Female Pattern Hairloss

Female pattern hair loss (FPHL), or female patterned alopecia, is a form of nonscarring, patterned hair loss occurring commonly in postmenopausal adult women that is characterized by a progressive reduction in hair density on the crown of the scalp with sparing of the frontal hairline (Ludwig scale).

 

The part width progressively increases, most prominently anteriorly, and demonstrates thinning rather than baldness. Temporal recession occurs to a lesser degree in females than in males. A genetically determined shortening of the anagen phase of growth with a constant telogen phase leads to a gradual conversion of terminal (large, thick, and pigmented) hairs into vellus (short, thin, nonpigmented) hairs.1

Pathogenesis

The hallmark feature of FPHL is the progressive transformation of terminal hair follicles (large, thick, pigmented) to vellus hair follicles (short, thin, nonpigmented), in part due to a genetic predisposition influenced by androgens4,5. Although the process of miniaturization is not fully elucidated, it is known that androgen-responsive hair follicles gradually shorten their anagen (growth phase of the hair follicle) phase, resulting in fewer terminal follicles and more follicles in the shedding phase (telogen). Miniaturization is thought to be induced by the conversion of testosterone to dihydrotestosterone (DHT) by the enzyme 5α- reductase. Androgens exert their effect on hair by means of circulating testosterone derived from the adrenal glands, testes, or ovaries. Only free testosterone has the ability to enter cells and undergo conversion to DHT, which then acts on the androgen receptor in susceptible scalp hair follicles to facilitate the unwanted conversion to a miniaturized follicle6. Interestingly, only a minority of females with patterned hair loss have evidence of hyperandrogenism, such as those with polycystic ovarian syndrome, making the role of increased androgen levels in FPHL unclear 7.Studies suggest that women may have less severe hair loss than men due to lower levels of 5α-reductase and higher levels of aromatase, an enzyme which converts testosterone to estradiol, in susceptible hair follicles8. This pattern of hair loss also can be induced by events independent of androgens9. The role of estrogen in the pathogenesis is also not definitive, although the increasing prevalence of FPHL in postmenopausal women and the hair loss that occurs following aromatase inhibitor therapy suggest that estrogens may stimulate hair growth 10,11. Conversely, genetic studies implicate that an aromatase gene variant resulting in higher levels of estrogen may be associated with the development of FPHL12. Interestingly, the scalps, especially the frontal hair lines, of young women have higher levels of aromatase compared with male scalps, which may explain the decreased severity and relative sparing of the frontal hairline in FPHL. Recently, sequence variation in the gene encoding aromatase, CYP19A1 (cytochrome P450, family 19, subfamily A, polypeptide 1), has been associated with higher circulating levels of estrogens and might influence the risk of developing FPHL 12.

Classification

There are three main patterns described in women.

1.      One of the commonly used classification is the centrifugal pattern of hair loss described by Enrick Ludwig. He described 3 grades of severity of hair loss, and the main emphasis in this pattern is the preservation of the frontal fringe.

LUDWIG’S     Grading
Grade IThinning of hair seen over the anterior part of the crown with minimal widening of the parting width.
Grade IIThinning of the crown more pronounced with more widening of the parting width, increase in the number of thinner and shorter hairs.
Grade IIICrown is more or less bald with significant widening of the parting width. The frontal hairline is still maintained

1.      Olsen has described a Christmas tree pattern with frontal accentuation. She noticed that instead of the diffuse loss over the vault of scalp, they can have increasing hair loss towards the frontal scalp with encroachment on and sometimes breach of the frontal hairline.

2.      Male pattern or fronto-parietal pattern described by Hamilton characterized by bi-temporal recession. He reported that about 13% of premenopausal and 37% of postmenopausal women had Hamilton types II-IV male pattern baldness.

Clinical manifestations

FPHL usually presents as a gradual onset slowly progressive loss of hair, in a diffuse pattern over the crown area, with preservation of the frontal hairline. It can also present

with widening of partition, and in few cases similar to the male pattern with bi-temporal or fronto-temporal recession. The main diagnostic feature is the presence of miniaturization, that helps to differentiate from other conditions.

