LA PITIRIASIS ROSADA Y EL HERPES VIRUS HUMANO,
ACTUALIZACIÓN.
THE PITYRIASIS ROSEA AN THE HUMAN HERPES VIRUS, UPDATE.
ACTUALIZADO 2.025
EDITORIAL ESPAÑOL
===================
Hola amigos de la red, DERMAGIC de nuevo con ustedes con el tema:
PITIRIASIS ROSADA ACTUALIZACIÓN.
1.) HISTORIA:
La pitiriasis Rosada es una de esas enfermedades ancestrales, descrita
por Primera vez por el medico Frances
Camille Melchior GIBERT,
en 1860.
- OTROS AUTORES LA DESCRIBIERON CON OTROS NOMBRES, a saber:
- Eritema Anulatum (Rayer).
- Herpes tonsurans maculoso y escamoso (Hebra).
- Liquen annulatum serpiginoso (Wilson).
- Pitiriasis circinada (Honrad).
- Pitiriasis diseminada (Hardy).
- Pitiriasis marginada y circinada ((Vidal).
- Pitiriasis Rubra aigu disseminee (Bazin).
- Seudoexantema eritemato descamativo (Besnier).
- Roseola Annulata (Wilan).
- Roseola furfuracea herpetiforme (Beherend).
- Roseola escamosa (Nicolas y Chapard).
Pero definitivamente el primero en describirla fue CAMILLE GIBERT en ese
año de 1860.
2.) ETIOLOGÍA:
Hoy en día han pasado mas de 160 años desde la época que inmortalizo a
GIBERT, y se discuten los probables agentes causales de la enfermedad,
entre ellos bacterias y virus de la familia herpes, siendo estos últimos
los
VIRUS HERPES 6 y 7
los mas asociados con la enfermedad.
- La
LEGIONELLA MICMADEI, (pneumophila) una bacteria gramnegativa bacilar, ha sido encontrada en algunos casos de
Pitiriasis rosada, mas no se le atribuye como agente causal
confirmado.
- Esta bacteria esta involucrada en la llamada Neumonía de Pittsburg,
Enfermedad del Legionario y también en la llamada Fiebre de
Pontiac.
- También han sido encontrado anticuerpos contra el VIRUS
EPSTEIN BARR (EBV), en algunos casos se ha encontrado MYCOPLASMA PNEUMONIA,
y CITOMEGALOVIRUS y virus del tipo
PICORNAVIRUS (resfriado
comun); tampoco son considerados agentes causales de esta
patología.
- Por ultimo, se han descrito casos de
ERUPCIONES SIMILARES a la
PITIRIASIS ROSADA, producida por medicamentos, entre ellos:
barbitúricos,
metronidazol,
alopurinol, diureticos (hidroclorotiazida), e
inhibidores de la enzima convertidora de la angiotensina (ECA), es
decir
antihipertensivos:
Captopril,
Enalapril,
Lisinopril,
Ramipril,
Perindopril,
Quinapril,
Benazepril, Fosinopril,
Trandolapril
y Moexipril. A estas erupciones se les conoce con el nombre de
PITIRIASIS ROSADA-LIKE.
3.) CARACTERÍSTICAS CLÍNICAS:
- La PITIRIASIS ROSADA tiene un comportamiento netamente ESTACIONAL, donde en una época del año (otoño e invierno) ocurren la mayoría de los
casos.
- Es más frecuente en la mujer que el hombre, en una proporción de 2 -1,
también se presenta en niños y adolescentes.
- Aunque CLÁSICAMENTE no produce lesiones en cara, palmas y plantas, yo
he visto tales manifestaciones y están descritas en la literatura.
- La clásica mácula o
PLACA HERÁLDICA
representa el inicio de la enfermedad y luego de 1 a 2 semanas, se
presenta un brote metamérico descrito como en
"árbol de navidad"
clásico de tal enfermedad.
- Por lo general son placas ovales, eritematosas, que en el centro
presentan una descamación descrita como "papel de cigarrillo".
- La enfermedad puede ser auto-limitada, (pocas lesiones), o presentarse
como una dermatosis GENERALIZADA, respetando solo palmas, plantas y cara
(ver fotos).
4.) CLASIFICACIÓN:
Durante muchos años se consideraba una sola presentación, que es la mas
común y es la forma en placas, pero luego se describieron otras variantes,
de modo que hoy dia se le clasifica así:
A.) FORMA TÍPICA: la
mas común ya descrita, que son PLACAS, con la clásica distribución en
"árbol de navidad" y PLACA HERÁLDICA.
