Sunday, 28 December 2014

Pityriasis versicolor: Regaining the lost pigmentation



Among the metabolites the Malassezia synthesizes is pityriacitrin that absorbs ultraviolet (UV) light. The hypopigmentation is accentuated if the surrounding unaffected skin becomes tanned. 

Patients should be informed that the hypopigmentation will take time to resolve and is not a sign of treatment failure.  Repigmentation may take several months even when the organisms have been destroyed. After the fungal disease is cured, an effort can be made to regain the lost pigmentation through UV light exposurePrevention of recurrence is also important. 









The patient chose to shorten the time needed for repigmentation by receiving UV light sessions. 



This page was last updated in December 2014

Monday, 15 December 2014

Friday Meetings: Friday 27/2/2015




Friday 27/2/15 4 pm Cairo Time Google Plus Hangout

Discussion of cases in Dermato-Venereology  


We resumed the meeting in another Google Hangout Room (because of electricity problem in 6 October City, Egypt). 


Free talks via Google Hangout on Fridays have been arranged. These Friday Meetings have been audiovisual online meetings where we have typed, talked and screen shared. The Handouts, when available, can be emailed on request unless they become out-of-date. 

Similarly, Thursday Meetings have been developed to discuss Rook's Textbook of Dermatology on Google Hangout

Friday, 7 November 2014

Lichen nitidus pathogenesis



Once considered a tuberculoid reaction, lichen nitidus (Latin nitidus, shiny) is currently regarded as a disorder of unknown aetiology. However, history of exposure to tuberculosis in the “setting of lichen nitidus” should be investigated and when appropriate antituberculosis treatment is initiated.  Actually, lichen nitidus needs to be distinguished from lichen scrofulosorum. While the infiltrate in lichen nitidus ‘hugs’ the epidermis and expands the dermal papilla, the granulomas in lichen scrofulosorum do not cause widening of the papillae. Furthermore, in lichen scrofulosorum, there may be mild spongiosis and exocytosis of neutrophils into the epidermis and the granulomas are typically centred on the hair follicles or sweat ducts.

An “allergen” may cause antigen-presenting cells to activate a cell-mediate response, initiate lymphocyte accumulation, and form the discrete papules.  Actually, Langerhans cells are present in large numbers in the infiltrate. Cytokines may shift the T lymphocyte response towards the T helper (CD4+) 2 subset that has the potential to produce the superficial dermal granulomas seen in lichen nitidus (in comparison, CD8+ lymphocytes play an important role in lichen planus (LP) where there are no granulomas). At each lateral margin of the infiltrate, rete ridges tend to extend downwards and seem to clutch the infiltrate in the manner of a claw clutching a ballDirect immunofluorescence examination of lichen nitidus is usually negative (in comparison, direct immunofluorescence examination of LP shows colloid bodies in the papillary dermis, staining for complement and immunoglobulins, particularly IgM. An irregular band of fibrin is present along the basal layer in most cases. Often there is irregular extension of the fibrin into the underlying papillary dermis).


Lichen nitidus eruption is found on any part of the body but the sites of predilection are the forearms, penis, abdomen, chest and buttocks

Early, tiny LP papules may be clinically and histopathologically indistinguishable from lichen nitidus. Coexistence with LP is common. It might also be associated with atopic dermatitis.

It has been suggested that cases reported in the past as summertime actinic lichenoid eruption (SALE) should be reclassified as actinic lichen nitidus, also called “pinpoint, papular polymorphous light eruption” (PMLE).

Lichen nitidus has followed hepatitis B vaccine and appeared during treatment of hepatitis with interferon-α.

There is not usually an associated systemic condition but associations with some conditions such as Down’s syndrome have been reported. Functional impairment in cellular immunity has been reported in generalised lichen nitidus and lichenoid photo-eruption similar to lichen nitidus has been associated with HIV infection.

Köbner’s phenomenon might occur. Perforating lichen nitidus has been described.


No genetic factors of the disease have been identified; however, familial presentation might be seen. Most cases occur in children or young adults. Its course is unpredictable; it may clear in a few weeks or last a very long time, and may show little or no response to treatment.






Lichen nitidus following hepatitis B vaccine



The lesions are minute shiny flesh coloured papules but can be reddish with various tints. 