Other associated features of hyperandrogenism should always be ruled out in females and clinical examination can reveal such features like acne, seborrhea, hirsutism, irregularities in menstrual cycles along with hair loss.

    Diagnosis

The diagnosis is mainly clinical and biopsy is usually not necessary. Dermoscopy is useful to detect early FPHL and to distinguish FPHL from other hair disorders that can cause hair thinning13. The hair pull test, which is a maneuver performed by the examiner that gently pulls tufts of hairs along the scalp, is usually positive in the affected scalp as miniaturization causes shortening of the hair cycle with increased telogen shedding. When positive in all scalp areas it indicates associated telogen effluvium. Dermoscopic examination of the scalp correlates with the clinical classifications of FPHL, revealing variability in the hair shaft diameter that affects at least 20% of hairs14 and increased number of vellus hairs, parameters which are linked to follicle miniaturization 15. Patients with FPHL may have other skin or general signs of hyperandrogenism such as hirsutism, acne, irregular menses, infertility, galactorrhea and insulin resistance, but most do not. The most common endocrinological abnormality associated with FPHL is polycystic ovarian syndrome (PCOS). Hyperandrogenism is often a common feature between the two conditions and in both, the manifestation of this hyperandrogenism may not correlate with the circulating androgen levels because total circulating testosterone is mostly bound to albumin and sex-hormone binding globulin. But even then, both conditions can be treated with anti-androgens, androgen receptor blockers and enzyme inhibitors to avoid the effects of the androgens in the target organs. Another important association with FPHL is metabolic syndrome because of increased cardiovascular risks. Possible mechanisms to explain the association between these conditions are the presence of 5 alpha-reductase and DHT receptors in the vessels. Patients must also be investigated for systemic and newly diagnosed illnessess within the past year before the signs of alopecia manifested, as well as about significant weight loss, eating habits and medications that can cause hair loss or increase androgen levels 16.

Differential Diagnosis

1.      Chronic Telogen effluvium : this is the most often confused diagnosis. However there is often a  triggering factor for this condition and it is associated with sudden onset of  massive hair fall. The hair loss is generalized and there is no widening of the central partition or bi temporal recession in this case. The hair pull test is positive and there is no miniaturization.

2.      Cicatricial alopecia, especially frontal fibrosing alopecia : the presence of a band like hair loss over the frontal area in post menopausal females with features of scarring helps in differentiating this condition from FAGA.

3.      Diffuse  alopecia areata : this usually occurs in an acute manner with diffuse hair loss. Dermoscopy reveals exclamation mark sign and presence of yellow dots. Biopsy is confirmative

4.      Anagen effluvium : occurs due to intake of cytotoxic drugs

5.      Trichotillomania

6.      Syphilitic alopecia

7.      SLE

Treatments
Nutritional supplementation

The benefit of oral supplementation with amino-acids, biotin, zinc, and other micronutrients in hair loss of any origin is controversial.  Similarly, an apparent lack of correlation between low serum ferritin levels (<10 g/l) in apparently healthy women with FPHL, CTE, or both raised doubt if iron supplementation will be helpful. 17

Medical treatment

Pharmacological treatments for FPHL may be topical and oral. They can also be divided into drugs with androgen-dependent and independent mechanisms of action.

Topical

Minoxidil topical solution (MNX): MNX is approved for use in FPHL in a 2% formulation as twice daily application of 1 ml solution over dry scalp. Minoxidil increases follicular vascularity (as a potassium channel opener), prolongs anagen, shortens telogen, and converts partially miniaturized (intermediate) to terminal hairs.

Combination of MNX with aminexil (1.5%), a reverser of perifollicular fibrosis, with tretinoin and azelaic acid, and with topical finasteride are also commercially available, but their superiority over MNX alone in FPHL is not established.

