne patients, male and female, excrete on average more sebum than
normal subjects and the level of secretion correlates well with the severity of the acne (Fig 1)
Sebaceous activity is dependent on male sex hormones of gonadal or adrenal origin.
Abnormally high levels of sebum secretion could thus result from high overall androgen production or increased availability of free androgen because of deficiency in sex-hormonebinding globulin (SHBG). Equally, they could involve an amplified target response mediated
either through 5-reduction of testosterone or the capacity of the intracellular receptor to bind
the hormone.
There is general agreement that plasma testosterone levels are not abnormally high in
males with acne. In females with acne the situation is more complicated.

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Etiology
Some investigators have found testosterone levels to be normal whilst others have found
raised levels, albeit to only a fraction of the concentration in the male. There is general
agreement that mean SHBG levels are significantly below normal, with free testosterone consequently, above normal. However, for each endocrine assay, there is a considerable overlap
between the acne and normal ranges. Thus, Lawrence and co-workers found that only 41%
of their acne patients had free testosterone levels above normal. Lucky and
co-workers
measured a number of androgens and their precursors, as well as SHBG, and found that
52% of non-hirsute women with acne had at least one abnormal hormone level. Darley and
co-workers found high testosterone in 26%, low SHBG in 45% and high prolactin in 45% of 38
women with acne. However, 24% of the total had no hormonal abnormality.
Thus androgenic hormonal balance is disturbed in 5075% of female acne patients.
However, this does not establish that it is the critical factor, and at least a quarter of all cases
remain unexplained.
These conclusions are supported by clinical observations. There is no correlation between
severity of acne, hirsutism and menstrual irregularity. Moreover, if the development of acne
were simply related to systemic hormone levels, it should have a similar frequency on the
face, back and chest, but this is not so. The fact that acne does not occur simultaneously on
all susceptible sites is consonant with the finding that sebum excretion varies from follicle
to follicle. An enhanced peripheral response must thus be considered as a factor in many
subjects. The possible role of increased 5-reduction of testosterone to its more active
metabolite is indicated both by the demonstration that sebaceous glands in acne-prone
regions show abnormally high 5-reductase activity in vitro and by the finding of abnormally
high amounts of 5-andro-stanediols in the urine of female acne patients. Data on androgen
receptors in acne suggests that androgen action on the sebaceous gland may be independent of serum hormone levels.
Finally, the possibility that other hormones affect the sebaceous glands either directly or by
enhancing their response to androgens should not be neglected. In acromegalics the rate of
sebum excretion correlates with skin thickness and growth hormone levels and sebum
excretion rate is low in individuals with isolated growth hormone deficiency.
Irrespective of the rate of sebum excretion, could acne be related to change in skin lipid
composition? Sebum consists of a mixture of squalene, wax and sterol esters, cholesterol,
polar lipids and triglycerides. As the sebum moves up the duct, bacteria, especially Propionibacterium acnes (P. acnes), hydrolyse the triglycerides to free fatty acids. The role of individual
lipid components in causing acne is uncertain. They may be involved in ductal hypercornification or may be essential to the growth of bacteria. Patients with acne tend to have higher
levels of squalene and wax esters, lower levels of fatty acids and a more frequent occurrence
of particular free fatty acids. Linoleic acid is significantly reduced in epidermal and comedonal
lipids and this may relate to ductal hypercornification.
Ductal hypercornification. Acne patients show ductal hypercornification, which produces
blackheads and whiteheads. There is a significant correlation between the severity of acne
and the number and size of follicular casts, which are a measure of comedogenesis.
The reason for this ductal hypercornification is unclear. Electron microscopy of early noninflamed lesions taken from prepubertal and early pubertal individuals has demonstrated
few or no bacteria. Quantification of comedonal bacteria suggests that follicular colonization
may be unrelated to comedo-genesis. Biopsy and culture of early non-inflamed lesions has
shown that 30% of these are without bacteria, suggesting that ductal bacteria are not needed
for the initiation of ramification. Examination of polar lipids recovered from comedones
shows that the acyl ceramides contain only 6% linoleate amongst the esterified fatty acids,
compared with 45% in normal human epidermis, Similarly, linoleic acid is reduced in sebum
from acne subjects but returns to normal following treatment with isotretinoin and antiandrogens.

