Solar lentigo

What is solar lentigo?

Solar lentigo is a harmless patch of darkened skin. It results from exposure to ultraviolet (UV) radiation, which causes local proliferation of melanocytes and accumulation of melanin within the skin cells (keratinocytes). Solar lentigos or lentigines are very common, especially in people over the age of 40 years. Sometimes they are also known as an “old age spot” or “senile freckle”.

What does a solar lentigo look like?

A solar lentigo is a flat, well-circumscribed patch. It can be round, oval or irregular in shape. Colour varies from skin-coloured, tan to dark brown or black, and size varies from a few millimetres to several centimetres in diameter. They can be slightly scaly.

Solar lentigines are found as groups of similar lesions on sun-exposed sites, particularly the face or the back of hands. They occur in light and dark skin but tend to be more numerous in fair-skinned individuals. Solar lentigines may be seen in younger patients often following an acute episode of sunburn

They are commonly on face in younger patients and they appear on face, back of hand and forearms in older person.

Solar lentigo

 


 


 


 

 


 


 


 


How is a solar lentigo diagnosed?

Solar lentigo is often diagnosed on its clinical appearance. On occasion, it can be difficult to differentiate an irregular solar lentigo from melanoma, a potentially dangerous form of skin cancer, and the term atypical solar lentigo may be used.

Examination using dermatoscopy can clarify the diagnosis. If there is still diagnostic doubt, a skin biopsy may be performed for histological examination.

Dermatoscopic features

  • Shows homogenous pattern & colouration with commonly has a particular “moth-eaten” or “Jelly-like” edge.
  • They can show diffuse colouration with circular hypopigmented follicular openings, called pseudo-network (like in seborrheic keratosis)


Histological features of solar lentigo

There is linear increase in melanocytes at the dermo-epidermal junction with extension of rete ridges to form bud-like processes. There is increased deposition of melanin in the basal keratinocytes. Sometimes there are large melanocytes that are monomorphous, equidistant from one another and unassociated with nests of melanocytes. Solar elastosis is present in the papillary dermis, with or without incontinence of pigment (melanophages).


Changes within solar lentigo

Seborrheic keratoses may arise within solar lentigines. This results in localised thickening and change in texture within the lentigo.

Solar lentigines may become inflamed, when they are called lichenoid keratoses or lichen-planus like keratoses (due to the pattern of inflammation seen on histopathology). Lichenoid keratoses gradually disappear.

Clinical differential diagnosis:

lentigo maligna may be clinically mistaken as solar lentigo especially on face as they may show the same features: regular & homogenous appearance, small size, lacking the ABCD signs of malignancy.

Dermatocopy is helpful in this distinction. Dermatoscopic features of lentigo maligna include asymmetrical pigmented follicular openings, and slate-grey aggregated dots around the hair follicles proceeding to dark-brown or black streaks.

What treatments are available for solar lentigo?

If left untreated, solar lentigo will most likely persist indefinitely. Cryotherapy and laser surgery can destroy them, but treatment may leave a temporary or permanent white or dark mark.

Bleaching agents such as hydroquinone are not effective.

Preventative measures include minimizing sun exposure and use of sunscreens, but this needs to start early in life.

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This photo/content belongs to DermNet and the use of this photo/content is in accordance with DermNet’s Creative Commons Attribution-NonCommercial-NoDerivs 3.0 (New Zealand) Licence, available here. No changes were made to this photo/content. Dermnet does not endorse any changes made to photo / content. 
For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Neurofibroma

Neurofibroma:

Relatively common benign peripheral nerve sheath tumour composed of a mixed population of Schwann cells, fibroblasts, and perineurial or perineurial-like cells, with scattered intermingled axons.
It is most often a sporadic tumour, but it can also occur as manifestation of the genetic syndrome Neurofibromatosis (NF1).

Neurofibromas may assume one of three growth patterns: localized, diffuse, or plexiform. The localized form is seen most commonly as a superficial, solitary tumour in normal individuals. Diffuse and plexiform neurofibromas have a close association with NF1, the latter being nearly pathognomonic of the disease.