Patient should be counseled about the increased hair loss following MNX application followed by stabilization and then noticeable increase in 8-12 weeks that usually peaks after 16 weeks. Minoxidil is a safe treatment; most common adverse effects being unsightly deposits on the hair-simulating dandruff, scalp irritation, and occasionally contact dermatitis that is due to vehicle propylene glycol rather than active molecule. Availability of MNX in gel and foam formulations enhances treatment acceptability. Secondly, as compared with men, women are more likely to develop hypertrichosis on the face (typically cheeks and forehead) and even on other remote sites especially with higher concentrations (5% > 2%). It is reversible on treatment break or reduction of concentration (within 4-6 months) and in some without cessation of treatment. 18 This side-effect may be minimized by wiping face and ears with a wet cloth after MNX application. The MNX being reasonably safe and effective should be considered as the first-line treatment for FPHL.

Oral

Androgen-dependent oral drugs for FPHL include 5α-reductase inhibitors and anti-androgens. Due to their propensity to cause feminization of the male fetus, they are contra-indicated in pregnant women and it is advisable to combine them with oral contraceptive pills (OCPs), especially in pre-menopausal women.

5α-Reductase inhibitors: Although compared with men, women have lower levels of this enzyme in the dermal papilla; inhibitors of this enzyme have been found to be effective in arresting hair loss in FPHL.

Anti-androgens
Anti-androgens act primarily through blockade of the ARs.
Cyproterone acetate: This drug blocks ARs and inhibits gonadotropin- releasing hormone. In many countries such as India, it is available in combination with estradiol as an OCP. The beneficial role of cyproterone acetate (CPA) in isolation or in combination with OCPs in reducing hair shedding and increasing hair density is known and seems to be greater in patients with evidence of hyperandrogenism. In two studies using Diane-35 for 6-9 months and as 2 mg CPA plus 50 μg ethinylestradiol daily plus additional 20 mg CPA on days 5-20 of the menstrual cycle, respectively, decrease in shedding and thinning of hair were observed. While one randomized comparative trial revealed that minoxidil 2% was more effective in women without evidence of hyperandrogenism, whereas CPA was more effective in those with hyperandrogenism, the efficacy of CPA versus spironolactone was found comparable in another trial. 20,21 The overall balance of evidence supports a role for CPA in FPHL, especially in presence of hyperandrogenism.

The most effective treatment dose seems to be 100 mg/day on days 5-15 of the menstrual cycle supplemented by 50 μg ethinylestradiol on days 5-25. 22 The adverse effects include menstrual disturbances, weight gain, loss of libido, depression, breast tenderness, and gastrointestinal upsets.

Surgical treatment

Hair transplantation is advantageous in being less invasive and a permanent hair cover can be re-established. A number of procedures have been tried, of these, follicular unit transplantation (FUT) is in vogue. In FUT, follicular units of 1-4 hairs are transplanted in high densities. Hair transplantation works on the principle of “donor dominance,” which means that the hairs from the donor region (the occiput) inherently lack the androgen-sensitive receptors, a property that is retained even after transplantation into the fronto-parietal region. It is indicated in patients with extensive hair loss or thinning of frontal scalp, but with the pre-requisite of high-donor hair density. 28

References

1.      L Lauren, J Jason. Female Pattern Alopecia : Current Perspectives. Int J of Women Health.  2013; 5: 541–556.

2.      Norwood OT. Incidence of female androgenetic alopecia (female pattern alopecia. Dermatol Surg 2001;27(1): 53-4.

3.      Wang TL, Zhou C, Shen YW, Wang XY, Ding XL, Tian S, et al. Prevalence of androgenetic alopecia in China: A community-based study in six cities. Br J Dermatol 2010;162:843-7.

Dermaroller

  • Dermaroller or microneedling, as the term indicates,means the use of microneedles to achieve therapeutic effect.
  • Roller system –It is a unique rolling device for the transdermal delivery of the substances that enhances the action of transdermal drug delivery and hair restoration.

MICRONEEDLING
•    Microneedling, originally known as collagen induction therapy or percutaneous collagen induction, is now a well documented treatment option for many dermatological condions.

•    The technique of microneedling was
innovated by    Fernandes in 2006.

