Lack of UV-A Protection In Daily Moisturising Creams

Came across another interesting article in the May edition of ‘The Archives of Dermatology’ 2011. The article is entitled ‘Lack of UV-A Protection In Daily Moisturising Creams’ on page 618. 

 

Ultraviolet radiation (UV) contains UVA, UVB and UVC subtypes. The major source of UV exposure for humans is sunlight. The earths ozone layer blocks approximately 98% of all UV radiation and the 2% which reaches the earths surface 99% is of the UVA subtype. UVB can cause direct DNA damage whereas UVA causes indirect damage of DNA via the formation of free radicals. Therefore it is important any sunscreen solution contains both UVA and UVB filters. 

This article reported the estimated long-range UVA1 protection of 29 creams.

Major points of note from the article include

- Most daily facial creams contain ingredients known as UV filters claiming broad spectrum UV protection.

- Sun protection factor (SPF) doesn’t reflect UV-A1 protection.

- UVA penetrates window glass whereas UVB is blocked, therefore women working indoors need to protect themselves from UVA exposure.

- Of the 29 creams 6 didn’t contain any UVA1 filters.

I recommend reading the full article as it is an interesting read. Below is a link to the article.

Lack of UV-A Protection in Daily Moisturizing Creams
Steven Q. Wang; Jacqueline M. Goulart; Henry W. Lim
Arch Dermatol. 2011;147(5):618-620

 

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Melanoma Research – Sex differences in survival of cutaneous melanoma are age dependent

Came across an interesting article in the latest issue of the Melanoma Research journal regarding differences in survival rates based on sex. It has been previously observed that women have a better survival rate for melanoma than men. This has also been observed in other cancers such as lung adenocarcinoma and colon cancer.

 

The study reveals that the slight survival benefit women with melanoma experience, disappears after the age of 60. This is mirrored, but also conflicts with other studies referenced within the article.

Proposed reasons for this female survival benefit include women being more prudent in the personal examination of the skin, women having a greater percentage of lower limbs melanomas which are associated with a better prognosis and immune gender differences.

Below is a link to the article abstract

http://journals.lww.com/melanomaresearch/Abstract/2011/06000/Sex_differences_in_survival_of_cutaneous_melanoma.11.aspx

 I recommend getting the whole article if it is possible.

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Solar Keratosis and Its Histological Subtypes

Solar keratosis is defined by the World Health Organization as ‘a common intraepidermal neoplasm of sun-damaged skin characterized by variable atypia of keratinocytes.’

Subtypes that are recognised are hypertrophic, atrophic, acantholytic, pigmented. lichenoid and bowenoid. All subtypes usually display the common features of hypogranulosis, parakeratosis along with keratinocyte atypia confined to the bottom two layers of the epidermis (basal and spinous). Below is some of the histological features commonly seen in the subtypes apart from the features mentioned above.

HYPERTROPHIC

This variant exhibits hyperkeratosis, acanthosis, papillomatosis, rete ridge elongation, telangiectasia and parakeratosis. The parakeratosis can be seen alternating with the hyperkeratosis.

ATROPHIC

This variant exhibits epidermal atrophy, basal epidermal budding with adnexal extension.

LICHENOID

This variant exhibits exocytosis, keratinocytic vacuolation, keratinocytic apoptosis, colloid bodies, band-like superficial dermal lymphocytic infiltrate and pigment incontinence.

ACANTHOLYTIC

This variant exhibits acantholysis (with possible extension down adnexae), suprabasal clefting and dyskeratosis.

PIGMENTED

This variant exhibits increased pigmentation of atypical keratinocytes with associated dermal melanophages.

BOWENOID

Although most pathologists consider this Bowen’s disease, some say bowenoid solar keratosis exhibits less than full thickness atypia and sparing of follicles.

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Basal Cell Carcinoma and It’s Histological Growth Types

Basal cell carcinoma (BCC) is the most common skin malignancy and it’s incidence is on the increase. Below is a description of the four main different histological growth types and what is features are associated with each of them.

Superficial

Superficial BCC presents as a scaly, reddish patch ranging in size from a few mm to over 100mm. Due to this clinical appearance there is often confusion with psoriasis. Superficial BCCs are most commonly found on the trunk and account for 10-30% of all BCCs. Histologically they are characterised by superficial collections of atypical basaloid cells projecting from the epidermis or from the sides of adnexal structures such as hair follicles or eccrine ducts. Due to the 2 dimensional processing of histology specimens most superficial BCCs appear multifocal but recent studies using digital imaging techniques show that the tumours nests are actually all interconnected. Truly multifocal superficial BCCs do occur but these are less common. 

