24 marzo 2017

Revisión sobre infecciones dermatológicas

Filed under: Artículos — Tania Izquierdo @ 11:54

Las infecciones de la piel y de los tejidos blandos son el resultado de la invasión microbiana de la piel y de sus estructuras de soporte. El manejo está determinado por la severidad y localización de la infección y por las comorbilidades del paciente. Las infecciones pueden clasificarse como simples (sin complicaciones) o complicadas (o no necrotizantes necrotizantes), o como supurativas o no supurativas. La mayoría de las infecciones adquiridas en la comunidad son causadas por Staphylococcus aureus resistente a la meticilina y por estreptococo beta-hemolítico. (more…)

Última actualización

Filed under: Actualización — dermatologia @ 11:22

Última actualización de contenidos: 26/04/2021

Sitio creado: 28 de junio 2011

7 marzo 2017

The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma

Filed under: Artículos — dermatologia @ 13:50

Atopic dermatitis (AD) is an inflammatory disease characterized by pruritic skin lesions. The pathogenesis of AD may include disrupted epidermal barrier function, immunodysregulation, and IgE-mediated sensitization to food and environmental allergens. AD is also part of a process called the atopic march, a progression from AD to allergic rhinitis and asthma. This has been supported by multiple cross-sectional and longitudinal studies and experimental data.

Vea el artículo completo.

Zheng T, Yu J, Oh MH, Zhu Z. The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma. Allergy, Asthma & Immunology Research. 2011;3(2):67-73. doi:10.4168/aair.2011.3.2.67.

27 octubre 2016

Enfoque terapeutico del prurito

Filed under: Clinica y Terapeutica — dermatologia @ 0:36

El prurito. Enfoque terapéutico en la atención primaria de salud

El prurito es una manifestación subjetiva y desagradable por la cual consultan frecuentemente los pacientes en la atención primaria de salud, debido a la frecuencia con que se presentan las afecciones cutáneas pruriginosas, y a los múltiples trastornos sistémicos que cursan con este síntoma.1-4

Después de un examen físico minucioso y de una anamnesis exhaustiva, el médico de asistencia primaria estará en condiciones de crear 2 grandes grupos de casos, por un lado los que consultan por prurito y tienen evidencias clínicas de enfermedad cutánea definida, y por otro, los que presentan el síntoma sin las evidencias señaladas.2,5-7

Con el caso definido de esta forma, se podrá concluir y tratar a un grupo considerable de pacientes a nivel primario de atención médica, así como conducir mucho mejor al grupo que necesite de la interconsulta con otras especializaciones médicas.

Artículo completo

9 octubre 2016

Herpesvirus 7

Filed under: Clinica y Terapeutica — Tania Izquierdo @ 12:33

Human Herpesvirus 7 in Dermatology
What Role Does it Play?
Werner Kempf
Department of Dermatology, University Hospital, Zurich, Switzerland
Abstract Human herpesvirus 7 (HHV-7) was discovered in 1989 as a new member of the β-herpesvirus

Primary infection occurs early in life and manifests as exanthema subitum, or other febrile

illnesses mimicking
measles and rubella. Thus, HHV-7 has to be considered as a causative agent in a variety of

rashes in children. In addition, HHV-7 was found in some cases of other inflammatory skin

disorders, such as
psoriasis. There are controversial data on the detection of HHV-7 in pityriasis rosea, but so far

there is not enough
evidence for a pathogenetic association of HHV-7 with this exanthematic skin disease. Although

HHV-7 can be
found in some cases of Hodgkin’s disease, there are no data supporting a direct causative role in

this lymphoma
type nor in other nodal or primary cutaneous lymphomas. In various epidemiologic forms of

Kaposi’s sarcoma,
infection of monocytic cells with HHV-7 was demonstrated, which may indirectly influence tumor

biology. In
the context of immunosuppression, HHV-7 has recently been identified as an emerging pathogen in

recipients and may exacerbate graft rejection in renal transplant recipients. The ability of

HHV-7 to induce
cytokine production in infected cells could make HHV-7 an important pathogenetic co-factor in

and neoplastic disorders. Moreover, the restricted cellular tropism of HHV-7 may render this

virus an interesting
vector for gene therapy. Thirteen years after the discovery of HHV-7, there has been considerable

progress in
characterizing its genetic structure, virus-induced effects on infected host cells and in the

development of
diagnostic tools. Nevertheless, the role of HHV-7 in various skin diseases and the clinical

manifestations of
reactivation of HHV-7 infection have still to be defined.
LEADING ARTICLE Am J Clin Dermatol 2002; 3 (5): 309-315
© Adis International Limited. All rights reserved.
During the last 3 decades, three new human herpesviruses
have been discovered. Two of these, human herpesvirus 6 (HHV-
6) and human herpesvirus 7 (HHV-7), are closely related to cytomegalovirus
(CMV) and constitute the Roseolovirus genus of the
β-herpesvirus subfamily (for a review see Black & Pellett[1]).
Similar to other human herpesviruses, infections with HHV-6 and
HHV-7 can manifest with cutaneous involvement. Exanthema
subitum and other childhood rashes were shown to be clinical
manifestations of primary infection.[2-4] Recently, HHV-7 was
suggested to be a causative cofactor in pityriasis rosea and other
inflammatory skin disorders. In addition, HHV-7 has been detected
in neoplasms, such as Kaposi’s sarcoma and lymphoproliferative
disorders. To date, more than 300 publications on
HHV-7 have been published and are listed in Index Medicus/
Medline. For this review, we have selected mostly original
papers for discussion, in particular publications providing epidemiologic
and experimental data on HHV-7 in skin diseases. This
review aims to provide information on the biology of HHV-7, to
summarize the data on its presence and the putative role of HHV-7
in various inflammatory and neoplastic skin diseases.
1. The Biology of Human Herpesvirus 7 (HHV-7)
In 1989, Frenkel et al.[5] isolated a new herpesvirus, which
was designated as HHV-7, from activated peripheral blood lymphocytes
(PBL) of a healthy individual. Genetically, it is closely
related to human herpesvirus 6A, human herpesvirus 6B (HHV-
6B) and CMV, with sequence homologies of up to 75%.[6] The
genome of 145-kB was cloned and encodes approximately 80
genes.[7,8] Various strains of HHV-7 were identified, which differ
mainly in regard to virus growth in different cell cultures.[9,10]
HHV-7 is still, even 13 years after its discovery, a little-studied
herpesvirus, which is in part because of its restricted growth in
cultured cells. So far, HHV-7 can only be propagated in vitro, in
cord blood lymphocytes, activated T cells and in SupT1 cells
(lymphoblastoid T cell line),[11,12] but viral replication remains
low even under optimized conditions.
† This manuscript is dedicated to Prof. Gabriella Campadelli Fiume, University of Bologna,