B.) FORMAS ATÍPICAS: se han descrito variantes,
VESICULARES, PAPULARES, y
PURPÚRICAS
(hemorragicas) de la misma afección. Las vesiculares y papulares son
mas frecuentes en niños, y las purpuricas son las mas raras, (adolescentes
y adultos jóvenes).
5.) EVOLUCIÓN:
Un dato interesante de la PITIRIASIS ROSADA, es que en la mayoría de los
casos NO REPITE LA ENFERMEDAD, aunque en algunos casos a los años puede presentarse una segunda
manifestación IGUAL a la primera vez; incluso se han descrito casos de 3
brotes en periodos cortos de años.
- Se hace esta aclaratoria, porque en las primeras descripciones de la
enfermedad se decía que dejaba INMUNIDAD TOTAL, hecho que posteriormente
se comprobó no era cierto.
- Si tomamos como válida la RECIENTE afirmación que la PITIRIASIS ROSADA
esta asociada a los
HERPES VIRUS 6 Y 7.
- Y que EL CAMBIO ESTACIONAL (otoño, invierno) ACTIVA la virulencia
de estos virus, provocando la enfermedad, al cambiar el clima de nuevo
(verano), LOS VIRUS PIERDEN ACTIVIDAD y disminuye el porcentaje de
casos.
- Otro dato INTERESANTE a tomar en cuenta es que la
PITIRIASIS ROSADA DE GIBERT
NO ES CONTAGIOSA, a pesar de que el agente causal mas asociado con la enfermedad son los
HERPES VIRUS 6 y 7.
- NO TODOS los familiares o
personas en contacto con los afectados MANIFIESTAN LA ENFERMEDAD, ?? esto
se explicaría por el grado de protección inmunológica que tienen las
PERSONAS CONTRA ESTOS HERPES VIRUS.
- TAMBIÉN EXISTEN PERSONAS A
LAS CUALES nunca las dio la ENFERMEDAD, otra prueba mas de la protección
inmunológica que poseen genéticamente.
6.) EVOLUCIÓN:
- La pitiriasis rosada puede durar hasta 90 días en algunos casos
luego de aparecer la mancha Heráldica, con o sin tratamiento y en
algunos casos desaparece sola. Pero lo recomendable es acudir al
dermatólogo para su tratamiento adecuado.
- La enfermedad NO DEJA
SECUELAS de ningún tipo.
- Los casos SEVEROS, requieren TRATAMIENTO y REPOSO en casa.
7.) TRATAMIENTO:
Las opciones de tratamiento para esta enfermedad son:
1.) Tratamiento sintomático: antihistamínicos para el prurito o
comezón.
2.) Corticosteroides tópicos.
3.) Hidratantes.
4.) ANTIVIRALES. se demostrado en muchos casos el éxito de el
ACICLOVIR, y
VALACICLOVIR
(debido a su etiología viral).
5.) Antibióticos: ERITROMICINA, CEFADROXILO y CEFALOSPORINAS, también han
sido utilizado con éxito en algunos casos.
8.) RESUMEN:
La clásica PITIRIASIS ROSADA se comporta CASI igualmente en todos los
pacientes, con un RASH eruptivo, luego de un tiempo de incubación marcado
por la placa HERÁLDICA.
Se han descrito casos de lesiones en mucosas (boca), y más del 98% de los
casos deja inmunidad definitiva.
Considerada de causa desconocida en sus comienzos, en la década de los 90
se le comprobó su ETIOLOGÍA INFECCIOSA (principalmente VIRAL).
En base a los HECHOS de 1.) ETIOLOGÍA VIRAL
(como las clásicas eruptivas), y
2.) La mayoría deja
INMUNIDAD DEFINITIVA, podría decirse que se comporta como una CLÁSICA ERUPTIVA.
En base a ello se ha asomado la posibilidad de considerarla como LA SEXTA
ENFERMEDAD, en el grupo de las eruptivas:
1.)
SARAMPIÓN:
Virus Morbilivirus (virus de ARN)
6.) PITIRIASIS ROSADA: Herpes
virus 6 y 7.
NOTA: Después de la Pandemia del virus Sars-Cov 2 (COVID 19) se han descrito casos de brotes de PITIRIASIS ROSADA, después de las vacunaciones.
En este enlace encontraras la primera publicación que hice sobre la
PTIRIASIS ROSADA, BUSCANDO UN AGENTE CAUSAL, donde todavía no se sabia con certeza que los HERPES VIRUS 6 y 7, eran
los agentes mas involucrados en esta patología.