Nodular

Nodular BCC most commonly appear as pale, pearly nodules often with macroscopically visible dilated blood vessels coursing over the top of the lesion. Nodular BCCs are most often found on the more sun exposed areas of the body (eg. face and neck). Histologically they are characterised by large, solid lobules of atypical basaloid cells exhibiting a peripheral palisade and often invading as far as the reticular dermis.  Other commons features including the classical BCC retraction artefact and tumour cystic degeneration.

Micronodular

Micronodular BCC most often present as slightly elevated/flat pale lesions. They are most commonly found on the back. Histologically, micronodular BCC appears as an invasive BCC with the tumour islands between 3-10 cells in width (approximately the size of a hair bulb). These smaller tumour islands commonly exhibit perineural invasion. Compared to nodular BCC, the excision margins of micronodular BCC can be more commonly underestimated leading to a higher recurrence rate. 

Infiltrating

Infiltrating BCC presents most commonly as an indurated, pale lesion whose clinical margins appear poorly demarcated. They are mostly found on the face and upper trunk. Histologically they appear as diffuse cords, strands, columns of atypical basaloid cells infiltrating deep into the dermis and that rarely exhibit a retraction artefact or peripheral palisade. Due to the highly diffuse infiltrating nature of this tumour perineural invasion is extremely common therefore recurrences are common. 

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Prognostic Factors of Cutaneous Squamous Cell Carcinoma

Below is a brief description of the prognostic factors involved with cutaneous squamous cell carcinoma, ie. SCC of the skin.

Site

The actual site of the SCC provides much prognostic information, most importantly that SCCs from sites such as the ear, lip and sole have an increased rate of metastasis.

Size

The physical size of the tumour is also related to prognosis, generally speaking the larger the tumour the poorer the prognosis.

Invasion

If the SCC is seen to be invasive this reflects a poorer prognosis. The actual depth of invasion is again prognostic, ie. the deeper the invasion, the poorer the prognosis.

Tumour differentiation

Histologically SCCs are graded for their differentiation with them being either well, moderately or poorly differentiated. The poorer the tumour differentiation, the poorer the prognosis.

Other

There are many other factors which can affect the prognosis of cutaneous squamous cell carcinoma including immune status of the patient, HPV infection status, age and genetic predisposition.

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Melanoma – Prognostic Factors – Quick Overview

Listed below are the most important prognostic factors with regard to cutaneous melanoma.

AGE – the older the patient, the poorer the prognosis.

SEX – generally females have a better prognosis than males.

BODY SITE – melanomas on the extremities (eg. legs and arms) have a better prognosis than those on the neck, trunk and face.

INVOLVEMENT OF LYMPH NODES – presence of tumour lymph node involvement has a poorer prognosis. Generally the more nodes involved the poorer the prognosis.

TUMOUR THICKNESS – the thicker the melanoma the poorer the prognosis.

ULCERATION – the presence of ulceration indicates a poorer prognosis.

MITOTIC RATE – the higher the mitotic rate the poorer the prognosis.

REGRESSION – presence of regression in thin melanomas indicates a poorer prognosis.

There are a few other prognostic factors such as Clarks level, tumour-infiltrating lymphocytes, BRAF mutations and LDH (lactate dehydrogenase) serum level.

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Special Stains for Amyloid - Method and Tips

Amyloid is a common substance found in the skin, in association with a number of disorders including, lichen amyloidosis, macular amyloidosis and also basal cell carcinoma. Amyloid results from the death of cells (apoptosis).

The presence of amyloid maybe diagnostic (as in the case with lichen amyloidosis) or coincidental (as in basal cell carcinoma where its has no prognostic significance). Since the presence of amyloid is sometimes coincidental there is no need to do a special amyloid stain as it would not add any diagnostic value.

Amyloid can sometimes be easily recognised on a standard H+E stain as amorphous eosinophilic material, especially if it is ubiquitous in the sample. If only small amounts of ?amyloid are present (as may be in the case of lichen amyloidosis) this is where the amyloid special stain can come into play. Since the presence of amyloid can make or break the diagnosis the scientist needs to ensure his/her method and technique is up to scratch.

The Congo Red method, which requires light polarizing equipment, seems to remain the gold standard amongst most laboratories with the thioflavin method also popular. I have included below my favoured method for amyloid as is it very quick, only needs light microscopy and produces a very good visual result.