PRINCIPLE OF MICRONEEDLING
•    It relies on the principle of neocollagenesis and neovascularisation that occurs as a result of the release of growth-factors following needle piercing of the stratum corneum.

•    These growth-factors are believed to be responsible for the beneficial effects of the procedure in the treatment of different dermatological conditions like scars , photoaging ,AGA etc
•    There are two hypothesis to explain the mechanism of action of microneedling.

1. Formation of microchannels with resultant healing response.

Following microneedling, thousands of microchannels or tiny wounds are produced through the epidermis into the papillary dermis of the treatedskin.These microchannels act as a powerful stimulus for the release of various growth factors such as platelet derived growth factors (PGF), transforming growth factor alpha and beta , and fibroblast growth factor (FGF),which initiate the normal process of wound healing by stimulating the migration and proliferatrion of fibroblasts that promote collagen deposition.

2. Production of a demarcation current

•    When the microneedles penetrate the skin , a demarcation current is produced among cells. It is the demarcation current that triggers a cascade of growth factors that stimulate the healing phase. In resting state, the interior of epidermal cells have a negative electric potential of    – 70mv where as interstitium and epidermal surfaces have a positive potential. The increase in the potential difference between the interior of the cell and the exterior environment triggers the migration of fibroblasts to the site of injury where they proliferate and lay down collagen.
INSTRUMENTS USED FOR MICRONEEDLING
•    The instrument used for microneedling is known as Dermaroller.
•    It is a simple hand held instrument consisting of a handle with a cylinder studded with sterile,fine stainless steel needles of 0.5- 2mm in length.
•    There are 192 needles and they are spaced at
regular distances from each other.
•    In order to achieve a uniform depth of penetration,the needles are placed at an inclination of 15 degrees in relation to the surface of dermaroller

•    To achieve the therapeutic benefit this needle studded cylinder is rolled on the skin in multiple directions and hence thename dermaroller.

HOW THE PROCEDURE IS DONE
•    Micro needling is usually performed under the
influence of a topical anaesthetic cream and is applied for a minimum of 45 mins before the procedure is started.

•    For treating acne and other scars the needle length should be selected on the basis of depth of the scars present. 1.5 -2mm is usually used for acne and other scars.

•    For ageing and wrinkles,the needle should be 0.5 or 1.0mm

•    After achieving adequate anaesthesia, the area to be treated is washed with saline water and then ethanol solution to obtain an aseptic fied.
•    The instrument is then held in the right hand like a pencil and rolled in three different directions on the treatment area

•    The procedure is performed after stretching the skin mildly with the left hand, so that the base of the scar is treated correctly.

•    Uniform formation of small pinpoint bleeding points mark the treatment endpoint.

POST PROCEDURE CARE

•    The treated area is simply washed off with saline solution and a patient is given a non comedogenic antibiotic cream for 3 -4 days after the prtocedure.

•    Sun avoidance and regular use of sunscreen is recommended in the post treatment area.

•    The bleeding points heal within 2-3 days with no post treatment sequelae.

•    Treatment with dermaroller is performed at 4 -8 weeks interval.

APPLICATIONS OF DERMAROLLER IN DERMATOLOGY

•    Although dermaroller was initially proposed as a treatment modality mainly for scars and wrinkles, its use has also been extended to stretch marks, facial rejuvenation and transdermal drug delivery.
ADVANTAGES
•    There are a number of advantages of using dermaroller.
•    In a nutshell,they are,
•    Far less invasive
•    Quick recovery time
•    Lower risk of complications
•    All skin types can be treated
•    No risk of permanent structural damage
•    No sun sensitivity after the treatment
•    No skin color loss or hyperpigmentation after treatment.
•    Dermaroller can also be used on the areas that are not suitable for peeling or laser such as near the eyes.
ADVERSE EFFECTS

•    A few adverse effects have been reported with dermaroller treatment.These include,

•    Pain during the procedure
•    Transient erythema and oedema

APPLICABLE AREA

•    Face,neck, arms,abdomen,legs,hair.
COMBINATION OF DERMAROLLER WITH OTHER PROCEDURE

•    To maximise the results of dermaroller,it can be combined with other procedures like subscision for acne scars, chemical peels, microdermabrasion and fractional resurfacing.