En las referencias los hechos
Saludos !!!
Dr
José Lapenta R.
Dr. José M. Lapenta.
ENGLISH EDITORIAL
===================
Hello friends of the network, DERMAGIC is back with you with
the topic:
PITYRIASIS ROSEA UPDATE.
1.) HISTORY:
Pityriasis rosea is one of those ancient diseases, first
described by the French physician
Camille Melchior Gibert
in 1860.
- OTHER AUTHORS DESCRIBED IT WITH OTHER NAMES, namely:
- Erythema Annulatum (Rayer).
- Maculosa and Squamous Herpes
Tonsurans (Hebra).
- Serpiginous Lichen Annulatum (Wilson).
-
Circinate Pityriasis (Honrad).
- Disseminated Pityriasis
(Hardy).
- Pityriasis marginata and circinata (Vidal).
-
Pityriasis rubra aigu disseminee (Bazin).
-
Pseudo-erythematous-desquamative exanthem (Besnier).
- Roseola
annulata (Wilan).
- Roseola furfuracea herpetiforme
(Beherend).
- Roseola squamosa (Nicolas and Chapard).
But definitively, the first to describe it was Camille Gibert
in 1860.
2.) ETIOLOGY:
Today, more than 160 years have passed since the time
that immortalized Gibert, and the probable causative agents of the
disease are debated, including bacteria and viruses of the herpes
family, with herpes viruses 6 and 7 being the most associated with the
disease.
-
LEGIONELLA MICMADEI, (pneumophila) a gram-negative rod-shaped bacterium, has been
found in some cases of pityriasis rosea, but it is not considered a
confirmed causative agent.
- This bacterium is involved in what is called Pittsburgh Pneumonia,
Legionnaires' Disease, and also in what is called
Pontiac Fever.
- Antibodies against
EPSTEIN BARR
VIRUS (EBV)
have also been found, and in some cases,
MYCOPLASMA PNEUMONIAE, PICORNAVIRUS type virus (common cold), and CYTOMEGALOVIRUS
have been found; these are also not considered causative agents of
this condition.
- Finally, cases of rashes similar to
PITYRIASIS ROSEA have been
described, caused by medications, including:
barbiturates, metronidazole,
allopurinol, diuretics (hydrochlorothiazide), and angiotensin-converting enzyme (ACE) inhibitors, i.e.,
antihypertensives: captopril, enalapril, lisinopril, ramipril,
perindopril, quinapril, benazepril, fosinopril, trandolapril, and
moexipril. These rashes are known as PITYRIASIS ROSEA-LIKE rashes.
3.) CLINICAL CHARACTERISTICS:
- PITYRIASIS ROSEA has a distinctly
SEASONAL pattern, with
most cases occurring during a specific time of year (autumn and
winter).
- It is more common in women than men, in a ratio
of 2:1, and also occurs in children and adolescents.
-
Although it classically does not produce lesions on the face, palms,
and soles, I have seen such manifestations, and they are described in
the literature.
- The classic MACULE
or
HERALD PATCH
represents the onset of the disease, and after 1 to 2 weeks, a
metameric outbreak appears, described as a classic
"Christmas tree"
pattern.
- These are generally oval, erythematous plaques
with a central scaling pattern described as "cigarette paper."
-
The disease can be self-limiting (few lesions) or present as a
generalized dermatosis, sparing only the palms, soles, and face (see
photos).
4.) CLASSIFICATION:
For many years, only one presentation was considered, the
most common being the plaque form. However, other variants were later
described, so today it is classified as follows:
A.) TYPICAL FORM:
the most common form, as described above, which consists of plaques
with the classic "Christmas tree" distribution and
herald patch.
B.) ATYPICAL FORMS: VESICULAR, PAPULAR
and PURPURIC (hemorrhagic)
variants of the same condition have been described. Vesicular and
papular forms are more frequent in children, while purpuric forms are
the rarest (adolescents and young adults).
5.) EVOLUTION:
An interesting fact about
GIBERT PITYRIASIS ROSEA is that in most cases the disease DOES NOT RECURR,
although in some cases a second outbreak, identical to the first, may
appear years later; cases of three outbreaks in short periods of years
have even been described.
This clarification is made
because early descriptions of the disease stated that it conferred
total immunity, a claim that was later proven false.
- If
we accept the recent assertion that pityriasis rosea is associated
with
HERPES VIRUS TYPES 6 and 7.