This page was last updated in March 2017

Saturday, 11 October 2014

Herald patch



A herald is a sign that something is soon going to happen and the herald patch (mother patch) of pityriasis rosea is a solitary larger and more conspicuous patch that precedes other patches. The herald patch and the succeeding patches are similar histopathologically (mild psoriasiform hyperplasia; spongiosis and exocytosis of lymphocytes leading to ‘mini-Pautrier simulants’ simulating Pautrier microabscesses because of the aggregation of lymphocytes; focal parakeratosis). The interval is usually a week or so, but may be as short as a few hours or as long as 2 months.  This is a characteristic evolutionary sequence seen in this skin condition that is believed to be due to reactivation of HHV-6 and/or HHV-7. The incidence is highest between the ages of 15 and 40, and the disease is most prevalent in the spring and autumn/winter. Females are more frequently affected than males. The herald patch is absent or undetected in about 20% of cases. Rarely, there may be more than one herald patch. The mother patch may be the sole manifestation of the disease! The reported epidemiological evidence for infectivity of pityriasis rosea includes occasional family or household outbreaks, seasonal and year-to-year fluctuations and statistical evidence for clustering in space and time. Interestingly, clusters of cases of herpes zoster have also been reported, and it is suggested that exposure to exogenous varicella zoster virus may trigger reactivation of latent virus in such circumstances.


The herald patch is a sharply defined oval or round salmon-red patch or slightly raised plaque with a marginal collarette of scale attached inside the periphery, with the free edge of the scale internally. Actually, the word collarette is used because the scale is attached inside the periphery and loose towards the centre of the lesion. The herald patch rapidly reaches its maximum size, usually 2–5 cm in diameter but occasionally much larger. The scales are silvery grey. The centre tends to clear and assumes a tawny colour. When stretched across the long axis, the scale tends to fold across the line of stretch, the “hanging curtain” sign. The herald patch is usually on the thigh or upper arm, the trunk, suprapubic skin, the groin or the neck; rarely may it be on the face, scalp or the penis.


The succeeding patches (resembling the mother patch or being non-scaly) begin to appear in crops at 2 to 3-day intervals over a week or so. Less often, new lesions continue to develop for several weeks. The long axes of the lesions characteristically are parallel to the ribs on the upper chest and back. There may be slight or moderate itching. The eruption is usually generalized, affecting chiefly the trunk and sparing sun-exposed surfaces but involvement of the face and scalp is quite common, especially in children. Palms and soles are rarely involved. The eruption may be limited to a few lesions, often around the herald patch. At times, the eruption is confined to a single region, or may be maximal on the extremities almost sparing the trunk.  An inverse distribution, sparing covered areas, is not rare. Unilateral pityriasis rosea has been reported. When irritated lesions my develop vesicles simulating erythema multiforme (pityriasis rosea irritata). 














Although pityriasis rosea is twice as common in black individuals as white, the same seasonal peaks and preceding herald patch occur. However, in black skin, individual lesions are smaller and more papular (micropapular) often urticated and may even be vesicular. An inverse distribution of pityriasis rosea is more frequent in black skin and involvement of the face is seen in 30%, especially in children. The scalp is also more often affected. Lesions in black patients tend to be quite itchy and are more persistent.


Chuh has drawn up a list of diagnostic criteria for pityriasis rosea. Essential features for the diagnosis include: (i) discrete circular or oval lesions; (ii) scaling on most lesions; and (iii) collarette scaling with central clearance of at least two lesions. Optional clinical features of which one must also be present include: (i) truncal and proximal limb distribution, with less than 10% of lesions distal to the mid-upper arm and mid thigh; (ii) distribution of most lesions along the ribs; and (iii) a herald patch appearing at least 2 days before the generalized eruption. Histopathological features were not added to the criteria, being relatively non-specific. However, Weedon states that histopathological features are sufficiently characteristic to allow the diagnosis to be made. Moreover, histopathological evaluation can be especially helpful in excluding the conditions with which pityriasis rosea may be confused.


Without treatment, the disease duration usually varies between 4 and 10 weeks. A few persist for as long as 3 months. A longer duration, except in localized forms, is very unusual. There may be temporary hyper- or hypopigmentation, but usually the lesions vanish without trace. Postinflammatory hyperpigmentation occurs in almost half of black patients, but hypopigmentation may also occur.  Rarely, a partial or complete relapse of a fading pityriasis rosea may be seen. Second attacks occur in about 2% of cases. Pityriasis rosea during pregnancy is of concern (miscarriages and premature deliveries have been reported). 