Bologna, Italy.
HHV-7 uses the CD4 molecule as a critical component of
the cellular membrane receptor.[13] Synthesis and expression of
cell surface CD4 becomes dramatically down-regulated in
HHV-7–infected cells.[14] In contrast to many other herpesvirus,
the range of host cells which can be infected by HHV-7 is small.
Apart from CD4+ T cells, macrophages have been identified as
target cells in vivo and in vitro.[15,16] Moreover, simultaneous replication
of HHV-7 and HHV-6B was found in CD68+ positive
cells of monocytic lineage in Kaposi’s sarcoma.[16] Infectious virus
can be isolated from the saliva of up to 75% of healthy individuals,[
17,18] but is only rarely found in breast milk.[19] Therefore,
saliva is considered as the main route of transmission.[20] Worldwide,
high seroprevalence rates have been reported (for a review
see Black & Pellett[1]). Primary infection mostly occurs within
the first 5 years of life, resulting in seroprevalence rates of 70 to
90% in young children and adolescents.[21,22] During primary infection,
HHV-7 DNA sequences can be detected in peripheral
blood mononuclear cells (PBMC) at acute and convalescent
stages. HHV-7 DNA is excreted into saliva and transiently into
stool at an early convalescent stage.[23]
After primary infection, HHV-7 is able to establish a latent
infection in PBMC, from which it can be reactivated.[24] In addition,
the presence of viral antigens indicative of viral replication
has been demonstrated in salivary glands and in a wide variety of
normal tissues, indicating chronic persistent HHV-7 infection.[
25,26] Although neutralizing antibodies and T cells specifically
targeting HHV-7 infected cells are generated,[11,27] little is
known about the immune response controlling HHV-7 infection.
The genetic similarities between HHV-7 and other members
of the β-herpesvirus subfamily render the development of
HHV-7–specific diagnostic tools a challenging project. Unique
nucleotide sequences allow for HHV-7–specific detection by
polymerase chain reaction (PCR), Southern blot and in situ hybridization.
By PCR, HHV-7 DNA can be detected in up to 90%
of PBL of healthy adults.[28,29] The evaluation of various immunoassays
for detection of virus-specific serum antibodies indicated
that most human sera contain cross-reactive antibodies
against HHV-6 and HHV-7, and that the degree of cross-reactivity
varies between individual serum specimens.[30] Immunogenic
proteins of HHV-7 and HHV-7–infected cells have been identified.[
31] An 85-kDa phosphoprotein (pp85) represents an immunodominant
protein specific for HHV-7,[32] and is localized to
the tegument substructure of the HHV-7 virion.[33] In addition, a
89-kDa protein was identified as a HHV-7–specific serologic
marker by immunoblot assay.[34] Recombinant proteins have been
developed, which can be used for diagnostic purposes.[35] In most
studies, PCR is the method most often applied for the detection
of HHV-7. However, in particular in studies focusing on a pathogenic
association between HHV-7 and diseases, PCR-based data
have to be interpreted with caution, in respect to the latent and
chronic persistent infection of HHV-7 found in various host tissues.[
2. Disease Association
HHV-7 is reactivated from latently infected PBL by T cell
activation, whereas HHV-6B can not be reactivated under similar
conditions. However, latent HHV-6B can be recovered after the
cells become infected with HHV-7.[24] Once reactivated, the
HHV-6B genomes become prominent and HHV-7 disappears.
The ability of HHV-7 to reactivate HHV-6B from latent infections
complicates interpretation of data which focus on the association
of HHV-7 with diseases and results in ongoing debate about the
pathogenic role of HHV-7 in the investigated disorders.
2.1 Primary Infection
Based on seroepidemiologic data, primary infection occurs
early in life. Exanthema subitum (or roseola infantum) is a common
childhood disease characterized by fever, rash and neurologic
complications in some patients. HHV-6B was originally
identified as the primary causative agent of exanthema subitum.[
36] Seroconversion and isolation of HHV-7 from PBMC in
children with exanthema subitum, but without evidence of prior
or concurrent HHV-6 infections, prove that primary infection
with HHV-7 can manifest as exanthema subitum.[2,4] However,
some patients had previous HHV-6–related exanthema subitum[
37] and a simultaneous rise in anti–HHV-6 antibodies. These
observations, and the fact that HHV-6 is usually acquired earlier
in life than HHV-7,[4] raise the possibility that HHV-7 infection
may contribute only indirectly to exanthema subitum by reactivation
of HHV-6 in some children.[38] Neurologic complications
of HHV-7–associated illness seem to be quite frequent. Seizures,
febrile convulsion and even hemiplegia have been reported in the
context of primary infection with HHV-7,[4,39] and encephalitislike
symptoms have occurred in a child after bone-marrow transplantation.[
Primary infection of HHV-7 has also been attributed to cases
clinically manifesting as rubella and measles.[3] Moreover, macular
or maculopapular rashes, considered to be drug eruptions
resulting from antibiotics and mononucleosis-like disease, may
in fact be manifestations of primary infection with HHV-7 or
co-infections together with Epstein-Barr virus (EBV).[41,42] Thus,
HHV-7 should be considered as a cause in a variety of macularpapular
rashes in children.
310 Kempf
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)
2.2 HHV-7 and Pityriasis Rosea, Psoriasis and Other
Inflammatory Skin Diseases
Pityriasis rosea is an exanthematic, inflammatory, and spontaneously
resolving skin disease. There is substantial evidence for
an infectious etiology of pityriasis rosea and various infectious
agents, including viruses, have been proposed as causative agents
(for a review see Kempf and Burg[43]). In 1997, Drago et al.[44,45]
reported the detection of HHV-7 in all skin, plasma and PBMC
specimens from 12 patients with pityriasis rosea, by nested PCR.
Moreover, cytopathic effects were observed in SupT1 cells
(lymphoblastoid T cell line) after co-cultivation with the PBMC
of patients with pityriasis rosea, and herpesvirus-like particles
were found in the supernatants of co-cultures by electron microscopy.
The authors concluded that ‘the finding of HHV-7 DNA in
plasma which reflects viral replication and virulence strongly
supports its causative role in pityriasis rosea’,[45] or an association,
not necessarily causative, between HHV-7 and the disease.[
Subsequently, several other investigators analyzed the presence
of HHV-7 in patients with pityriasis rosea (see table I). Most
of these studies have been performed in Italy and Japan. Two
groups applied the same PCR protocol for detection of HHV-7 as
Drago et al.,[44,45] but HHV-7 DNA was completely absent or
found in only 16 of 36 (44%) plasma samples of patients with
pityriasis rosea.[46,47] Moreover, immunoglobulin M antibodies
against HHV-7 were not detected, and there was no increase in
immunoglobulin G titers (except for one case), although both
antibodies would have been expected to rise in primary and/or
reactivation infections.[46,48] Additionally, investigations of skin
biopsies of pityriasis rosea lesions mostly showed an absence, or
very low detection rate, of HHV-7 DNA.[49-51] In our study, we
focused on the presence of HHV-7 in skin biopsies of herald
patches and secondary pityriasis rosea lesions.[49] Two detection
methods, a nested PCR protocol[6] and an immunohistochemical
approach using a well-characterized monoclonal antibody directed
against the structural phosphoprotein pp85 of HHV-7,
were employed. HHV-7 was detected in only 1 of 13 (8%) archival
skin biopsies of pityriasis rosea lesions, which represented a
smaller incidence than in controls of normal skin [2 of 14 biopsies
(14%)].[49] In several studies, HHV-7 DNA was found in similar,
or even lower, percentages in the PBL or PBMC of patients with
pityriasis rosea compared with controls.[50,52-54] Two studies of
HHV-7 DNA in plasma, which serves as a marker of active infection,
demonstrated the absence of HHV-7,[54,55] whereas in one
study HHV-7 DNA was present in only 16 of 36 (44%) of plasma
Controversial data might be partly because of geographic
variations in the prevalence of HHV-7 infections, as well as dif-
Table I. Viral studies on human herpesvirus 7 in pityriasis rosea
Reference Study country Investigated material Detection methods Results
Drago et al.[44,45] Italy Skin, PBMC, plasma PCR, EM, cell culture HHV-7 DNA in all 12 PR