- And that seasonal changes (autumn, winter) activate the
virulence of these viruses, causing the disease, while with the return
of summer, the viruses become less active and the percentage of cases
decreases.
- Another interesting fact to consider is
that PITYRIASIS ROSEA IS NOT CONTAGIOUS is not contagious, even though herpes virus types 6 and 7 are
the most commonly associated causative agents of the disease.
-
NOT ALL family members or people
in contact with those affected SHOW THE DISEASE. This could be
explained by the degree of immunological protection that PEOPLE have
AGAINST THESE HERPES VIRUSES.
- THERE ARE ALSO PEOPLE WHO NEVER GET THE DISEASE,
further proof of the immunological protection they possess
genetically.
6.) EVOLUTION:
- PITYRIASIS ROSEA can last up to 90 days in
some cases after the appearance of the herald patch, with or without
treatment, and in some cases it disappears on its own. However, it is
recommended to see a dermatologist for appropriate treatment.
- The disease DOES NOT LEAVE ANY SEQUELAE.
- SEVERE cases
require TREATMENT and REST at home.
7.) TREATMENT:
The treatment options for this disease are:
1.)
Symptomatic treatment: antihistamines for pruritus or itching.
2.)
Topical corticosteroids.
3.) Moisturizers.
4.)
Antivirals.
ACYCLOVIR
and VALACYCLOVIR have proven successful in many cases (due to
their viral etiology).
5.) Antibiotics:
ERYTHROMYCIN, CEFADROXIL, and CEPHALOSPORINS have also
been used successfully in some cases.
8.) SUMMARY:
Classic PITYRIASIS ROSEA presents almost identically in all patients, with an eruptive
rash following an incubation period marked by the heraldic patch.
Cases
of mucosal lesions (in the mouth) have been described, and
more than 98% of cases result in permanent immunity.
Initially considered to be of unknown cause, its
INFECTIOUS ETIOLOGY (primarily viral) was confirmed in the
1990s.
Based on the
FACTS of 1.) VIRAL ETIOLOGY
(like classic eruptive diseases), and 2.) that most cases
confer DEFINITIVE IMMUNITY, it could be said that it behaves like a CLASSIC ERUPTICAL
DISEASE.
Based on this, the possibility has arisen of
considering it as THE SIXTH DISEASE, within the group of eruptive diseases:
1.)
MEASLES:
Morbillivirus (RNA virus)
2.) CHICKENPOX:
Varicella-zoster virus
3.) RUBELLA:
Rubivirus
4.) ROSEOLA INFANTILE:
Human Herpesvirus 6 and 7
5.) FIFTH DISEASE (ERYTHEMA INFECTIOSUM): Parbovirus B19
6.) PITYRIASIS ROSEA:
Human Herpesvirus 6 and 7
NOTE: After the Sars-Cov 2 virus (COVID 19) pandemic, cases of
outbreaks of PITYRIASIS ROSEA have been described
following vaccinations.
In this link you will find the first publication I made about
PITYRIASIS ROSEA, LOOKING FOR A CAUSAL AGENT, where it was not yet known for certain that HERPES VIRUS 6 and 7 were
the agents most involved in this pathology.
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1.) Papular pityriasis rosea.
2.) Human herpes virus-like particles in pityriasis rosea lesions: an
electron microscopy study.
3.) Human herpesviruses 6 and 7.
4.) Human herpesvirus 7 in dermatology: what role does it play?
5.) [Myerson nevus as a primary patch of Gibert pityriasis rosea. A case
report]
6.) Rash orientation in pityriasis rosea: a qualitative study.
7.) Skin diseases associated with human herpesvirus 6, 7, and 8
infection.
8.) Collarette scaling in pityriasis rosea demonstrated by digital
epiluminescence dermatoscopy.
9.) [Etiopathogenic importance of human herpes viruses type 6, 7 and 8
in manifestations of certain skin diseases]
10.) Prospective case-control study of chlamydia, legionella and
mycoplasma infections in patients with pityriasis rosea.
11.) Pityriasis rosea is associated with systemic active infection with
both human herpesvirus-7 and human herpesvirus-6.
12.) Detection of human herpesvirus 7 in pityriasis rosea by nested
PCR.
13.) An epidemiological study of pityriasis rosea in the Eastern
Anatolia.
14.) Human herpesvirus 7 in patients with pityriasis rosea. Electron
microscopy investigations and polymerase chain reaction in mononuclear
cells, plasma and skin.
15.) A pityriasis rosea-like eruption secondary to bacillus
Calmette-Guerin therapy for bladder cancer.