Localized Neurofibroma

Localized neurofibroma is usually a painless cutaneous nodule or polypoid lesion presenting in adulthood and affect the genders equally. Although usually solitary, neurofibromas can occasionally be multiple; this occurrence does not necessarily imply a diagnosis of

NF1.

The anatomic distribution of localized neurofibroma is wide, because it can involve nerves of any size and any location, including deep soft tissues and viscera. Deep-seated tumours are more often associated with Neurofibromatosis 1 (NF1) and carry a small risk of malignant transformation that is absent, or negligible, in small superficial lesions

Localized cutaneous neurofibromas
are small, well delineated but unencapsulated nodular lesions that arise in the dermis and subcutaneous fat. They have relatively low cellularity and. adnexal structures are sometimes entrapped at the edges of the lesion.

Diffuse Neurofibroma

Diffuse neurofibroma is uncommon but clinically distinctive variant that usually presents in young adults as an ill-defined plaque of subcutaneous and dermal thickening, most commonly in the trunk or head and neck area. The lesion tends to be large and sometimes disfiguring. The risk of malignant transformation is minimal. The association with NF1 is variable.

This tumour has morphologic features similar to those seen in localized cutaneous neurofibromas, but exhibits a distinctly different growth pattern. The tumour diffusely infiltrates the dermis and subcutaneous connective tissue, entrapping fat and appendage structures and producing a plaque-like appearance. Some of these neurofibromas can grow to large sizes. Focal collections of cells mimicking the appearance of Meissner corpuscles (so-called pseudo- Meissner corpuscles or tactile-like bodies) are an associated feature.

Plexiform neurofibroma

Is essentially diagnostic of NF1, affecting 20% to 40% of patients with this syndrome.
It is defined by its growth pattern, consisting of multiple tortuous cords and nodules of variable size that correspond to nerve fascicles replaced and expanded by neurofibromatous tissue. The lesions most often present in children, and they may be deep but are more often superficial.

Neurofibroma in Neurofibromatosis

Any histologic type of neurofibroma can be found in patients with NF1. Such a neurofibroma should be carefully followed clinically and with imaging techniques to intervene in case of malignant transformation.

Numerous cutaneous localized neurofibromas are the hallmark of NF1. However, several localized neurofibromas can occur sporadically and occasionally in some individuals with NF2.

Large deep localized neurofibromas may also rarely be sporadic, but these should raise the possibility of NF1 and prompt a detailed clinical evaluation of the patient. With very rare exceptions, plexiform neurofibroma is only seen in patients with NF1.

Malignant Transformation in Neurofibroma

The risk of malignant transformation is variable for different forms of neurofibroma. Localized cutaneous neurofibroma almost never undergoes malignant transformation, and diffuse neurofibroma only rarely does so. When a residual neurofibroma is identified adjacent to Malignant peripheral nerve sheath tumour (MPNST) from a patient with NF1, it is usually either a plexiform neurofibroma or a localized intraneural neurofibroma involving a large or

medium-sized nerve or nerve plexus.

Malignant transformation of neurofibromas in NF1 is associated with constitutive activation of RAS proteins
and inactivation of p16 through homozygous deletion of CDKN2A.
At the gene expression level, malignant transformation from neurofibroma to MPNST is associated with loss of expression of a large number of genes and dysregulation of microRNAs involved in the p53 pathway such as miR-34a


Neurofibroma


Plexiform neurofibroma

References:

  • Practical Soft Tissue Pathology by Jason L. Hornick, MD, PhD
  • Enzinger and Weiss’s Soft Tissue Tumours, 5th Edition by Sharon W. Weiss MDJohn R. Goldblum MD FCAP FASCP FACG , Andrew L. Folpe MD
  • Robbins & Cotran Pathologic Basis of Disease, 9th Edition By Vinay Kumar, MBBS, MD, FRCPath, Abul K. Abbas, MBBS and Jon C. Aster, MD, PhD
  • DermNet NZ (images)

Attribution:
This photo/content belongs to DermNet and the use of this photo/content is in accordance with DermNet’s Creative Commons Attribution-NonCommercial-NoDerivs 3.0 (New Zealand) Licence, available here. No changes were made to this photo/content. Dermnet does not endorse any changes made to photo / content.
For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/