Pityriasis rosea may be atypical in the appearance or distribution of the lesions or in its course. Examples include erythema multiforme-like variants, classic lesions admixed with follicular papules or purpura, and papular pityriasis rosea (absent herald patch). Thus the diagnosis can be challenging.  In the typical, fully developed case, the diagnosis is usually straightforward, as the distribution, morphology and the usual absence of constitutional symptoms are sufficiently distinctive. In pityriasis circinata et marginata of Vidal, sometimes regarded as a special form of pityriasis rosea and seen mainly in adults, the lesions are few and large, and are often localized to one region of the body, especially the axillae or groins. They tend to become confluent and may persist for several months. This form may follow a typical generalized pityriasis rosea, but it usually occurs alone. Pityriasis rosea might mimic other viral exanthema. Ackerman used to propose that pityriasis rosea and erythema annulare centrifugum are clinical variations of a single pathological process, and that pityriasis rosea gigantea is pityriasis rosea concurrent with erythema annulare centrifugum.


Seborrhoeic dermatitis may be pityriasiform (pityriasiform type of seborrhoeic dermatitis). There is no herald patch. The lesions often develop slowly and the are more widely distributed; being most numerous on the upper trunk near the midline, on the neck and in the scalp, and they are duller in colour with thicker and greasier scales. Small, scaly, follicular papules may also be present. The eruption is persistent if untreated.


The usual absence of lymphadenopathy, and infrequent mucous membrane lesions help to distinguish pityriasis rosea from secondary syphilis (useful points: remains of a chancre might be seen/history of chancre - no herald patch - roseolar or maculopapular lesions assume a brownish tint with palmoplantar involvement - condylomata lata - mucous membrane lesions – lymphadenopathy - presence of plasma cells on histopathology - positive nontreponemal and treponemal tests).


Some patterns of drug eruption may have to be excluded. An acute onset without a herald patch, itching and a tendency for the lesions to become lichenoid in appearance are suggestive features. A progressive, irritable, atypical pityriasiform eruption in a patient taking a drug, which is known to provoke reactions of this nature, can be provisionally accepted.


Guttate psoriasis and pityriasis lichenoides may sometimes need exclusion. In both, the lesions are papular and persistent. In psoriasis they are surmounted by thicker silvery scales. In pityriasis lichenoides they are polymorphic, some showing haemorrhagic crusting and some adherent thicker scales.


The hypopigmented patches with dry, branny scales of pityriasis alba are most frequent on the face, and are seen mainly in young children. Discoid dermatitis has no collarette of scale and is usually not oval. Tiny vesicles are common. 


The acute urticarial forms in childhood can sometimes not be identified with complete certainty on first examination unless a herald patch can be discovered. Re-examination after 2 days enables a confident diagnosis to be confirmed.


The herald patch and the localized forms such as pityriasis circinata et marginata of Vidal can be easily confused with ringworm. The lesions of ringworm are red and oedematous, may show marginal vesiculation and are usually not oval. Scale is usually at the periphery of plaques rather than inside the periphery. The pigmented form of pityriasis versicolor does not show marginal scaling. In case of doubt microscopic examination of scales is performed to differentiate these two conditions.


Scabies and lichen planus may be confused with the papular type of pityriasis rosea.


If itch is troublesome, or the appearance distressing, a topical steroid, usually of moderate strength can be helpful. The standard dose regimen of aciclovir is ineffective, but high-dose acyclovir (herpes zoster treatment dosage), used early after the onset of the eruption, may lead to a more rapid clearance of skin lesions. It has been stated in Fitzpatrick’s Dermatology in General Medicine textbook that this form of therapy should be considered in pityriasis rosea patients presenting early in their disease course who demonstrate associated flu-like symptoms and/or extensive rash.



Herald patch


The centre tends to clear and assumes a tawny (brownish-yellow) colour, with a marginal collarette of scale attached inside the periphery, with the free edge of the scale loose internally.