Androgenic
hormonal balance
is disturbed in
5075% of
female acne
patients.

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Etiology
Monoclonal antibodies to keratins 6 and 16 confirm that comedones are hyperproliferative
but impaired corneocyte separation is also likely to be important. Hypercornification appears
to involve persistence of desmosomes, desmosomal bodies and a decrease in the number of
membrane-coated granules, but it is not clear whether such changes are primary or
secondary. The factors which convert a normal follicle into either a whitehead (closed
comedo) or a blackhead (open comedo) are equally obscure. Possibly hydration of the ductal
exit may cause a non-inflamed lesion to become inflamed. This might provide a partial
explanation for tropical acne.
Acne and bacteria. Acne is not infectious. The three major organisms isolated from the
surface of the skin and the duct of patients with acne are P. acnes, S. epidermidis and
Malassezia furfur (Pityrosporum). There are three major subgroups of the propionibacteria (P.
acnes, P. granulosum and P. avidum). Almost certainly P. acnes and, to a lesser extent,
P. granulosum, are the most important. Nevertheless, as they live in association with the
S. epidermidis and M. furfur it is likely that these oganisms have some control over the growth of
P. acnes.
Adolescence and its attendant seborrhoea are associated with a significant increase in P.
acnes but there is little or no relationship between the number of bacteria on the skin
surface or in the ducts and the severity of acne. Sebum excretion rate and ductal cornification
by contrast, both correlate well with clinical severity.
The environment of the bacteria is probably more important than their absolute numbers for
the development of lesions. Oxygen tension, pH and nutrient supply markedly affect the
growth of P. acnes in vitro and the bacterial production of active substances such as lipases,
proteases, hyaluronate lyase, phosphatase and smooth muscle contracting substances. In
vivo the pH of blackheads markedly varies between 3.6 and 6.7, and this is likely to affect the
bacteria. Such factors could determine whether or not a follicle develops into a non-inflamed
comedo and subsequently, into an inflamed lesion.
The once-fashionable 'lipase' theory for acne no longer has much support, since injection of
fatty acids into the skin produces only mild inflammatory reactions. Lipids are not found in the
inflammatory infiltrate of acne and a specific lipase inhibitor produces no improvement in
acne.
Mediation of inflammation. The dermal inflammation is not caused by bacteria in the dermis, since these are rarely demonstrable by routine and immunofluorescent methods. It
probably results from biologically active mediators which diffuse from the follicle where they
are produced by P. acnes.
The precise factors which induce inflammation in acne lesions are unknown.
Propionibacterium acnes produces many enzymes, including three proteases, lipase,
phosphatases and hyaluronate lyase, all of which might in theory be implicated. Ductal
corneocytes produce interleukins (IL-1 and IL-2) and tumour necrosis factor, and are upregulated by antibiotics, in particular minocycline. These cytokines may be involved in
inflammation. The lymphocyte is the first-cell to infiltrate the dermis (Fig. 2) and duct rupture is
seen in only 33% of papules at 36 h and 67% at 72 h. Thus, the early inflammation is probably due to mediators moving through the duct wall. Propionibacterium acnes, in
particular
its cell-wall fraction, is a potent chemo-attractant for polymorphonuclear and mononuclear
cells. It also produces a prostaglandin-like substance, which might be involved, since non- Fig. 2 An inflamed papule showing
rapture of the duct with a symmetristeroidal anti-inflammatory drugs have an anti-acne effect.
cal lymphocytic infiltration.
Direct immunofluorescent studies have shown that in early non-inflamed and inflamed
lesions there is activation of the classical and alternative complement pathways. As the
lesions progress, types 3 and 4 immune reactions increase at the expense of complement.
Circulating immune complexes are not evident in acne sera. Skin testing with a heat-killed
suspension of P. acnes demonstrated that subjects with severe acne produced a greater
inflammatory response at 48 h than other subjects, suggesting that the host response may
be important. Observed changes in neutrophil chemotaxis may be a secondary event. It is

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Etiology
uncommon to see females with very severe acne and it may be that females muster a better
defense mechanism than males against P. acnes.
Resolution of acne. While the evolution of acne has received considerable attention, its
resolution has been largely ignored. Limited studies suggest that the resolution is not related
to reduction of sebum production or surface bacteria. The relationship between ductal
hypercornification, inflammatory mediators, changes in the host response and resolution is
obscure. Pierard has shown that in acne patients the individual sebaceous glands function at
different rates. Resolution may be associated with specific changes in these acne-prone
hypersecreting glands.
Biological significance of sebum and P. acnes. Activity of the sebaceous glands is unlikely
to be necessary for healthy skin since prepubertal skin appears perfect. Yet the ubiquity of
both hypersecretion and of P. acnes suggests that their apparent undesirability may be outweighed by some selective advantages. It has been suggested that P. acnes, which enhances
immune responses, may provide protection against malignant haematological disease,
though not against solid tumours.