Crystal Violet
1. Sections to water
2. Stain with crystal violet solution (same as one used in Gram stain) for 2 – 3 mins.
3. Wash in water then diff in very weak (~0.2%) acetic acid for about 5 secs.
4. Wash in water and mount using aqueous mounting media
5. If wanted seal coverslip around the edges with nail varnish.

This is a metachromatic stain with the amyloid appearing pink/purple and the surrounding tissue staining purple.

I would invite anyone to submit their favoured amyloid staining technique along with its advantages and disadvantages.

 

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Cutaneous Spindle Cell Tumour Immunohistochemistry Panel

This post is about cutaneous spindle cell tumours and their immunohistochemistry (IHC) profiles. I get many questions from laboratory staff about why we perform certain IHC and in what situations are they used. Since spindle cell tumours require IHC for their correct specific diagnosis I thought I would do a post on them (plus I was also involved in a recent published journal article about this very subject).

Cutaneous spindle cell tumours include atypical fibroxanthoma (AFX), spindle cell melanoma, leiomyosarcoma and spindle squamous cell carcinoma. Why can’t the pathologist diagnose these tumours simply on H+E without the need for IHC? Well, cutaneous spindle cell tumours look extremely similar on H+E and the effects of misdiagnosing a spindle cell melanoma (which obviously is extremely serious) as, for example, an AFX (which has a rather benign, indolent clinical course despite it’s alarming histopathology appearance) can be diastrous for the patient. 

Below is a table which provides an example panel leading to the diagnosis of AFX and the reasons for the use of each particular antibody.

S100 – Negative. Essential to exclude melanoma.  Also highlights Langerhans cells, which can be prominent in some AFX.

Melan A - Negative    Optional, if S100 is negative.

HMB45 – Negative    Optional, if S100 is negative.

Broad spectrum cytokeratin (e.g. MNF116, AE1 & 3) – Negative   Beware of included normal adnexal structures or hyperplastic epidermal downgrowths.

34betaE12 – Negative    Highlights some squamous cell carcinomas more prominently than broad spectrum cytokeratins.

Smooth muscle actin – Positive    ~75% of AFX tumors are positive.

Desmin – Negative    Useful to exclude leiomyosarcoma in actin positive cases.

CD68 – Positive    ~90% of AFX tumors are positive.

CD10 – Positive    Although most AFX are positive, the specificity of this antibody is low, making it of limited discriminatory value.

At a minimum an S100 ( to exclude melanoma), CD68 (positive for AFX), a keratin (preferably 34betaE12 as this stains most spindle squamous cell carcinomas) and desmin (positive for leiomyosarcoma), should be performed on all cutaneous spindle cell tumours. 

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The Need For Greater Education of Medical Scientists in Histopathology Laboratories

As you can tell from the title I am an advocate for the ongoing job-specific training of medical / biomedical scientists in pathology and in particular histopathology (as this is the area of which I am involved).

 

By “job-specific” I really do mean that. My experience with ongoing education of medical scientists within many laboratories involves mainly attending conferences which in fact do provide presentations on many interesting and varying medical subjects but do not translate into increased knowledge within the pathology sector that they are employed. Yet attendance at these conferences do fulfill the “ongoing education” condition of governing accreditation bodies. For example a conference attended by this author attended by many medical scientists of employed over all the different disciplines (eg. histology, microbiology, haematology), had many interesting talks (eg. the effect of a local major natural disaster and the providing of medical assistance from neighbouring countries), but he could not see how these talks would translate to increased laboratory knowledge beneficial to the conference attendee. 

It appears to this author that there is very limited opportunities offered to pathology laboratory employees which in turn is resulting in these employees not possessing an ever-growing knowledge base of their chosen discipline. Another example observed by this author is the huge majority of histopathology scientists not being able to recognise the simplest of skin tumours histologically (eg. BCC, SCC, melanoma), which is the ‘bread and butter’ of skin pathology.

What is the purpose of scientists being able to recognise tumours histologically I hear you say? If scientists can recognise these simplest of tumours, this talent can be put to a number of uses including cutting deeper levels on initial sections that are non-diagnostic before the initial sections are given to the pathologist thus increasing the efficiency of reporting. This example of course depends on the confidence of the pathologist to trust the scientist to recognise a case that requires deeper levels. 

Thank you very much for reading this post and hopefully you found it of interest.

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