Cytopathic effect in co-cultures; herpesvirus-like particles in
supernatant of co-cultures
Kempf et al.[49] Switzerland Skin PCR, IHC HHV-7 in 1/13 PR samples and 2/14 controls
Yoshida[47] Japan Peripheral blood DNA PCR HHV-7 DNA in all samples of 4 patients with PR and 3

Yasukawa et al.[52] Japan PBMC PCR, cell culture, SA HHV-7 DNA in 1/14 samples
Watanabe et al.[46] Japan Plasma PCR, SA HHV-7 DNA in 16/36 (44%) plasma samples of patients with

but not in 31 control samples. No detection of IgM and no increase
in IgG titers of antibodies against HHV-7
Kosuge et al.[53] Japan Serum, PBL PCR HHV-7 DNA in 13/30 (43%) and 14/25 (56%) PBMC samples of
patients and controls, respectively
Rise in titers of anti–HHV-7 antibodies in 2/44 cases
Offidani et al.[50] Italy PBMC, skin scales,
saliva and urine
PCR HHV-7 DNA in saliva of 5/12 (42%) patients and 14/20 (70%)
controls. No detection of HHV-7 DNA in all other samples
Chuh and Peiris[55] China Plasma, PBL PCR, SA No HHV-7 DNA in plasma in all 3 patients; HHV-7 DNA

in PBL of
only 1/3 patients
Chuh et al.[54] China Plasma, PBL PCR, SA No HHV-7 DNA in plasma, but in PBL samples of 7/15

patients with PR and 5/15 (33%) controls
Antibodies in serum of all 15 patients and 15 controls
Wong et al.[51] Taiwan Skin PCR, viral culture HHV-7 DNA or virions in none of the biopsies of 24

patients and 20
EM = electron microscopy; HHV-7 = human herpesvirus 7; IgG = immunoglobulin G; IgM =

immunoglobulin M; IHC = immunohistochemistry; PBL = peripheral
blood lymphocytes; PBMC = peripheral blood mononuclear cells; PCR = polymerase chain reaction; PR