Clinical Features
Acne is a polymorphic disease which occurs predominantly on the face (99%) and, to a lesser
extent, on the back (60%) and chest (15%). In young men it affects mainly the face, and in
older males the back. Seborrhoea is an almost universal feature. Non-inflamed lesions
(comedones) are more frequent in the younger patients and consist of blackheads (open
comedones), in which the black colour is due to melanin not dirt, whiteheads (closed
comedones) (Fig. 3) and the so-called intermediate non-inflamed lesions which show features
of both blackheads and whiteheads. Inflammatory lesions may be superficial or deep and some
arise from non-inflamed lesions. The superficial lesions are usually papules and pustules
(5 mm or less in diameter), and the deep lesions are deep pustules and nodules. Often
forgotten is the macule, a lesion well on the way to regression, but one which can last for
many weeks and contribute markedly to the general inflammatory appearance.

Fig. 3 Multiple whiteheads.

Classification of lesions is arbitrary and the types may merge. Nodules, especially if
exudative or haemorrhagic, and cysts are particularly disfiguring. They may extend over areas
of a few to many centimetres and the nodules may be remarkably deep with very little
surface involvement. Sinus formation between nodules may also occur, with devastating
disfigurement. The deeper inflammatory lesions are often associated with scarring. Pyogenic
granulomata develop very infrequently.
The exact incidence of scars is not known but it is decreasing with improved therapy. Scars
may show increased collagen (hypertrophic scars and keloids) or be associated with loss of
collagen (i.e. ice-pick scars, depressed fibrotic scars, superficial and deep, soft scars and
atrophic macular atrophy). Keloids are the least common and are most prevalent on the
trunk. Atrophic macular scars normally retain a purple colour for many months before
becoming white and less conspicuous. Ice-pick scars, depressed fibrotic scars and keloids
probably change very little, but the superficial and deep, soft scars may improve with time. A
common type of scarring on the back and chest consists of relatively inconspicuous small,
follicular, macular atrophic lesions the so-called perifollicular elastolysis.
A rare complication of scarring is calcification. A common feature of darkly pigmented skin is
the relatively persistent postinflammatory pigmentation (Fig. 4).

Fig. 4 Postinflammatory
pigmentation: a characteristic
feature associated with acne
in black skin.

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Grading
Grading is very helpful in the assessment of acne in the clinic. A grading scale similar to that
shown in Figs 5, 6, 7 & 8 is recommended. A good light and palpation, as well as inspection,
are required. The acne can be graded on a 07 scale on the face, back and chest. Little practice
is required to become reasonably efficient, and it does not matter if the grading used is somewhat different from those techniques published, so long as the observer is consistent.

Fig 5 Patient with grade

0.5 acne (Leeds Scale)

Side Effects of Conventional Therapy

The most widely used topical therapies are benzoyl peroxide, vitamin A acid and antibiotics.
Many topical pre-parations produce a primary irritant dermatitis (Fig. 9) and the patient must
be warned so that treatment will not stop prematurely. Gastrointestinal effects, especially
colic and diarrhea may occur in 5% of patients. Vaginal candidiasis occurs in 6% (male sexual
partners may also need treatment for candidiasis).

Fig 6 Patient with grade

1.5 acne (Leeds Scale)

Uncommon complications of oral therapy include onycholysis, oesophagitis with ulceration,

widespread or fixed drug eruptions and photosensitivity, including porphyria-like
cutaneous changes, especially with the longer-acting tetracyclines.
Doxycycline causes a phototoxic rash in 4% of patients.
Tetracyclines, especially minocycline, may produce benign intracranial hypertension: this
presents with headache, loss of concentration and sometimes papil-loedema, and quickly
disappears on stopping therapy. Another rare problem is oesophageal ulceration with tetracycline.
Minocycline produces a blueblack pigmentation in a dose-dependent way and presents
in three ways: in inflamed acne lesions, in scars (acne and non-acne) and, more rarely, as a
generalized dark-grey discoloration. The pigmentation is due to a melanin-drug complex and it
lasts for about 815 months post-therapy.