This page was last updated in February 2016

Thursday, 25 September 2014

Quiz











A white patch (black arrows) is seen after stroking of the skin (note the presence of a flare, red arrow). Which diagnosis is excluded now


  1. Tuberous sclerosis
  2. Naevus anaemicus
  3. Naevus depigmentosus
  4. Hypopigmented mycosis fungoides 
  5. Pityriasis versicolor




This page was last updated in August 2014.

Monday, 22 September 2014

Quiz







Fixed drug eruption (FDE) appearing few hours after ingestion of a tetracycline. FDE lesions usually develop 30 minutes to 8 hours after drug intake. On continuing the course the involved site flared with each exposure. He first ingested a tetracycline a year ago without having a drug eruption. What is this period called? Positive patch test reactions are observed at the site of previous lesions harbouring significant numbers of intraepidermal CD8+ T cells with an effector–memory phenotype. What is the refractory period in this regard? What is non-pigmenting FDE? What is wandering FDE?



This page was last updated in August 2014.

Wednesday, 17 September 2014

Differential diagnosis of Becker’s naevus (melanosis)




Becker’s naevus is a relatively common anomaly, affecting most racial groups, and about five times more frequent in males than females. The basal and suprabasal keratinocytes are heavily pigmented, and melanocyte density is variably reported as increased or normal, with a few melanophages in the upper dermis. There are no junctional or intradermal naevus cells. It may present in childhood, but is usually first noticed during adolescence, initially pale in colour and becoming more conspicuous after sun-exposure. Classically, Becker naevus is unilateral but it is rarely bilateral. The usual site is shoulder, anterior chest or scapular region, but lesions may occur on any area of the body. It starts as an area of irregular macular pigmentation, which spreads to a diameter of several centimetres, new macules developing beyond the margin and fusing with it, giving a geographical contour. The skin may thicken towards the centre of the lesion. Increased terminal hairs may appear on and around the lesion.

Becker’s naevus has been reported to follow Blaschko’s lines, but the usual lack of conformity to Blaschko’s lines may be due to the relatively late occurrence of a causative mutation. The mutant skin clone is presumably predisposed not only to pigmentation but also to androgen sensitivity, since Becker’s naevus is prone to acne and hypertrichosis (increased expression of androgen receptors within lesional skin). Many dermatologists would not regard Becker’s naevus as an epidermal naevus.  Once present, Becker’s naevus remains indefinitely. Almost all epidermal naevi follow the pattern of lines documented by Blaschko from drawings of epidermal naevi. The pattern is attributed to the lines of migration and proliferation of epidermal cells during embryogenesis. The lines do not correspond to any known nervous, vascular or lymphatic structures. The bands of abnormal skin represent clones of cells carrying a mutation in a gene expressed in the skin. Mosaicism impact on the phenotype relates to the proportion of cells that harbour the mutation and their distribution. Mosaic describes an art form in which pictures are produced by joining together tiny pieces of different coloured stone or glass. The term is used in genetics to describe individuals composed of cells of different genotypes, such as patients with Turner syndrome who have both 45, XO and 46, XX cells. The pattern may vary according to cell type and timing of mosaicism. In the skin, genetic mosaicism classically appears as Blaschko's lines. The term "pigmentary mosaicism" encompasses different phenotypic expressions of common pathogenic process caused by genetic mosaicism that specifically disrupt expression of pigmentary genes.

Cutaneous conditions have been reported to colocalize with Becker’s naevus and include e.g. pityriasis versicolor (I have seen one case), granuloma annulare and lichen planus. The term Becker’s naevus syndrome has been proposed to describe the association of a Becker’s naevus with ipsilateral non-cutaneous abnormalities.


A well-developed Becker’s naevus is unmistakeable.

Differential diagnosis of less developed lesions includes:


  • Progressive cribriform and zosteriform hyperpigmentation: This might be a non-hypertrichotic variant of Becker’s naevus or a localised form of linear and whorled naevoid hypermelanosis. 
  • (Diffuse) linear and whorled naevoid hypermelanosis
  • Idiopathic eruptive macular hyperpigmentation: The lesions disappear gradually over several months to years.
  • Acquired smooth muscle hamartoma: It has similar clinical and histopathological features, but in different proportions, with less pigmentation and more smooth muscle. Lesions described in the literature as ‘congenital Becker’s naevi’ could have actually been congenital smooth muscle hamartomas. However, it is possible that in some cases there is clinical/histopathologic overlap with Becker’s naevus.
  • Partial unilateral lentiginosis/agminated lentiginosis: Two similar conditions if not identical. 
  • Café-au-lait macule/spot/patch: Café-au-lait macules are common (found in approximately 15% of individuals), but increased numbers of such lesions are a component of many disorders.
The condition has been misdiagnosed by a dermatologist as pityriasis versicolor for several months.




