Videodermoscopy Evaluation in Non-scarring Alopecia of Scalp Part-2

Dr.

Dr.

$ 6 cells (50.0%) have expected count less than 5. ^ Column data pooled and Chi-Square Test reapplied.

$ 6 cells (50.0%) have expected count less than 5. ^ Column data pooled and Chi-Square Test reapplied.

Table 8: Association of Brown Peripilar Sign among the cases between- Alopecia areata, Androgenetic alopecia and Telogen effluvium groups

$ 5 cells (41.7%) have expected count less than 5. ^ Column data pooled and Chi-Square Test reapplied.

In our study alopecia areata 93.3% had yellow dots and 6.7%. In alopecia areata subjects 50% had black dots. In alopecia areata 56.6% had small vellous hairs. In Alopecia areata 60% of the subjects had exclamation mark hair. In alopecia areata 16.6% had brown peripilar sign.

In another study byLacarrubba F et al the first group consisted of 200 patients affected by acute (140 patients) and chronic (60 patients) AA, and the second group of 100 patients affected by AGA. In both groups, the clinical diagnosis was confirmed by pull tests and trichograms. The third group consisted of 50 patients with clinically undifferentiated hair loss. In all groups, videodermatoscopy was performed at magnifications ranging from 20x to 600x.[13,14,15]

In our study alopecia areata 93.3% had yellow dots and 6.7%. In alopecia areata subjects 50% had black dots. In alopecia areata 56.6% had small vellous hairs. In Alopecia areata 60% of the subjects had exclamation mark hair. In alopecia areata 16.6% had brown peripilar sign.

In another study by Lacarrubba F et al the first group consisted of 200 patients affected by acute (140 patients) and chronic (60 patients) AA, and the second group of 100 patients affected by AGA. In both groups, the clinical diagnosis was confirmed by pull tests and trichograms. The third group consisted of 50 patients with clinically undifferentiated hair loss. In all groups, videodermatoscopy was performed at magnifications ranging from 20x to 600x.[13,14,15]

The study results in acute AA (n = 140), three videodermatoscopy patterns were identified, characterized by: (i). 'exclamation point' and/or 'cadaveric' hairs (n = 62); (ii). 'vellus' hairs, in some cases with increased proximal shaft thickness and pigmentation (n = 38); and (iii). coexistence of all the features from (i). and (ii). [n = 40]. In chronic AA (n = 60), in those cases who were recently converted to chronic form from acute AA (n = 35), videodermatoscopy showed a scalp skin that appeared smooth and thin, with evident follicular openings. In cases of long-standing chronic AA (n = 25), hair follicle openings appeared to be obstructed by keratotic plugs. However, whether the two follicular patterns were related to disease duration or to some unknown factors is unclear. In some patients with chronic AA, videodermatoscopy also revealed hair regrowth, which appeared either as homogeneous, indicating early disease remission (upright

'vellus' hairs), or as sparse, thin, and twisted vellus hairs that were usually lost in a few weeks time. In AGA patients, videodermatoscopy observation allowed an accurate assessment of the ratios of miniaturized to normal hairs, a finding that was interpreted as a prognostic feature. Interestingly, videodermatoscopy clearly demonstrated the hair abnormalities corresponding to both diseases in those patients with concomitant causes of hair loss, as we observed in five patients simultaneously affected by AA and AGA. In the third group, videodermatoscopy allowed identification of early or minimal forms of AA (n = 20), AGA with mild hair loss of the centro-parietal area of the scalp (n = 20), and scarring alopecia (n = 10).

The study concluded that the results indicate that videodermatoscopy represents a very useful tool in the evaluation of hair loss, both for differential diagnosis (especially in early, transitional and mild forms) and for prognostic evaluation. It allows rapid, detailed, and noninvasive observation of the scalp skin and hair, and it provides highresolution quality imaging.

In our study a total of 140 subjects were studied, 30 alopecia areata, 40 androgenetic alopecia, 30 telogen effluvium and 40 controls.

Of the total 140 subjects, the cases were divided into alopecia areata 30 (21.4%), androgenetic alopecia 40 (28.6%), telogen effluvium 30 (21.4%) and control cases 40(28.6%).

In alopecia areata 93.3% had yellow dots. In androgenetic alopecia 57.5% had yellow dots. In telogen effluvium 16.7% had yellow dots. In controls 7.5% had yellow dots.

In alopecia areata subjects 50% had black dots. In androgenetic alopecia 5% had black dots. In telogen effluvium and controls none of the subjects had black dots. The p-value was significant with a value of 5.64E-08 where E stands for 10 to the power of minus.