= pityriasis rosea; SA = serologic assays.
HHV-7 in Dermatology 311
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)
ferences in the sensitivity and specificity of the applied detection
methods. Moreover, to assess the role of HHV-7 in inflammatory
diseases, several compartments (skin, plasma and PBL) of the
affected individuals should be evaluated for the presence of HHV-
7 virions, antigens or nucleic acids. In summary, so far there are
no consistent data supporting an association of HHV-7 and pityriasis
In a recent article, β-herpesviruses (CMV, HHV-6 and HHV-
7) were investigated as possible causative antigens in psoriasis.
Skin biopsies from ten patients with chronic plaque psoriasis
were investigated by PCR for the presence of HHV-7 DNA, but
HHV-7 could not be detected in involved or uninvolved skin.
Although viruses or viral antigens may play a role in the pathogenesis
of psoriasis, none of the β-herpesviruses seem to be
linked to this common skin disease.
Ongradi et al.[56] reported simultaneous infection of HHV-7
and parvovirus B19 in papular-purpuric gloves-and-socks syndrome,
but it cannot be excluded that HHV-7 was merely reactivated
during infection with parvovirus B19. Apart from these
diseases, no other inflammatory skin diseases have yet been examined
for the presence of HHV-7, and the clinical manifestations
of HHV-7 reactivation are still to be identified.
3. HHV-7 and Immunosuppression
Recently, HHV-7 has been identified as an emerging pathogen
in transplant recipients. HHV-6 and HHV-7 are considered to
induce immunosuppression by targeting lymphocytes, natural
killer cells and monocytes.[57] After kidney transplantation, HHV-
7 DNA was detected (by PCR) in PBMC in 39% of the patients,
whereas only 9% of healthy controls showed ‘HHV-7 DNAemia’.[
58] In this study, so called ‘CMV disease or post-transplant–
occurring viral disease’ was associated with rising antibody titers
to HHV-7. Patients with detectable HHV-7 DNA in their plasma
had significantly higher plasma CMV loads.[59] Recently, Kidd et
al.,[60] in a prospective study by clinicopathologic analysis,
showed that in patients with rejection, the presence of HHV-7
DNA in peripheral blood samples was associated with more episodes
of rejection. Two studies revealed that there was a significant
increase in ‘CMV disease’ occurring in patients with CMV
and HHV-7 co-infection, compared with those with CMV infection
alone.[60,61] Therefore, HHV-7 may act as a possible cofactor
in the development of ‘CMV disease’ in renal transplant patients
and may potentially exacerbate graft rejection. In liver transplant
recipients, HHV-7 may be the cause of some episodes of hepatitis
and pyrexia.[62] In contrast, no correlation between HHV-7 and
acute graft-versus-host disease or delayed engraftment could be
observed in patients with allogenic bone marrow transplantation.[
Since CD4 is also used as a cellular receptor by HIV, the
interactions between HHV-7 and HIV have been intensively studied.
Both viruses can reciprocally block infection of CD4+ lymphoid
cells, as well as in macrophages in vitro.[13,15] In vivo, HHV-
7 was more frequently found in the lymph nodes of patients with
AIDS, than in individuals who were HIV-seronegative.[64] Contradictory
data of the viral load of HHV-7 in the saliva of patients
infected with HIV have been reported and may result from fluctuations
of viral load in the saliva within the same individual over
time.[65,66] However, the data are controversial and further studies
are needed to clarify the in vivo interaction between HHV-7 and
4. HHV-7 and Neoplasms
No transforming genes of HHV-7 have been identified, thus
rendering it rather implausible that HHV-7 is involved in the direct
tumorigenesis of neoplasms. However, since the cellular tropism
of HHV-7 is mainly restricted to cells of lymphoid origin,
the question arose whether lymphoid neoplasms are linked to this
lymphotropic herpesvirus. Hodgkin’s disease, which is considered
to be of viral origin, has been intensively examined for the
presence of HHV-7. Viral DNA was found by nested PCR in 33
of 88 (38%) Hodgkin’s disease biopsies, with seven of those cases
showing co-infection with HHV-6, and 11 cases containing EBV
DNA.[67] In another study, HHV-7 DNA was detected significantly
more often by PCR in Hodgkin’s disease biopsies independently
of the histological type, compared with reactive lymph
nodes.[68] However, quantitative PCR revealed only a low level
of viral load in the majority of the examined samples. Moreover,
in situ hybridization for HHV-7 DNA was positive in a low number
of small T lymphocytes, and consistently negative in Hodgkin
and Reed-Sternberg cells, which also appeared negative for HHV-
7 at immunohistochemistry.[68] In contrast to EBV, β-
herpesviruses are therefore unlikely to have a role in the etiology
of Hodgkin’s disease. The presence of HHV-7 is most probably a
result of recruitment of nonmalignant, reactive T cells in Hodgkin’s
disease tissue.[68] In regard to non-Hodgkin’s lymphomas,
HHV-7 could not be found by Southern blot hybridization in 32
lymph node specimens with non-Hodgkin’s lymphomas.[69]
Evaluating primary cutaneous T and B cell lymphomas,
Nagore et al.[70] detected HHV-7 DNA in 9 of 64 (14%) samples
comprising mycosis fungoides, CD30+ large cell lymphoma, follicle
center cell lymphoma and one case of marginal zone lymphoma.[
70] We have previously analyzed 37 fresh, frozen and formalin-
fixed, paraffin-embedded biopsies of lymphomatoid
312 Kempf
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)
papulosis, which belongs to the spectrum of primary cutaneous
CD30+ T cell lymphomas, and found HHV-7 DNA sequences by
nested PCR in 5 of 37 (14%) biopsies.[71] Thus far, these data do
not indicate an association between HHV-7 and nodal or primary
cutaneous T or B cell lymphomas.
Human herpesvirus 8 (HHV-8) has been identified as a causative
factor in the pathogenesis of Kaposi’s sarcoma, a vascular
neoplasm occurring in various epidemiologic forms.[72,73] HHV-8
is a ‘conditio sine qua non’ for Kaposi’s sarcoma development,
but other cofactors are involved in the maintenance and propagation
of tumor growth. Studies on the presence of other viruses in
Kaposi’s sarcoma, including HHV-7, revealed controversial data
(for a review see Kempf & Adams[74]). We found HHV-7 DNA
and structural antigens (pp85) in 9 of 32 (28%) patients with
AIDS-associated Kaposi’s sarcoma and in 1 of 7 patients with
classical-sporadic HIV-negative Kaposi’s sarcoma,[16] whereas
HHV-7 could not be detected in non–AIDS-related Kaposi’s sarcoma
forms by others.[75] In some of the Kaposi’s sarcoma tumors,
co-infection of CD68+ cells of monocytic lineage with
HHV-6B and HHV-7 could be observed. HHV-7 infection has
been shown to cause significant immunomodulatory effects with
increased levels of cytokines (tumor necrosis factor-α, transforming
growth factor-β and interferon-γ).[76] Thus, we hypothesize
that infection of tumor-infiltrating CD68+ cells by HHV-6 and
HHV-7 may contribute to tumor propagation via secretion of tumor
growth-enhancing cytokines.
5. HHV-7 and Antivirals
With increasing evidence of HHV-7 as a cofactor for ‘viral
disease’ in transplant recipients, it becomes more important to
analyze antivirals for their efficacy to inhibit HHV-7 replication.
HHV-7 lacks a homologue of the thymidine kinase gene. Therefore,
HHV-7 replication is largely unaffected by thymidine kinase–
dependent drugs, such as aciclovir and its derivatives.[10,77] There
are controversial data on the effect of ganciclovir on HHV-7 in
renal transplant recipients. Brennan et al.[78] reported that
ganciclovir, administered either orally or intravenously, had no
effect on the prevalence of HHV-7 viremia,[78] whereas antiviral
therapy with ganciclovir reduced the load of CMV, HHV-6 and