USES OF DERMAROLLER

Besides acnescars ,dermarollerhas also been used in the treatment of,

1.    Varicella scars
2.    Post herpetic facial scars
3.    Hypertrophic and burn scars
4.    Antiaging
5.    Transdermal drug delivery
6.     Hair disorder
7.    Large pores
8.    Wrinkles
9.    Stretch marks
10.   Cellulite
11.   Facial rejuvenation
CONCLUSION

•    Dermaroller is an underused treatment option
•    It can serve as a cheap alternative to fractional laser resurfacing in multiple indications
•    Therapeutic applications of this modality are going to increase opver the years tocome.

Treatment Of Diffuse Hyper Pigmentation Of Face Due To Koebner Inducible Lichen Planus Pigmentosus

Abstract:- 

Lichen Planus pigmentosus of the face will cause diffuse pigmentation over the face, following sun exposure and trivial injuries. Common sites of Lichen planus Pigmentosus are face arms and other sun exposed areas and if Koebner Phenomenon is present, the Hyper pigmentation will recur periodically with mildest and trivial injuries like even shaving the face. So for no shorter treatment is available for this type of Koebner inducible Hyper pigmentation, usually the pigmentation will settle only after two years, in spite of vigorous treatment with all modalities of treatments.

One young man of age 40 years came with diffuse pigmentation of face in the sun exposed area (sides of face) of six months duration.  He has been treated with high potent steroids and the following drugs at various consultations, Tretinoic acid cream, kojjc acid cream and vitamin c, Tacrolimus, pimecrolimus and Topical metronidazole gel. Patient became anxious and depressed. I had put him on Topical mild potent steroid Hydrocortisone cream mixed with    kojjc acid and vitamin c cream and applied over the lesion at night and a sunscreen in the daytime. Patient was advised to visit my clinic once in a week for mesotherapy with water. It has been done as follows, patient was asked to apply the mixture of kojjc and Hydrocortisune over the pigmented area followed by the water mesotherapy. Water is a harmless agent even when applied in a Jet form. This is continued at an interval of once in a weak for 20 weeks. This mesotherapy was done in a slow speed, over the cream applied pigmented area. After 20 weeks there was a marked improvement in the pigmentation. 75 percentage of clearance of lesion and color change was noted. Serial photos were taken and compared the efficacy. This procedure was carried out with the consent of the patient. Mesotherapy with water will enhance the absorption of drugs applied over the skin.

Conclusion:-

Since koebner phenomenon positive pigment Lichen planus is a difficult problem for early healing and clearance; we are in a position to go for a novel innovative treatment for early improvement. The above method seems to be a safe and effective technic for early clearance of pigmentation; and for the psychologically affected patients with recurrent pigmentation.

The following advices are given to the patient.

1.      Avoid Sun exposure.

2.      Use adequate sunscreen lotions.

3.      Avoid trivial injuries.

4.      Avoid shaving, instead trimming best.

A Warty Issue

A multitude of therapeutic strategies for treatment of warts exist, with no one therapy universally preferred. Location, size, type and number of warts merit consideration of therapy, while choosing a therapeutic modality along with patient pain tolerance, patient preference and physician preference.

The immune response of the host to HPV is important for resistance to and resolution of infection, with or without treatment. Cutaneous warts often resolve spontaneously in immunocompetent patients, So why do we treat warts?.2,3  Spontaneous resolution may take months to years, in the interim  warts can grow and spread, cause pain and emotional distress due to their appearance.

Table: Treatments for cutaneous warts1-5

*It is proposed that ablative therapies and even therapies such as duct tape might expose the immune system to HPV antigen, causing a host immune reaction.

A 24 yr old male presented with extensive tiny warts in beard area with 3 month history of the same. It was so extensive that cryotherapy or co2 laser would have left a lot of appreciable scarring in the beard area leading to cosmetic disfigurement. Only keratolytics as topical therapy would have lead to more chances of recurrences.