16.) UVB phototherapy for pityriasis rosea: a bilateral comparison
study.
17.) Pityriasis rosea Gibert: detection of Legionella micdadei
antibodies in patients.
18.) Pityriasis rosea-like eruption after bone marrow
transplantation.
19.) Tongue and cheek: oral lesions in pityriasis rosea.
20.) Pityriasis rosea and discoid eczema: dose related reactions to
treatment with gold.
21.) [Pityriasis rosea-like skin eruptions caused by captopril]
22.) Recurrent pityriasis rosea. New episodes every year for five years.
A case report.
23.) Pityriasis rosea-like eruption associated with BCG vaccination.
24.) [Vesicular pityriasis rosea]
25.) [Benign familial chronic pemphigus and pityriasis rosea. Clinical
aspects and histology of the coexistence of both dermatoses]
26.) Human herpesvirus 6 and 7 DNA in peripheral blood leucocytes and
plasma in patients with pityriasis rosea by polymerase chain reaction: a
prospective case control study.
27.) The human herpesviruses and pityriasis rosea: curious covert
companions?
28.) Pityriasis rosea is not associated with human herpesvirus 7.
29.) Association of pityriasis rosea with human herpesvirus-6 and human
herpesvirus-7 in Taipei.
30.) Epidemiological study of human herpesvirus-6 and human
herpesvirus-7 in pityriasis rosea.
31.) Lack of evidence of active human herpesvirus 7 (HHV-7) infection in
three cases of pityriasis rosea in children.
32.) Pityriasis rosea associated with herpesvirus 7 DNA.
33.)Pityriasis rosea: one virus, two viruses, more viruses?
34.) Reactivation of human herpesvirus 6 in pityriasis rosea.
35.) Absence of picornavirus genome in pityriasis rosea.
36.) Human herpesvirus 7 in pityriasis rosea.
37.) Detection of human herpesvirus 7 in patients with pityriasis rosea
and healthy individuals.
38.) The association of pityriasis rosea with cytomegalovirus,
Epstein-Barr virus and parvovirus B19 infections - A prospective case
control study by polymerase chain reaction and serology.
39.) Pityriasis rosea associated with imatinib (STI571, Gleevec).
40.) Erythromycin in pityriasis rosea: A double-blind,
placebo-controlled clinical trial.
41.) A Remarkable Result of a Double-Masked, Placebo-Controlled Trial of
Erythromycin in the Treatment of Pityriasis Rosea.
42.) Case Clustering in Pityriasis Rosea
A Multicenter Epidemiologic Study in Primary Care Settings in Hong Kong
43.) Pityriasis rosea--a virus-induced skin disease? An update.
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HERPES VIRUS 6, 7 AND 8 … MORE
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44.) Association between human herpesvirus type 6 and type 7, and
cytomegalovirus disease in heart transplant recipients.
45.) Invasion by human herpesvirus 6 and human herpesvirus 7 of the
central nervous system in patients with neurological signs and
symptoms.
46.) Association of human herpesvirus 6 and human herpesvirus 7 with
demyelinating diseases of the nervous system.
47.) [Detection of human herpesvirus type 6, human herpesvirus type 7,
cytomegalovirus and human papillomavirus in cutaneous AIDS-associated
Kaposi's sarcoma]
48.) Influenza encephalopathy associated with infection with human
herpesvirus 6 and/or human herpesvirus 7.
49.) Human herpesvirus 6 and human herpesvirus 7 infections in renal
transplant recipients and healthy adults in Turkey.
50.) Detection of human herpesvirus-6 DNA in peripheral blood and
saliva.
51.) Human herpesvirus-6 and human herpesvirus-7 in the bone marrow from
healthy subjects.
52.) Lymphomatoid papulosis and human herpesviruses--A PCR-based
evaluation for the presence of human herpesvirus 6, 7 and 8 related
herpesviruses.
53.) Presence of human herpesvirus 6 variants A and B in saliva and
peripheral blood mononuclear cells of healthy adults.
54.) Detection of human herpesvirus 6 DNAs in samples from several body
sites of patients with exanthem subitum and their mothers by polymerase
chain reaction assay.
55.) Human herpesvirus-6 and human herpesvirus-7 infections in bone
marrow transplant recipients.
56.) High prevalence of HHV-6 DNA in peripheral blood mononuclear cells
of healthy individuals detected by nested-PCR.
57.) Clinical features and viral excretion in an infant with primary
human herpesvirus 7 infection.
58.)
Gestational Pityriasis Rosea:
Suggestions for Approaching Affected Pregnant Women.
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