HHV-7 in another study.[79] Nucleoside phosphonates, including
cidofovir, and inhibitors of DNA polymerases, such as foscarnet
(phosphonoformic acid), are promising drugs against HHV-7,
since they are potent inhibitors of HHV-7 replication.[80]
6. Conclusion
Thirteen years after the discovery of HHV-7, there has been
considerable progress in characterizing its genetic structure and
the virus-induced effects on infected host cells, and in the development
of diagnostic tools. Nevertheless, the role of HHV-7 in
various systemic diseases, as well as in skin disorders, has still to
be defined. Well-characterized, standardized and widely available
diagnostic tools are an important prerequisite to enable comparison
of study results and to increase our knowledge on the
biology and pathogenesis of HHV-7. In regard to the fact that
human herpesviruses in general are often linked to skin disorders,
and that HHV-7 infection can manifest with a variety of maculopapular
rashes in childhood, it can be expected that additional
clinical manifestations of primary and reactivated HHV-7 infection
will be identified in the future. Moreover, the ability of HHV-
7 to induce cytokine production in infected cells could make
HHV-7 an important pathogenic cofactor in inflammatory conditions,
and also in neoplastic processes where the cytokine milieu
is of utmost importance for the regulation of tumor growth. In
addition, the relatively restricted cellular tropism of HHV-7 for
lymphocytes and macrophages may render this virus an interesting
vector for gene therapy. Thus, HHV-7 is likely to become an
emerging pathogen in dermatology, and in general.
The author declares no conflict of interest or financial support for the
preparation of this manuscript.
1. Black JB, Pellett PE. Human herpesvirus 7. Rev Med Virol 1999; 9: 245-62
2. Torigoe S, Kumamoto T, Koide W, et al. Clinical manifestations associated with
human herpesvirus 7 infection. Arch Dis Child 1995; 72: 518-9
3. Black JB, Durigon E, Kite Powell K, et al. Seroconversion to human herpesvirus
6 and human herpesvirus 7 among Brazilian children with clinical diagnoses of
measles or rubella. Clin Infect Dis 1996; 23: 1156-8
4. Caserta MT, Hall CB, Schnabel K, et al. Primary human herpesvirus 7 infection: a
comparison of human herpesvirus 7 and human herpesvirus 6 infections in children.
J Pediatr 1998; 133: 386-9
5. Frenkel N, Schirmer EC, Wyatt LS, et al. Isolation of a new herpesvirus from human
CD4+ T cells. Proc Natl Acad Sci U S A 1990; 87: 748-52
6. Berneman ZN, Ablashi DV, Li G, et al. Human herpesvirus 7 is a T-lymphotropic
virus and is related to, but significantly different from, human herpesvirus 6 and
human cytomegalovirus. Proc Natl Acad Sci U S A 1992; 89: 10552-6
7. Nicholas J. Determination and analysis of the complete nucleotide sequence of
human herpesvirus. J Virol 1996; 70: 5975-89
8. Singer O, Frenkel N. Human herpesvirus 7 (HHV-7) DNA: analyses of clones
spanning the entire genome. Arch Virol 1997; 142: 287-303
9. Berneman ZN, Gallo RC, Ablashi DV, et al. Human herpesvirus 7 (HHV-7) strain
JI: independent confirmation of HHV-7. J Infect Dis 1992; 166: 690-1
10. Black JB, Burns DA, Goldsmith CS, et al. Biologic properties of human herpesvirus
7 strain SB. Virus Res 1997; 52: 25-41
11. Secchiero P, Berneman ZN, Gallo RC, et al. Biological and molecular characteristics
of human herpesvirus 7: in vitro growth optimization and development
of a syncytia inhibition test. Virology 1994; 202: 506-12
12. Cermelli C, Pietrosemoli P, Meacci M, et al. SupT-1: a cell system suitable for an
efficient propagation of both HHV-7 and HHV-6 variants A and B. New
Microbiol 1997; 20: 187-96
HHV-7 in Dermatology 313
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)
13. Lusso P, Secchiero P, Crowley RW, et al. CD4 is a critical component of the
receptor for human herpesvirus 7: interference with human immunodeficiency
virus. Proc Natl Acad Sci U S A 1994; 91: 3872-6
14. Furukawa M, Yasukawa M, Yakushijin Y, et al. Distinct effects of human herpesvirus
6 and human herpesvirus 7 on surface molecule expression and function
of CD4+ T cells. J Immunol 1994; 152: 5768-75
15. Crowley RW, Secchiero P, Zella D, et al. Interference between human herpesvirus
7 and HIV-1 in mononuclear phagocytes. J Immunol 1996; 156: 2004-8
16. Kempf W, Adams V, Wey N, et al. CD68+ cells of monocyte/macrophage lineage
in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma
are singly or doubly infected with human herpesviruses 7 and 6B. Proc Natl
Acad Sci U S A 1997; 94: 7600-5
17. Wyatt LS, Frenkel N. Human herpesvirus 7 is a constitutive inhabitant of adult
human saliva. J Virol 1992; 66: 3206-9
18. Hidaka Y, Liu Y, Yamamoto M, et al. Frequent isolation of human herpesvirus 7
from saliva samples. J Med Virol 1993; 40: 343-6
19. Fujisaki H, Tanaka Taya K, Tanabe H, et al. Detection of human herpesvirus 7 (HHV-
7) DNA in breast milk by polymerase chain reaction and prevalence of HHV-7
antibody in breast-fed and bottle-fed children. J Med Virol 1998; 56: 275-9
20. Takahashi Y, Yamada M, Nakamura J, et al. Transmission of human herpesvirus
7 through multigenerational families in the same household. Pediatr Infect Dis
J 1997; 16: 975-8
21. Tanaka Taya K, Kondo T, Mukai T, et al. Seroepidemiological study of human herpesvirus-
6 and -7 in children of different ages and detection of these two viruses
in throat swabs by polymerase chain reaction. J Med Virol 1996; 48: 88-94
22. Huang LM, Lee CY, Liu MY, et al. Primary infections of human herpesvirus-7
and herpesvirus-6: a comparative, longitudinal study up to 6 years of age. Acta
Paediatr 1997; 86: 604-8
23. Asano Y, Suga S, Yoshikawa T, et al. Clinical features and viral excretion in an
infant with primary human herpesvirus 7 infection. Pediatrics 1995; 95: 187-90
24. Katsafanas GC, Schirmer EC, Wyatt LS, et al. In vitro activation of human
herpesviruses 6 and 7 from latency. Proc Natl Acad Sci U S A 1996; 93: 9788-92
25. Sada E, Yasukawa M, Ito C, et al. Detection of human herpesvirus 6 and human
herpesvirus 7 in the submandibular gland, parotid gland, and lip salivary gland
by PCR. J Clin Microbiol 1996; 34: 2320-1
26. Kempf W, Adams V, Mirandola P, et al. Persistence of human herpesvirus 7 in
normal tissues detected by expression of a structural antigen. J Infect Dis 1998;
178: 841-5
27. Yasukawa M, Yakushijin Y, Furukawa M, et al. Specificity analysis of human
CD4+ T-cell clones directed against human herpesvirus 6 (HHV-6), HHV-7,
and human cytomegalovirus. J Virol 1993; 67: 6259-64
28. Wilborn F, Schmidt CA, Lorenz F, et al. Human herpesvirus type 7 in blood
donors: detection by the polymerase chain reaction. J Med Virol 1995; 47: 65-9
29. Kidd IM, Clark DA, Ait Khaled M, et al. Measurement of human herpesvirus 7
load in peripheral blood and saliva of healthy subjects by quantitative polymerase
chain reaction. J Infect Dis 1996; 174: 396-401
30. Black JB, Schwarz TF, Patton JL, et al. Evaluation of immunoassays for detection
of antibodies to human herpesvirus 7. Clin Diagn Lab Immunol 1996; 3: 79-83
31. Foa Tomasi L, Avitabile E, Ke L, et al. Polyvalent and monoclonal antibodies
identify major immunogenic proteins specific for human herpesvirus 7-infected
cells and have weak cross-reactivity with human herpesvirus 6. J Gen
Virol 1994; 75: 2719-27
32. Foa Tomasi L, Fiorilli MP, Avitabile E, et al. Identification of an 85 kDa phosphoprotein
as an immunodominant protein specific for human herpesvirus 7-infected
cells. J Gen Virol 1996; 77: 511-8
33. Stefan A, Secchiero P, Baechi T, et al. The 85-kilodalton phosphoprotein (pp85)
of human herpesvirus 7 is encoded by open reading frame U14 and localizes
to a tegument substructure in virion particles. J Virol 1997; 71: 5758-63
34. Black JB, Schwarz TF, Patton JL, et al. Evaluation of immunoassays for detection