The condition has been misdiagnosed by a dermatologist as pityriasis versicolor for several months.



This page was last updated in September 2014. 

Wednesday, 3 September 2014

Treatment of epidermodysplasia verruciformis



Epidermodysplasia verruciformis (EV) is a rare inherited susceptibility to widespread and persistent infection with specific HPV genotypes giving rise to plane warts, pigmented warts, pityriasis versicolor–like lesions and seborrhoeic keratoses-like lesions. It is inherited as an autosomal recessive trait, though autosomal dominant and X-linked patterns have been reported. The susceptibility for EV was localised to chromosome 17q25 and mutations in EVER1 and EVER2 genes from the same region were identified. There is a failure to mount an effective immune response to the HPV infection hence the recurrence after treatment. The lesions usually develop rapidly in childhood but may first appear at any age. They are most numerous on the face and neck and backs of the hands and feet, and may be restricted to these sites, but there are often scattered lesions elsewhere and the lesions may be generalized over the entire body surface. EV is remarkably persistent and may remain unchanged for decades. However, slow spontaneous regression has been reported. Carcinomas develop mainly in sun-exposed lesions* suggesting that ultraviolet radiation is an important factor. Viral particles can be identified ultrastructurally not only in the spinous cells, but also in basal cells. EV HPV may be required only in early phases of carcinogenesis and therefore may not be found in well-developed cancer.  Skin cancers are less common in African patients, suggesting a protective effect of skin pigmentation.  EV-like lesions have been observed in the setting of immunosuppression and are sometimes called acquired EV. Remission of EV-like eruptions can occur in HIV infected patients after the commencement of highly active antiretroviral therapy. In addition to the host genetic background, the EV-HPVs are activated by UV exposure and immunosuppression


Strict sun avoidance and protection should be started as soon as the syndrome is diagnosed. Diligent use of an effective sunscreen should be advised. An approach similar to that for patients with xeroderma pigmentosa can be instituted. No specific treatment exists for EV lesions. Therapy with electrodesiccation, cryotherapy, topical retinoids, and surgery are generally unsatisfactory. Mixed results have been seen with topical 5% imiquimod cream. Many other therapies have been tried e.g. oral retinoids, oral cimetidine and topical vitamin D analogues. Whether dysplastic or malignant change can be prevented by oral retinoids is unknown. If skin grafting is required, the grafts should be taken from sun-protected skin, such as the buttocks or inner upper arm. 




*Partridge ME, Pariser RJ. Ocular and cutaneous squamous cell carcinoma in an African American man with epidermodysplasia verruciformis resulting in blindness and death. J Am Acad Dermatol. 2003; 49 (suppl 5): 262 – 264.


Face involvement - Her grandmother (father's side), her father, and her two sisters and brother had the same condition. 


Hand involvement - Her grandmother (father's side), her father, and her two sisters and brother had the same condition.  

This page was last updated in September 2014

Friday, 15 August 2014

Shiny trachyonychia



Trachyonychia (Gk trachys rough, onychos nail) presents as a rough surface affecting the entire nail plate in up to 20 nails. Thus trachyonychia may involve one, several or all digits and when most or all digits are involved, the term twenty-nail dystrophy is commonly used. Trachyonychia may affect patients from all age groups although it is most commonly diagnosed in children. Familial forms exist. Spontaneous resolution might occur.

Based on appearance, trachyonychia is divided into two types*: (1) Opaque trachyonychia where nail is ridged and rough, and is deprived of its natural lustre. The nail appears sandpapered in a longitudinal direction (severe trachyonychia). (2) Shiny trachyonychia where the nail plate is shiny with numerous, closely aggregated, small superficial pits. This shiny appearance may be accentuated by a camera flash or by tangential light from a pen-torch (mild trachyonychia). The severity of trachyonychia frequently varies from nail to nail and the shiny and opaque varieties of the disease may coexist in the same patient.