Fig 7 This patient has grade 2

acne (Leeds scale) and also
shows the seborrhoea
characteristic of acne.

The possible clinical interactions between oral antibiotics and the contraceptive pill have not
been adequately studied, but a recent report showed a six- to sevenfold increase of pill failure,
and sexually active females should be made aware of this problem.

Homoeopathic Treatment
Generally speaking the treatment of acne consist of:
Fig 8 Patient with grade 4
1. Decrease sebum production
acne (Leeds Scale)
2. Reduce P. acnes (bacteria)
3. Normalize skin shedding
4. Eliminate inflammation
To achieve the above stated steps, the following remedies are used in successfully treating the
Acne:
1. Sulpur: It is used as a constitutional remedy or when indicated remedies fail to provide
cure.
2. Kali Brom: Acne on face, shoulder & neck. Most suitable to women.
3. Antim Crude: Acne associated with gastric derangements.
4. Natrum Mur: It has special effect on sebaceous glands as such very useful in Acne.
Fig 9 This patient has an al5. Berberis Aquafolium: To remove the scar of Acne. Useful to clear the complexion. Acne be- lergic contact dermatitis to
fore menses.
benzoyl peroxide.
6. Calcrea Pic: Acne of Young girls. Acne in crops.
7. Hepar Sulph: Acne Grade-II to IV; leaving scars.
8. Silicea: Acne that leaves scars.
9. Glycyrrhiza Glabera: Black spots / pigmentation from acne.

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Homoeopathic Treatment
10. Carbo Anim: Acne Grade-II to Grade IV, especially on cheeks.
11. Graphites: Acne, especially around mouth.
12. Sepia: Acne, especial before menses (Mag Mur)
13. Merc Sol: Acne with pus, leaving scars.Most suitable in Chronic cases.
14. Belladona: Acne, fiery red, painful, Grade-IV.
15. Bovista: cosmetic acne.
16. Asteris rub: Acne with small red base & black tips. (Kali Bro & Radium)
17. Causticum: Acne on Nose and in groups.
18. Mag Mur: acne on forehead, aggravated before menses.
Vibrionic Preparations:
1. Acne 200c
2. War 1M

General Guidelines
1.

Wash your face two times a day with a gentle soap. Change your wash cloth every
day (bacteria can grow on damp cloth). Wash as soon as possible after you exercise.

2.

Wash your hands more frequently and avoid putting your fingers and hands to your
face unnecessarily. Don't squeeze, pick, scratch, or rub your skin. Scars may form if
you squeeze pimples.

3. Keep a record of the foods you eat and try to figure out if any foods make your acne
worse. Avoid foods high in fat like chocolate, nuts, peanut butter, cheeses, potato
chips, and popcorn if they seem to make your acne worse.
In the marketing era there are Big Advertisements of Treatments that promise fast, miraculous or overnight results often capture the attention of acne sufferers hoping for
quick resolution. However, the fact remains that acne does not clear overnight.
In Homoeopathy or in any other system of medicine, on an average, 6 to 8 weeks are
needed to see initial results. Once acne significantly improves or clears, continued treatment is needed to keep acne from re-appearing. If acne does not improve in 6 to 8
weeks, treatment may need to be adjusted as not every acne treatment clears every case
of acne.
Dont try to follow the treatment of another person, as what is appropriate treatment for
one may not be right for another due to many factors affecting resolution, including the
cause(s) of the acne, a persons skin type and the kind of acne lesions present etc.
It is always advisable to keep your follow-up appointments with your doctor. Keep a
record of what has been tried and how it has worked. There are many alternatives for you
and your doctor to try, so don't give up!
WARNING:
Dont use any of the remedies described here without the consultation of Homoeopathic
Professional.

References
1. Text book of Dermatology By RH Champion, JL Burton & FJG Ebling
2. Materia Medica By Boreike
3. Kents Repertory

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