of antibodies to human herpesvirus 7. Clin Diagn Lab Immunol 1996; 3: 79-83
35. Stefan A, De Lillo M, Frascaroli G, et al. Development of recombinant diagnostic
reagents based on pp85(U14) and p86(U11) proteins to detect the human immune
response to human herpesvirus 7 infection. J Clin Microbiol 1999; 37: 3980-5
36. Yamanishi K, Okuno T, Shiraki K, et al. Identification of human herpesvirus-6 as
a causal agent for exanthema subitum. Lancet 1988; I: 1065-7
37. Ueda K, Kusuhara K, Okada K, et al. Primary human herpesvirus 7 infection and
exanthema subitum [letter]. Pediatr Infect Dis J 1994; 13: 167-8
38. Frenkel N, Wyatt LS. HHV-6 and HHV-7 as exogenous agents in human lymphocytes.
Dev Biol Stand 1992; 76: 259-65
39. Torigoe S, Koide W, Yamada M, et al. Human herpesvirus 7 infection associated
with central nervous system manifestations. J Pediatr 1996; 129: 301-5
40. Chan PK, Peiris JS, Yuen KY, et al. Human herpesvirus-6 and human herpesvirus-7
infections in bone marrow transplant recipients. J Med Virol 1997; 53: 295-305
41. Bruns R, Muller CE, Wiersbitzky SK, et al. Clinical presentations of infection by
the human herpesvirus-7 (HHV-7). Pediatr Hematol Oncol 2000; 17: 247-52
42. Chiu HH, Lee CY, Lee PI, et al. Mononucleosis syndrome and coincidental human
herpesvirus-7 and Epstein-Barr virus infection. Arch Dis Child 1998; 78: 479-80
43. Kempf W, Burg G. Pityriasis rosea, a virus-induced skin disease: an update. Arch
Virol 2000; 145: 1509-20
44. Drago F, Ranieri E, Malaguti F, et al. Human herpesvirus 7 in patients with pityriasis
rosea: electron microscopy investigations and polymerase chain reaction
in mononuclear cells, plasma and skin. Dermatology 1997; 195: 374-8
45. Drago F, Ranieri E, Malaguti F, et al. Human herpesvirus 7 in patients with pityriasis
rosea [letter]. Lancet 1997; 349: 1367
46. Watanabe T, Sugaya M, Nakamura K, et al. Human herpesvirus 7 and pityriasis
rosea. J Invest Dermatol 1999; 113: 288-9
47. Yoshida M. Detection of human herpesvirus 7 in patients with pityriasis rosea and
healthy individuals. Dermatology 1999; 199: 197-8
48. Lebbe C, Agbalika F. Pityriasis rosea and human herpesvirus 7, a true association
[letter]? Dermatology 1998; 196: 275
49. Kempf W, Adams V, Kleinhans M, et al. Pityriasis rosea is not associated with
human herpesvirus 7. Arch Dermatol 1999; 135: 1070-2
50. Offidani A, Pritelli E, Simonetti O, et al. Pityriasis rosea associated with herpesvirus
7 DNA. J Eur Acad Dermatol Venereol 2000; 14: 313-4
51. Wong WR, Tsai CY, Shih SR, et al. Association of pityriasis rosea with human
herpesvirus-6 and human herpesvirus-7 in Taipei. J Formos Med Assoc 2001;
100: 478-83
52. Yasukawa M, Sada E, MacHino H, et al. Reactivation of human herpesvirus 6 in
pityriasis rosea. Br J Dermatol 1999; 140: 169-70
53. Kosuge H, Tanaka Taya K, Miyoshi H, et al. Epidemiological study of human
herpesvirus-6 and human herpesvirus-7 in pityriasis rosea. Br J Dermatol 2000;
143: 795-8
54. Chuh AA, Chiu SS, Peiris JS. 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. Acta Derm Venereol 2001; 81: 289-90
55. Chuh AA, Peiris JS. Lack of evidence of active human herpesvirus 7 (HHV-7)
infection in three cases of pityriasis rosea in children. Pediatr Dermatol 2001;
18: 381-3
56. Ongradi J, Becker K, Horvath A, et al. Simultaneous infection by human herpesvirus
7 and human parvovirus B19 in papular-purpuric gloves-and-socks syndrome
[letter]. Arch Dermatol 2000; 136: 672
57. Dockrell DH, Paya CV. Human herpesvirus-6 and -7 in transplantation. Rev Med
Virol 2001; 11: 23-36
58. Osman HK, Peiris JS, Taylor CE, et al. ‘Cytomegalovirus disease’ in renal allograft
recipients: is human herpesvirus 7 a co-factor for disease progression? J Med
Virol 1996; 48: 295-301
59. Tong CY, Bakran A, Williams H, et al. Association of human herpesvirus 7 with
cytomegalovirus disease in renal transplant recipients. Transplantation 2000;
70: 213-6
60. Kidd IM, Clark DA, Sabin CA, et al. Prospective study of human
betaherpesviruses after renal transplantation: association of human herpesvirus
314 Kempf
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)
7 and cytomegalovirus co-infection with cytomegalovirus disease and increased
rejection. Transplantation 2000; 69: 2400-4
61. Chapenko S, Folkmane I, Tomsone V, et al. Co-infection of two beta-herpesviruses
(CMV and HHV-7) as an increased risk factor for ’CMV disease’ in patients
undergoing renal transplantation. Clin Transplant 2000; 14: 486-92
62. Griffiths PD, Ait Khaled M, Bearcroft CP, et al. Human herpesviruses 6 and 7 as
potential pathogens after liver transplant: prospective comparison with the effect
of cytomegalovirus. J Med Virol 1999; 59: 496-501
63. Wang FZ, Dahl H, Linde A, et al. Lymphotropic herpesviruses in allogeneic bone
marrow transplantation. Blood 1996; 88: 3615-20
64. Kempf W, Muller B, Maurer R, et al. Increased expression of human herpesvirus
7 in lymphoid organs of AIDS patients. J Clin Virol 2000; 16: 193-201
65. Di Luca D, Mirandola P, Ravaioli T, et al. Human herpesviruses 6 and 7 in salivary
glands and shedding in saliva of healthy and human immunodeficiency virus
positive individuals. J Med Virol 1995; 45: 462-8
66. Kidd IM, Clark DA, Aitkhaled M, et al. Measurement of human herpesvirus 7 load
in peripheral blood and saliva of healthy subjects by quantitative polymerase
chain reaction. J Infect Dis 1996; 174: 396-401
67. Schmidt CA, Oettle H, Peng R, et al. Presence of human beta- and gamma-herpes
virus DNA in Hodgkin’s disease. Leuk Res 2000; 24: 865-70
68. Secchiero P, Bonino LD, Lusso P, et al. Human herpesvirus type 7 in Hodgkin’s
disease. Br J Haematol 1998; 101: 492-9
69. Berneman ZN, Torelli G, Luppi M, et al. Absence of a directly causative role for
human herpesvirus 7 in human lymphoma and a review of human herpesvirus
6 in human malignancy. Ann Hematol 1998; 77: 275-8
70. Nagore E, Ledesma E, Collado C, et al. Detection of Epstein-Barr virus and human
herpesvirus 7 and 8 genomes in primary cutaneous T- and B-cell lymphomas.
Br J Dermatol 2000; 143: 320-3
71. Kempf W, Kadin ME, Kutzner H, et al. Lymphomatoid papulosis and human
herpesviruses: a PCR-based evaluation for the presence of human herpesvirus
6, 7 and 8 related herpesviruses. J Cutan Pathol 2001; 28: 29-33
72. Chang Y, Cesarman E, Pessin MS, et al. Identification of herpesvirus-like DNA
sequences in AIDS-associated Kaposi’s sarcoma. Science 1994; 266: 1865-9
73. Antman K, Chang Y. Kaposi’s sarcoma. N Engl J Med 2000; 342: 1027-38
74. Kempf W, Adams V. Viruses in the pathogenesis of Kaposi’s sarcoma: a review.
Biochem Mol Med 1996; 58: 1-12
75. Drago F, Raineri E, Rebora A. Non-AIDS-related Kaposi sarcoma tissues do not
contain DNA sequences of HHV-6, HHV-7, Epstein-Barr virus, cytomegalovirus
and HSV. Acta Derm Venereol 1998; 78: 485
76. Atedzoe BN, Menezes J, D’Addario M, et al. Modulatory effects of human herpes
virus-7 on cytokine synthesis and cell proliferation in human peripheral blood
mononuclear cell cultures. J Leukoc Biol 1999; 66: 822-8
77. Yoshida M, Yamada M, Tsukazaki T, et al. Comparison of antiviral compounds
against human herpesvirus 6 and 7. Antiviral Res 1998; 40: 73-84
78. Brennan DC, Storch GA, Singer GG, et al. The prevalence of human herpesvirus-7
in renal transplant recipients is unaffected by oral or intravenous ganciclovir. J
Infect Dis 2000; 181: 1557-61
79. Mendez JC, Dockrell DH, Espy MJ, et al. Human beta-herpesvirus interactions in
solid organ transplant recipients. J Infect Dis 2001; 183: 179-84
80. Safrin S, Cherrington J, Jaffe HS. Clinical use of cidofovir. Rev Med Virol 1997;
7: 73-84
Correspondence and offprints: Dr Werner Kempf, Department of Dermatology,
University Hospital, Gloriastrasse 31, Zurich, CH-8091, Switzerland.
HHV-7 in Dermatology 315
 Adis International Limited. All rights reserved. Am J Clin Dermatol 2002; 3 (5)