The most common presentation is as an isolated nail abnormality (idiopathic) where histopathology shows spongiosis and a lymphocytic infiltrate of the nail matrix. It can be associated with psoriasis (pitting of the fingernails may be the only manifestation for months or even years), alopecia areata, lichen planus (it may be its sole manifestation and some regard nail lichen planus as a distinct condition) and other conditions. Unilateral involvement may occur in complex regional pain syndrome. Localized trachyonychia in a judo player** from the repeated grabbing of opponents’ uniforms has been described. Routine biopsy is not recommended.

Treatment is often useless and several forms have been suggested. Tazarotene alone or in association with topical steroids may improve the condition. The safety of tazarotene has not been established in patients under the age of 18 years.



Shiny trachyonychia affecting all the fingernails 


*Baran RDuprè AChristol BBonafe JLSayag JFerrere JL'ongle grèsè peladique. Ann Dermatol Venereol 1978105:387392.

**Shelley WBShelley DE‘Judo’ nailsCutis 199556912.

This page was last updated in August 2014

Sunday, 3 August 2014

Palmar lichen planus



Plamar lichen planus can be difficult to diagnose if present as an isolated finding.  Itchy (or painful) erythematous scaly plaque is characteristic. The lesions tend to be firm and rough with a yellowish hue. It is one of the therapy-resistant variants of lichen planus. Although lesions on the volar aspect of the wrists are common, lesions on the adjacent palms are less common and lack the characteristic shape and colour of lesions elsewhere. They may be broadly sheeted or show up as punctate keratoses. Vesicle-like papules are recorded. Itching may be absent. Palmoplantar lichen planus may also present as erosive-ulcerative type. When such changes occur in isolation, diagnosis is difficult; and conditions such as eczema, tinea, secondary syphilis, psoriasis, porokeratosis, callosities and warts must be excluded. Histopathologically findings are identical to those of classic lichen planus.

The primary lesions of lichen planus are characteristic, almost pathognomonic violaceous, flat-topped, polygonal papules. Papules expand to plaques. The colour of the lesions initially is erythematous but well-developed lesions are violaceous, and resolving lesions are often hyperpigmented. The surface is shiny with scant adherent scales. On the surface, grey or white lines, known as Wickham’s striae, may traverse the surface of the papules. Dermoscopy may enhance the visualization of this important diagnostic element.  Most patients react to the itching of lichen planus by rubbing rather than scratching but itching can be absent. The four Ps-purple, polygonal, pruritic papule are a mnemonic to help you recall the findings that characterise lichen planus.   The centre of the papule shows irregular acanthosis of the epidermis, irregular thickening of the granular layer, and compact hyperkeratosis. A focal increase in thickness of the granular layer and infiltrate corresponds to the presence of Wickham’s striae. The basal damage is associated with a band-like infiltrate of lymphocytes and some macrophages which press against the undersurface of the epidermis. Occasional lymphocytes extend into the basal layer. The infiltrate however does not obscure the interface or extend into the mid-epidermis.  Pigmentary incontinence with dermal melanophages is characteristic. Postinflammatory pigmentation may persist for some time.

Potent topical corticosteroids (with or without occlusion) remain the treatment of choice for lichen planus in patients with classic and localized disease.





Improvement after use of very potent topical corticosteroid with occlusion 



This page was last updated in August 2014

Thursday, 31 July 2014

Varicella in an adult


Varicella occurs throughout the world but infection occurs at a younger age in temperate zones compared to the tropics. In temperate regions more than 90% of adults are immune to varicella while in tropical countries only 60% of adults are immune to it. Transmission is via the respiratory route and less commonly by direct contact with the lesions. A susceptible person may develop varicella following exposure to the lesions of herpes zoster. The severity of the disease is age-dependent, with adults having more severe disease and more complications. Varicella confers lasting immunity and second attacks are uncommon, especially in immunologically healthy people, but clinical reinfection with a mild varicella-like illness occasionally takes place.

The distinctive features of varicella are the centripetal distribution, the polymorphism in each affected site and the rapid progression of the individual lesion from vesicle to crust. Vesicles are common in the mouth, especially on the palate, and are occasionally seen on other mucous membranes, including the conjunctiva and genitalia. On the anal mucosa they may be followed by painful ulcers.