0.025 ml of Mw vaccine was initially injected intradermally in the deltoid region on both the sides, followed 2 weeks later by intralesional injection into the larger beard warts by drop and prick method using insulin syringe, total of no more than 0.1ml per sitting. The  intralesional injections were to be repeated 2 wkly. but patient came for second intralesional therapy after a month from the previous intralesional. he was advised to take tab ascazine thrice a day for at least 1 month. but the patient could take the medication just for 15 days. There was significant reduction of warts post first injection into the deltoid region and complete resolution of all the warts  after 2 sittings of intralesional injection. No recurrence was seen till 5 months of followup.

Immunotherapy is a safe, cost effective and efficient method of dealing with disseminated warts. Warts away from the injected warts also respond well due to generation of systemic immunity. Immunotherapy is worth considering in extensive or difficult to treat warts.

References 

1  Lynch MD, et al. Management of cutaneous viral warts. BMJ. 2014; 348: g3339 doi : 10.1136/bmj.g3339

2.       Kwok CS, et al. Topical treatments for cutaneous warts. Cochrane Database of Systematic Reviews 2012, Issue 9. Art. No.: CD001781. DOI: 10.1002/14651858.CD001781.pub3.

3.       Boull C, Groth D. Update: treatment of cutaneous viral warts in children. Pediatr Dermatol. 2011; 28: 217-29.

4.       Leung L. Recalcitrant nongenital warts. Aust Fam Phys. 2011; 40: 40-2.

5.       Lipke MM. An armamentarium of wart treatments. Clin Med Res. 2006; 4: 273-93.

Fractional Co2 Vs Other Modalities In Stretch Marks : 2 Year Perspective Of Arv Aesthetics, Gurgaon

They may also be influenced by hormonal changes associated with puberty, pregnancy, body building, obesity, crushing’s syndrome, marfan syndrome, hormone replacement therapy and misuse of oral and topical steroids as well as that of protein supplements. Both genders may be affected though females are a bit more prone to it

By definition they are dermal scars associated with epidermal atrophy. They appear as linear bands that are initially erythematous to violaceous and gradually fade to become skin colored or hypo-pigmented atrophic lines that may be thin or wide. Cause largely remains unknown but closely relates to changes in structure that provide the skin with its tensile strength an elasticity. Mechanical stretch of skin in association with hormonal factors has been postulated with its pathogenesis. Some hormones like estrogen, relaxin and adreno cortical hormones decrease the adhesiveness between collagen fibers and increase ground substance which result in formation of striae. They may also form due to structural connective tissue changes that include realignment and decreased expression of collagen,fibronectin elastin and fibrillin.However, in most of studies there is no direct correlation between degrees of striae from extent of skin stretching. Affected areas appear empty and are mostly soft to touch. They can appear anywhere on body where large amounts of fat are stored. Abdomen, breast, upper arm, back, thigh hip are the areas more involved. Although no significant medical problem, aesthetically striae are cause of great concern and are responsible of psychological stress too.

Stretch marks are not medically of any concern but aesthetically the marks can be a cause of concern and anxiety for many women, and affects their quality of life as they are disfiguring.

Stretch marks cannot be treated completely but there are various treatments available that improves the appearance of skin. Various topical treatments and procedures are available which helps in improving color and texture of skin by dermal regeneration and epidermal thickening .

Treatment and prevention:

Prevention: although there is no significant data regarding the efficacy of the emollients applications during the early months of pregnancy to prevent the stretch marks but various preparations containing vit E, hyaluronic acid, olive oils etc. are available in market.  Probably the emollient causes improvement in the dryness of skin and hence less scratching.

Topical:

Vitamin c: Vitamin C is a potent antioxidant drug that can be used topically in dermatology. Vit. C is essential for collagen biosynthesis.it influences quantitative collagen synthesis in addition to stimulating qualitative changes in the collagen molecule. Clinical studies have shown that the topical use of Vit. C increases collagen production. Used as a topical preparation to reduce striae alone and in combination of glycolic acid and hyaluronic acid.