Radicales Libres y Enfermedades de la piel

Filed under: Debates interesantes,Interesante — dermatologia @ 2:14



Los Radicales Libres o Especies Reactivas de Oxigeno constituyen los elementos patológicos que inducen al estrés oxidativo y a partir de este a múltiples enfermedades en el ser humano.

El sistema cardiovascular, el nervioso, el aparato ocular, el sistema respiratorio, el aparato osteoarticular, el tubo digestivo, el riñón, la glándula mamaria y el útero, son ejemplos de sistemas diana para los radicales libres y el estrés subsiguiente.

La piel es el órgano mas extenso del ser humano, estructuralmente contiene altas cantidades de lípidos, proteínas y DNA, elementos que la hacen extremadamente sensible a los procesos oxidativos. El daño cutáneo por especies reactivas de oxigeno puede ser de origen endógeno, ambiental o en la propia piel (1,2)

El Vitiligo y el Daño Solar son los ejemplos mas destacados y estudiados en los últimos años sobre el efecto de los radicales libres y el estrés oxidativo sobre el tegumento. (3,4,5)


El Vitiligo es una afección cutánea clásica, pues es evidente para todos y porque afecta solo a la piel, pudiera decirse que es una de las afecciones de la piel que más rechazo provoca, nótese que en la India le dicen manchados y que cuando una persona comienza a padecer vitiligo, la pareja sexual tiene derecho a divorciarse sin ningún beneficio para el enfermo. Se le denomina también, Leucoderma Adquirida Idiopática, y vulgarmente se le conoce como: Pinto, Pintado, Nostálgico, Manchado y Carare por citar algunos ejemplos (6, 7,8)

Clínicamente se caracteriza por la presencia de manchas o máculas acrómicas, la enfermedad se caracteriza por exclusivamente por lesiones cutáneas, las cuales consisten en áreas sin pigmentación sin otra alteración de la piel a su nivel, el color es blanco marfil, habiendo sido comparado con la leche y el queso (6, 7,8)



Las lesiones pueden aparecer en cualquier sitio de la superficie cutánea, aunque tienen predilección por: dorso de las manos, alrededor de la boca y los ojos, regiones genitales y perigenitales y dorso de los pies. (6, 7,8)

Tienen una simetría relativa, existiendo lesiones en puntos simétricos del cuerpo, sin que necesariamente sean lesiones en espejo; puede hallarse, un halo hipercrómico rodeando las maculas, lo que, aunque frecuente, no es en la actualidad tan constante como se considero e otros tiempos. Muchas veces las maculas o placas acrónicas tienen distintos tonos de perdida del pigmento en su configuración, lo que ha sido señalado, según el numero de tonalidades en el interior, como vitiligo dicrómico, tricrómico, cuadricrómico y hasta pentacrómico (6, 7,8)

La incidencia de la enfermedad varía entre el 0.5 y el 4% de la población mundial; sin embargo, en América Latina  llega hasta el 8.8%, destacándose México donde alcanza hasta un 15% de la población, es de señalar que en pacientes con enfermedades autoinmunes también existe un aumento de la incidencia del vitiligo que llega hasta el 10% (6,7,8)

Desde el punto de vista fisiopatológico, se han postulado múltiples teorías, entre las que se destacan: estrés, autoinmunidad, herencia, factores neurohumorales, autotoxicidad y exposición química exógena, o sea, que debe ser considerada como una enfermedad multifactorial (6,7,8)

Los estudios sobre el estrés oxidativo han demostrado un aumento de los radicales libres y una disminución de las defensas antioxidantes en las lesiones acrónicas de los pacientes que padecen vitiligo; por tanto, el estrés oxidativo juega un papel determinado en la fisiopatología de la afección (3)

Se ha documentado, tanto in vitro como in vivo la acumulación de peroxido de hidrogeno en asociación con bajos niveles de catalasa en la epidermis, explicable, pues la sobreproducción de peroxido de hidrogeno puede causar inactivación de la catalasa así como vacuolización de los melanocitos con una traducción clínica evidente, la pérdida de pigmento y la aparición del vitiligo (3,9,10)

Queda aún por responder el hecho de cómo y por qué se desencadena el estrés oxidativo en estos pacientes. Existe una alta relación entre el vitiligo y otras enfermedades autoinmunes, habiéndose demostrado la presencia de autoanticuerpos frente a los melanocitos epidérmicos entre estos pacientes. Se considera, además, que las catecolaminas podrían ser elementos de neurotoxicidad frente a los melanocitos, nótese que un gran número de pacientes asocian el debut de la enfermedad con fenómenos de estrés emocional, en estas condiciones y en individuos con predisposición genética a padecerla, los melanocitos podrían ser autotóxicos (6,7,8)

Vamos a partir del hecho de la predisposición genética a padecer vitiligo, y esto explica un tanto la asociación a otras enfermedades autoinmunes, en las cuales también existe una alta predisposición genética; estos individuos tendrían una hiperreactividad a los elementos neurotóxicos liberados en estados de estrés o tensión emocional, hecho que DESENCADENARIA el estrés oxidativo a nivel epidérmico con la acumulación de especies reactivas de oxigeno, inactivación de las defensas antioxidantes y vacuolización de los melanocitos, así, éstos últimos serian reconocidos por los elementos inmunes autoreactivos con la consiguiente producción de autoanticuerpos, se produciría un proceso de mayor estrés oxidativo y de mayor producción de autoanticuerpos con la traducción clínica hacia el vitiligo. Ya en aquel paciente con lesiones clínicas de vitiligo, el estrés oxidativo provocado por las radiaciones ultravioletas seria aun mas intenso que en individuos normales por lo que se agregaría otro elemento negativo tanto en la evolución del paciente como en la respuesta a los diferentes esquemas de tratamiento.

Seria entonces, el estrés oxidativo un eslabón importante en la génesis de la enfermedad y por tanto, una diana hacia las perspectivas terapéuticas de esta enfermedad. Deben incluirse; sin duda, los antioxidantes en cualquier esquema terapéutico destinado a la curación de la enfermedad.


El daño solar se produce por la exposición indiscriminada y sin protección  a las radiaciones ultravioletas, las cuales tienen efectos agudos y crónicos sobre el tegumento cutáneo

Respuestas cutáneas frente a la radiación ultravioleta:

 Agudas:

Engrosamiento cutáneo

 Crónicas:


Sin duda, los efectos crónicos de las radiaciones ultravioletas son los más temidos y los de mayor importancia clínica.