In alopecia areata 56.6% had small vellous hairs. Androgenetic alopecia and telogen effluvium did not have any significant association with the small vellous hairs.

In alopecia areata 60% of the subjects had exclamation mark hair. Exclamation mark hair was not seen in androgenetic alopecia, telogen effluvium and control subjects. p-value was significant with a value of 7.55E-12 (where E stands for 10 to the power of minus) showing a clear relationship of alopecia areata and exclamation mark hairs.

In another study by Inui S, Itami S et al dermoscopic examination of areas of hair loss on the scalp of 300 Asian patients with AA was performed using a DermLite II pro, which can block light reflection from the skin surface without immersion gels. Using the Spearman rankorder correlation coefficient by rank test, correlations between the incidence of each dermoscopic finding and the severity of disease and disease activity were examined. The sensitivity and specificity of the findings as diagnostic clues for AA were evaluated.[16]

The results showed characteristic dermoscopic findings of AA included black dots, tapering hairs, broken hairs, yellow dots, and clustered short vellus hairs (shorter than 10 mm) in the areas of hair loss. Black dots, yellow dots, and short vellus hairs correlated with the severity of disease, and black dots, tapering hairs, broken hairs, and short vellus hairs correlated with disease activity. For diagnosis, yellow dots and short vellus hairs were the most sensitive markers, and black dots, tapering hairs, and broken hairs were the most specific markers.

It was concluded in the study that dermoscopic characteristics, such as black dots, tapering hairs, broken hairs, yellow dots, and clustered short vellus hairs, are useful clinical indicators for AA.

In another study by Ihm w et al it was shown that exclamation mark (EM) hair can lead to the misdiagnosis of alopecia areata (AA) because it is widely considered as pathognomonic for AA. Typical EM hairs were also found in trichotillomania. EM hairs collected from 2 cases of trichotillomania and 9 cases of AA were compared under light microscopy. There were two sorts of EM hairs, one with frayed distal ends and the other with blunt distal ends. The majority (77.8%) of the EM hairs from AA had frayed distal ends, while the majority (82.2%) of that from trichotillomania had blunt distal ends. EM hairs, even with frayed distal ends, are not pathognomonic of AA.[17]

In our study in alopecia areata 60% of the subjects had exclamation mark hair. Exclamation mark hair was not seen in androgenetic alopecia, telogen effluvium and control subjects. p-value was significant with a value of 7.55E12 (where E stands for 10 to the power of minus) showing a clear relationship of alopecia areata and exclamation mark hairs.

In another study by Ozlem Karadag Kose et al 144 subjects of alopecia were involved with similar control subjects. The follicular features showed yellow dots, black dots, and broken hairs that was significantly more common in AA than in the other alopecias. Tapering hairs were detected only in AA. Short vellus hairs were noted in all types of alopecia, without a significant difference in frequency. Circular hairs and trichorrhexis nodosa were observed in AA or PCAs without a significant difference between the two groups. Hair diameter diversity was found in all subjects with AGA, and was significantly more common in this group than the others. Empty follicles, and peripilar sign were noted only in AGA. In AGA yellow dots were seen in 30.5%, black dots in 1.7%, hair diameter diversity in 100% of the patient’s empty follicles in 52.5% and peripilar sign in 59.3% white dots were seen in 15.3% of the patients. In AA yellow dots were seen in 83.7%, black dots in 63.3%, tapering hairs in 42.9%, broken hairs in 57.1%, short vellous hairs in 46.9% and hair diameter diversity in 32.7%. In telogen effluvium yellow dots were seen in 21.1%, short vellous hairs were seen in 47.7% and hair diameter diversity were seen in 10.5%. Black dots, tapering hairs and broken hairs were not seen in telogen effluvium. [8,18]

In our study alopecia areata 93.3% had yellow dots. In alopecia areata subjects 50% had black dots and 56.6% had small vellous hairs. In alopecia areata 60% of the subjects had exclamation mark hair. In alopecia areata 16.6% had brown peripilar sign.

In our study brown peripilar sign were seen in androgenetic alopecia in 95% of subjects compared to 42.5% in control volunteers, 43.3% in telogen effluvium and 16.6% in alopecia areata, showing a significant association of brown peripilar sign in androgenetic alopecia. Yellow dots were seen in alopecia areata in 93.3%. In androgenetic alopecia 57.5% had yellow dots. In telogen effluvium 16.7% had yellow dots. In controls

7.5% had yellow dots.