Hyaluronic acids: HA alone is not an effective treatment modality. But as an adjuvant in other topical preparations it helps in healing and collagenesis.

Glycolic acid : Glycolic acid used alone as a topical preparation or as a chemical peeling agent to treat the stiae but more effective when used as a topical preparation in combination with vit c or retinoic acid. Again helps in collagen synthesis.

Tretinoins: Tretinoin works through its affinity for fibroblasts also induces collagen synthesis. It works maximally in striae rubra and the response is poor and unpredictable in striae alba tretenoin promotes collagen and elastin production. When applied nightly into striae rubra, the appearance and texture of the lesions can improve significantly.

PROCEDURES:

Micro-derma abrasions:  Microdermabrasion is effective, well tolerated, and safe for treating striae distensae having more beneficial effect on striae rubra than striae alba with ability to up regulate type I procollagen mRNA expression involved in dermal matrix remodeling. Weekly microdermabrasion treatments gives dermal remodeling and improves appearance of striae. Chances of PIH is very low in case of microdermabrasion. Histological evaluation shows thickening of epidermis and more collagen and elastin fibers in dermis.

Micro needling: micro-needling by derma roller or derma pen is again collagen induction technique in which mechanical trauma is created in the affected area by fine needles. As of result of which columns of damaged and healthy skin are formed in skin and as a result neo-collagenesis occurs. Process of wound healing results in to thickening of epidermis and new collagen and elastin synthesis in dermis, resulting in to bridging the gap in the dermis. Shows significant improvement .can be combined with vitamin c application or hyaluronic acid application during micro needling.

Radio frequency: Tripolar RF and intradermal RF both can be used.  RF increases collagen production by inducing collagen type I mRNA expression. They produce heat, which converts electrical current to thermal energy which is uniformly dispersed in to various tissue depths. Multiple sittings are required. Also gives improvement in telangiectasia present in striae rubra. Should be combined with other procedures to get good results as it has got minimal or no effect on epidermal atrophy.

Fractional co2: The use of ablative lasers diminishes the appearance of stretch marks and can provide safe and effective reduction in the appearance of both striae rubra i.e.early striae and striae alba i.e. Old striae.

Fractional photothermolysis creates small zones of thermal damage or injury leaving normal skin columns in between.

Injury to the skin initiates cascade of events collectively known as wound healing which includes 3 overlapping stages of inflammation, granulation and remodeling. These sequential events results in to proliferation and deposition of collagen in to the dermis .formation of new micro capillaries in to the affected area and re-epithelization of the affected area. Fibroblast activity gives tensile strength to the wound ultimately the resulting tissue has epidermal thickening, dermal collagen deposits and fibroblasts and microvasculature of the area.

Multiple sittings of fractional co2 along with the topical applications results in to overall improvement of the stiae. Being it an invasive procedure the darker skin types are prone to develop PIH. Gradually due to the epidermal thickening and dermal remodeling with every sitting the skin quality improves.

Conclusion: complete remission of striae is not possible as it is a form of scarring but with treatment the skin condition can be improved up to a great extent. In involves topical treatments as well as procedures. Many treatment modalities have been tried so far. Many of them have been explained earlier in the article, all of them worked on the ailment to some extent.

Fractional co2 lasers emerged as a best treatment modality for improving the overall skin condition as it involves dermal remodeling as well as epidermal thickening both. With repeated sittings and due precaution the results are very satisfactory to the patient. And with proper sun protection the chances of PIH and other possible side effects are minimal.

BEFORE AFTER PICTURES:

Biologics and Biosimilars

Biological therapies

§  are recombinant molecules, derived from the genetic sequences of existing living organisms

§  are often similar or identical to proteins produced  by the human body

§  are generally administered by injection

§  have very specific molecular targets (e.g. receptors, cytokines)

Nomenclature: biologics ending with different words have different meaning suggesting source .

•      Monoclonal antibodies  (mab) .