Aciclovir is indicated for varicella in adults and for severe varicella at any age in the immunocompromised. Therapy does not appear to alter the development of adequate immunity to reinfection. 




Centripetal distribution


Resolving rash. The virus is transmitted by droplet infection from the nasopharynx. A brief first viraemic stage, when the virus can disseminate to other organs, is followed by a second viraemia coinciding with the onset of the rash. Patients are infectious to others from about 2 days before to 5 days after the onset of the rash and most non-immune people will contract the infection if exposed to someone in the infectious stage of varicella. Vesicle fluid contains a large amount of virus. Completely dry scabs are not infectious.



A characteristic feature is the presence of lesions at different stages in each site. Papules very rapidly become vesicles that appear over around 4 days with centripetal distribution.  Vesicles dry rapidly to become crusts within around 4 days. Crusts soon separate leaving shallow pink depressions that normally heal without scarring within around 2 weeks. Hyper- or hypopigmentation may persist for weeks and scars can occur in some.





This page was last updated in August 2014. 

Sunday, 20 July 2014

High-dose aciclovir hastening resolution of pityriasis rosea



The evidence that pityriasis rosea is a viral exanthem associated with reactivation of HHV-6 and/or HHV-7 is strong. Based on this concept, trials of antiviral drugs have been reported. The standard dose regimen of aciclovir is ineffective, but high-dose acyclovir (herpes zoster treatment dosage), used early after the onset of the eruption, may lead to a more rapid clearance of skin lesions. Here, the rash began to resolve soon after starting high-dose aciclovir (second photo taken at 2 weeks of starting aciclovir therapy). Without treatment, the disease duration usually varies between 4 and 10 weeks. Rarely, a partial or complete relapse of a fading pityriasis rosea may be seen. Second attacks occur in about 2% of cases. 

Interestingly, pityriasis rosea has been classified in Rook’s textbook of dermatology as a viral infection for many years before a viral cause was actually found. 
It has been stated in Fitzpatrick’s Dermatology in General Medicine textbook that this form of therapy should be considered in pityriasis rosea patients presenting early in their disease course who demonstrate associated flu-like symptoms and/or extensive rash.
 


Before treatment 

Two weeks of starting treatment
  





The eruption is usually generalized, affecting chiefly the trunk and sparing sun-exposed surfaces but involvement of the face and scalp is quite common, especially in children. An inverse distribution, sparing covered areas, is not rare.


This page was last updated in February 2015.


Main Works of Reference List (The first eight are my top favourites)

  • British National Formulary
  • British National Formulary for Children
  • Guidelines (BAD - BASHH - BHIVA - Uroweb)
  • Oxford Handbook of Genitourinary Medicine, HIV, and Sexual Health
  • Oxford Handbook of Medical Dermatology
  • Rook's Textbook of Dermatology
  • Simple Skin Surgery
  • Weedon's Skin Pathology
  • A Concise Atlas of Dermatopathology (P Mckee)
  • Ackerman's Resolving Quandaries in Dermatology, Pathology and Dermatopathology
  • Andrews' Diseases of the Skin
  • Andrology (Nieschlag E FRCP, Behre M and Nieschlag S)
  • Bailey and Love's Short Practice of Surgery
  • Davidson's Essentials of Medicine
  • Davidson's Principles and Practice of Medicine
  • Fitzpatrick's Colour Atlas and Synopsis of Clinical Dermatology (Klaus Wolff FRCP and Richard Allen Johnson)
  • Fitzpatrick’s Dermatology in General Medicine
  • Ganong's Review of Medical Physiology
  • Gray's Anatomy
  • Hamilton Bailey's Demonstrations of Physical Signs in Clinical Surgery
  • Hutchison's Clinical Methods
  • Lever's Histopathology of the Skin
  • Lever's Histopathology of the Skin (Atlas and Synopsis)
  • Macleod's Clinical Examination
  • Martindale: The Complete Drug Reference
  • Oxford Handbook of Clinical Examination and Practical Skills
  • Oxford Textbook of Medicine
  • Practical Dermatopathology (R Rapini)
  • Sexually Transmitted Diseases (Holmes K et al)
  • Statistics in Clinical Practice (D Coggon FRCP)
  • Stockley's Drug Interactions
  • Treatment of Skin Disease: Comprehensive Therapeutic Strategies
  • Yen & Jaffe's Reproductive Endocrinology