In another study Inui S the characteristic trichoscopic features of common hair loss diseases are described using a DermLite II pro or Epilight eight. Characteristic trichoscopic features of alopecia areata are black dots, tapering hairs (exclamation mark hairs), broken hairs, yellow dots and short vellus hairs. In androgenetic alopecia (AGA), hair diameter diversity (HDD), perifollicular pigmentation/ peripilar sign and yellow dots are trichoscopically observed. In all cases of AGA and female AGA, HDD more than 20%, which corresponds to vellus transformation, can be seen. In cicatricial alopecia (CA), the loss of orifices, a hallmark of CA, and the associated changes including perifollicular erythema or scale and hair tufting were observed. Finally, an algorithmic method for trichoscopic diagnosing is proposed.[4]

In our study a videodermoscope of 50*magnification from medicam company with a LED light and connectable to the computer hard disk drive with a USB cable through which videodermoscopic pictures can be recorded is used.

In another study by Rakowska A et al female androgenetic alopecia and telogen effluvium was studied. They compared to the healthy controls, hair thickness of patients with female AGA was significantly reduced in the frontal, occipital left temporal and right temporal area. The largest percentage of thin hairs was observed in female AGA in frontal area (20.9 + 12%) and it was significantly different compared to patients with telogen effluvium (10.4+ 3.9%) and healthy volunteers (6.15+ 4.6%, p<0.001).

The percentage of single-hair, double-hair and triple-hair units was evaluated. In patients with female AGA the mean percentage of single-hair pilosebaceous units was highest in the frontal area (65.2+ 19.9%). This was significantly more than in telogen effluvium (39.0 + 13.4%, p< 0.001) and healthy controls (27.3 + 13%, p<0.001).

Perifol liculardis coloration was significantly more often in female AGA as compared to healthy controls or patients with chronic telogen effluvium. The mean percentage of hair follicles with surrounding disco louration in female AGA was 32.4+4.7% in the frontal area and 6.6+2% in the occipital area p<0.001.[19]

In another study by Inui S, Nakajima T et al, they investigated the dermoscopic features and their incidence of androgenetic alopecia (AGA; n = 50 men) and female AGA (FAGA; n = 10 women) in Asian people. More than 20% hair diameter diversity (HDD), which reportedly is an early sign of AGA and corresponds to hair follicle miniaturization, was observed in the affected area of all AGA and FAGA cases, suggesting that HDD is an essential feature to diagnose AGA and FAGA. Peripilar signs, corresponding to perifollicular pigmentation, were seen in 66% (33/50) of AGA and 20% (2/10) of FAGA women. This incidence in the present study was lower than previously reported in white subjects possibly because the Asian skin color conceals slight peripilar pigmentation. Yellow dots were observed in 26% (13/50) of AGA and 10% (1/10) of FAGA cases and the number of yellow dots in AGA and FAGA was limited to 10 on the overall hair loss area. Yellow dots possibly indicate the coincidence of AGA and enlargement of the sebaceous glands caused by common end-organ hypersensitivity to androgen. In conclusion, dermoscopy is useful to diagnose

AGA and FAGA and provides insights into the pathogenesis of AGA.[20]

In our study brown peripilar sign were seen in androgenetic alopecia in 95% of subjects compared to 42.5% in control volunteers, 43.3% in telogen effluvium and 16.6% in alopecia areata, showing a significant association of brown peripilar sign in androgenetic alopecia. Yellow dots were seen in alopecia areata in 93.3%. In androgenetic alopecia 57.5% had yellow dots. In telogen effluvium 16.7% had yellow dots. In androgenetic alopecia 95% had brown peripilar sign compared to 42.5% in controls, 16.6% in alopecia areata and 43.3% in telogen effluvium. In controls 7.5% had yellow dots. P–Value was significant with a value of 6.37E where E stands for 10 to the power of minus. Relationship of yellow dots was 93.3% in alopecia areata and 7.5% in control subjects.

Conclusion

Videodermoscopy is an effective non-invasive tool of considerable potential in dermatological practice. It is gaining popularity as an accessory tool in differential diagnosis of hair loss. videodermoscopy has proved to represent a useful tool for differentiating between different types of alopecia, thus avoiding scalp biopsy in most of the cases, which is particularly important in patient compliance. Use of videodermoscopy in the clinical evaluation of scalp and hair disorders improves diagnostic capability beyond simple clinical inspection and reveals novel features of disease, which may extend clinical and pathogenetic understanding. Nowadays, they represent an important and relatively simple aid in daily clinical practice.

Financial support and sponsorship

Nil

Conflicts of interest

There are no conflicts of interest.