•      mo = mouse

•      u- human ,

•      xi=chimera ,

•      zu= humanised chimera

•       Immune  = lim

•      miscelleaneous tumor = tu

•      Receptor fusion protein (cept) alefacept

•      Receptor antagonist (ra) anakinara

What is Biopharmaceutical

– A drug created by means of  biotechnology, especially genetic engineering.

– A pharmaceutical inherently biological in nature and manufactured using biotechnology.

How biopharmaceuticals are made?

1.     Develop host cell

2.     Establish a cell bank

3.     Protein production

4.     Purification

5.     Analysis

6.     Formulation

7.     Storage and handling

Development of host cell

  • Identify the human DNA sequence for the desired protein
  • Isolate the DNA sequence
  • Select a vector to carry the gene
  • Insert the gene into the genome of a host (a suitable bacterial or eukaryotic cell)

 

The exact DNA sequence and the type of host cell used will significantly influence the characteristics of the product

Cell bank

  • A cell bank is then established, using an interative and elaborate cell screening and selection process, yielding a unique master cell bank.
  • No two master cell banks are exactly alike.

Making a generic drug is like making a bicycle whereas making a biologic is like making a Ferrari car.

What is biosimilar?

“A biosimilar is a biological product that is highly similar to an already approved biological product, not withstanding minor differences in clinically inactive components, and for which there are no clinically meaningful differences between the biosimilar and the approved biological product in terms of the safety, purity, and potency of the product”

  • Is a medicine which similar to biological /biopharmaceutical medicine that has already been authorized (the biological/ biopharmaceutical reference medicine).
  • The active substance of a biosimilar is similar to the one of biological/ biopharmaceutical reference medicine.

Used in the same dose to treat the same disease

What is the importance of biosimilar?

  • Biopharmaceuticals represent one of the fastest-growing segments of pharmaceutical industry.
  • By 2010 they are expected to represent 50% of the market.
  • Patent of original product expired.
  • Increase opportunity to healthcare services, decrease expenditures.

Biologics v/s Biosimilars

  • Biologics are highly targeted large molecule less side effects
  • Biosimilars follow on biologics2 or similar biological medicinal products
  • Generic version of biologics (Economical)
  • Similar in structure and function to reference products
  • It is similar but not identical

Storage and Handling

  • Biopharmaceuticals are very sensitive to temperature changes and/or shaking.
  • Strict storage and handling conditions are therefore  essential for maintaining product integrity and stability.
  • Poor adherence to (cold) storage requirements can affect clinical efficacy and safety.

Differences in manufacturing

  • The manufacturing process for a biopharmaceutical is far more complex than that for a low molecular weight drug.
  • For biopharmaceuticals, much more than for low molecular weight drugs, the quality of the end product (including therapeutic efficacy and safety) is depended on the manufacturing process.
  • Major hurdle for biosimilar manufacturers is they don’t have access to cell bank, molecular blueprint and data of manufacturing, purification and exact fermentation process that were used to develop original drug
  • Drug is similar but not the copy of existing original drug.

Biologics are driving force in pharma industry

  • 30% new entities are biologics
  • Small molecule growth is declining v/s biologics is increasing
  • Chronic diseases best treated à biologics
  • Under patent
  • Premium pricing
  • High barrier to competition
  • Monoclonal antibodies is fastest growing market in the world.

Problems with biologics

  • Immunogenicity
  • Antibody production
  • Poor response
  • Larger dose needed
  • Costs
  • Infections Tuberculosis
  • Cancers lymphomas

In India following biosimilars are available by different Indian companies

1.Etanercept

2.Rituximab

3.Infliximab

4.Adalimumab

Biologics available in India for dermatologists

1. Omalizumab (Xolair)

2. Secukinumab (Scapho)

3.  Etanercept (Enbrel)

4.  Rituximab (Mabthera)

5 . Infliximab (Remicade)

Summary

  • Biosimilars are effective and are the future
  • Economical  (Biosimilars  costs 1/5th  less of the original )
  • Reducing duration of disease with a better control over it
  • Thus, improving patients Quality  Of  Life