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Common fatty acid contributes to temperature and pain sensitivity in psoriasis plaques

Psoriasis is a chronic autoimmune skin condition that causes cells to build up rapidly on the surface of the skin. The excess skin cells form scales and red patches that are sometimes itchy and painful. The exact cause of psoriasis is unknown, but it is believed to involve a combination of genetic and environmental factors.

According the recent study findings showed a common fatty acid found in the western diet breaks down into compounds that contribute to increased temperature and pain but not itch sensitivity in psoriatic lesions. The finding could lead to better understanding of how lipids communicate with sensory neurons, and potentially to improved pain and sensitivity treatments for psoriasis patients. Linoleic acid is a fatty acid found in vegetable oils, nuts and seeds, and is one of the predominant fatty acids found in the western diet. Metabolites from linoleic acid - the products formed when the body breaks it down through digestion - play a role in skin barrier function.

The researchers noticed high levels of two types of lipids derived from linoleic acid in psoriatic lesions. That led us to wonder whether the lipids might affect how sensory neurons in these lesions communicate. They decided to investigate whether their presence could be related to the temperature or pain hypersensitivity that many psoriasis patients report. The research team used mass spectrometry to create lipid profiles of skin from psoriatic lesions. They focused on two types of linoleic acid-derived lipids, or oxylipids: 13-hydroxy-9,10-epoxy octadecenoate (9,13-EHL) and 9,10,13-trihydroxy-octadecenoate (9,10,13-THL). The first form, 9, 13-EHL, can convert into the more stable 9,10,13-THL form via interaction with certain enzymes.

The researchers found that while both forms bind to receptors on sensory neurons within the skin, the more stable form -9,10,13-THL - had a longer lasting effect than 9,13-EHL. They also found that once the lipids bind to the neuronal receptor, they activate the neurons expressing TRPA1 and TRPV1 receptors that are involved in temperature and pain hypersensitivity, opening communications channels to the central nervous system. Interestingly, the lipids did not have any effect on itch. It was surprising that these lipids could create hypersensitivity but not impact itch sensation, which is usually the most troublesome symptom associated with psoriasis. This most likely has to do with how the neuron is activated - a mechanism we still haven't uncovered. Now that an association between linoleic acid and hypersensitivity to temperature and pain has been established, the researchers want to further explore exactly how this response is being created. They hope that the answers may lead to solutions that can relieve these symptoms in psoriasis patients.

Researchers know that this lipid moves from one form to another, but don't yet know what causes that. They also know what protein the lipids are binding to, but not where the bond occurs. Answering these questions may hopefully lead to new therapies -or dietary solutions -for some psoriasis sufferers.

In cells, UV-emitting nail polish dryers damage DNA and cause mutations

The ultraviolet nail polish drying devices used to cure gel manicures may pose more of a public health concern than previously thought. Researchers studied these ultraviolet (UV) light-emitting devices, and found that their use leads to cell death and cancer-causing mutations in human cells. The devices are a common fixture in nail salons, and generally use a particular spectrum of UV light (340-395nm) to cure the chemicals used in gel manicures. While tanning beds use a different spectrum of UV light (280-400nm) that studies have conclusively proven to be carcinogenic, the spectrum used in the nail dryers has not been well studied.

If we look at the way these devices are presented, they are marketed as safe, with nothing to be concerned about. But to the best of our knowledge, no one has actually studied these devices and how they affect human cells at the molecular and cellular levels until now.

Using three different cell lines -adult human skin keratinocytes, human foreskin fibroblasts, and mouse embryonic fibroblasts - the researchers found that the use of these UV emitting devices for just one 20-minute session led to between 20 and 30 percent cell death, while three consecutive 20-minute exposures caused between 65 and 70 percent of the exposed cells to die. Exposure to the UV light also caused mitochondrial and DNA damage in the remaining cells and resulted in mutations with patterns that can be observed in skin cancer in humans.

Researchers saw multiple things: first, they saw that DNA gets damaged, they also saw that some of the DNA damage does not get repaired over time, and it does lead to mutations after every exposure with a UV-nail polish dryer. Lastly, they saw that exposure may cause mitochondrial dysfunction, which may also result in additional mutations. Researchers looked at patients with skin cancers, and we see the exact same patterns of mutations in these patients that were seen in the irradiated cells.

The researchers caution that, while the results show the harmful effects of the repeated use of these devices on human cells, a long-term epidemiological study would be required before stating conclusively that using these machines leads to an increased risk of skin cancers. However, the results of the study were clear: the chronic use of these nail polish drying machines is damaging to human cells.