El fotoenvejecimiento cutáneo o dermatoheliosis constituye el primer paso hacia la premalignidad y la posterior malignidad. Los individuos presentan una piel francamente engrosada, con elastosis (arrugas gruesas y evidentes) de un tinte bronceado mas o menos intenso y que se define claramente cuando comparamos áreas de piel expuestas al sol con áreas cubiertas por los vestidos habituales, se les denomina igualmente piel de marino o piel de campesino debido a que en ellos el sol deja su marca debido a sus labores habituales durante años de trabajo. (6,11)

Sobre esta piel dañada y preparada, aparecen lesiones premalignas y posteriormente lesiones malignas.

La premalignidad se caracteriza por la aparición de lesiones debidas al daño solar del tipo de las queratosis actínicas y el cuerno cutáneo que en un periodo mas o menos corto conducirían a la aparición de carcinomas cutáneos y la melanosis circunscrita de Dubreuilh que en un periodo similar conduciría a la aparición del melanoma maligno. Existen otras lesiones premalignas, que si bien no son dependientes directas del daño solar crónico, si son influenciadas negativamente por la exposición a las radiaciones solares y deben ser mencionadas. Cicatrices secundarias a lupus vulgar, leishmaniasis, lupus vulgar o quemaduras, ulceras cutáneas de larga duración, las dermatitis ocupacionales y la atrofia senil de la piel evolucionan a carcinomas cutáneos tanto mas rápido cuanto mayor sea el abuso de la exposición al sol. De igual manera los nevos pigmentados, sobre todo los y los displásticos evolucionan  melanoma maligno de forma mas rápida si la exposición interviene (11,12)

La malignidad cutánea es; sin duda, la más frecuente de todas, se estima que entre el 40 y el 50% de toda la población habrá padecido al menos de un tipo de cáncer cutáneo al llegar a los 65 años. Se destacan, entre otras, el carcinoma basocelular, el carcinoma espinocelular y el melanoma maligno (11,12)

Las radiaciones ultravioletas provocan un incremento en la producción de especies reactivas de oxigeno o radicales libres en la piel humana, los que son responsables del estrés oxidativo y del daño a proteínas, lípidos y sobre todo al DNA celular, daño que de no poder ser reparado por un exceso de radicales, por una disminución de las defensas antioxidantes o por ambos, conduce a la carcinogénesis (13,14)

Sin duda, la prevención del daño solar y sus consecuencias en el ser humano seria muy fácil si los individuos no se expusieran a las radiaciones solares; sin embargo, eso seria como cambiar el mundo, por lo que los mecanismos de prevención deben ir encaminados a la educación sobre cómo exponerse al sol y las medidas terapéuticas necesarias para evitar el efecto dañino de las radiaciones ultravioletas, momento en el cual los antioxidantes entran a jugar un rol de vital importancia

Los betacarotenos han sido los antioxidantes que preferentemente se han utilizado en la prevención del fotodaño; sin embargo, la vitamina C y la vitamina E también protegen eficazmente, de igual modo la coenzima Q 10 (CoQ10) para aplicación tópica en la fotoprotección, así como la ingestión de compuestos polifenólicos derivados del te verde con el mismo fin (15,16)

El modo de vida moderno conduce; a no dudar, a una mayor tendencia al uso del bronceado cutáneo como elemento de belleza tanto femenina como masculina; por otro lado, el indiscriminado deterioro de las capas atmosféricas protectoras provoca que el daño a las células expuestas sea cada vez mayor, deben buscarse entonces todos los elementos que sean capaces de protegernos de este inminente daño, estando los antioxidantes en la primera línea para la protección urgente y necesaria frente a ese enemigo presente y cada vez mas fuerte

Enseñemos a utilizar el vestuario correcto en labores que irremediablemente tienen una exposición al sol, eduquemos sobre las horas en que las radiaciones hacen mas daño, pero además, eduquemos sobre la ingestión diaria de productos antioxidantes en la dieta y prescribamos los antioxidantes necesarios para la prevención del dañó solar.

Referencias Bibliográficas.

1. Kohen R. Skin antioxidants: their role in aging and in oxidative stress – new approaches for their evaluation. Biomed Pharmacother, 1999;53(4):181-192

2. Robert B. Free radicals and tissue injury. Dialogues in Cardiovascular Medicine, 1998;3(1):3-21

3. Schallreuter KU, Moore J, Wood JM, Beazley WD, Gaze DC, Tobin DJ, et al. In vivo and in vitro evidence for hydrogen peroxide (H202) accumulation in the epidermis of patients with vitiligo and its successful removal by UVB-activated pseudocatalase. J Investig Dermatol Symp Proc 1999;4(1):91-96

4. Yaar-M, Cilchrest-BA Asing versus photoaging: postulated mechanism and effectors. J-Investig-Dermatol-Symp-Proc. 1998;3(1): 47-51

5. Podda-M; Traber-MG; Weber-C; Yan-LJ; Parker-L. UV – irradiation repletes antioxidants and causes oxidative damage in a model human skin. Free-Radic-Biol-Med. 1998; 24(1): 55-65

6. Arenas R. Atlas de dermatología, diagnostico y tratamiento. 2da edición. Interamericana 1996: 81-99

7. Agarwal-G. Vitiligo: an Ander-estimated problem. Fam-Pract. 1998; 15(suppl):S 19- 26

8. Mason-SH; Cohen-PR. Vitiligo. J-Gt-Houst-Dent-Soc. 1998; 69(7): 12-13

9. Masaki H, Okano Y, Sakurai H. Differential role of catalase and glutathione peroxidasa in cultured human fibroblast under exposure of H2O2 or ultraviolet B light. Arch Dermatol Res, 1998: 290(3): 113-118

10. Schallreuter KU. A review of recent advances on the regulation of pigmentation in the human epidermis. Cell Mol Biol, 1999:45(7): 943-949

11. Larrondo RJ, Hernández LM, González AR, Larrondo RP. Consideraciones sobre la prevención del cáncer de piel. Rev Cubana Med Gen Integr, 1996:12(3):284-288

12. Larrondo RJ, González AR, Hernández LM, Larrondo RP. Lesiones precancerosas en la piel del anciano. Estudio en 10 consultorios del médico de la familia Rev Cubana Med Gen Integr, 1996:12(1):20-23

13. Frikle T, Resl V, Racek J, Holecek V. Antioxidants and protection of skin against the effect of ultraviolet rays. Cas Lek Cesk, 2000:139(12):358-360

14. Lear JT, Smith AG, Strange RC, Fryer AA. Detoxifying enzyme genotypes and susceptibility to cutaneous malignancy. Br J Dermatol,2000:142(1):8-15

15. Hoppe U, Bergemann J, Diembeck W, Ennen J, Gohla S, Harris I, et al. Coenzyme Q10, a cutaneus antioxidant and energizer. Biofactors,1999:9(2-4):371-378

16. Katiyar SK, Matsui MS, Elmets CA, Mukhtar H. Polyphenolic antioxidant – epigallocatechin – 3 – gallate from green tea reduces UVB induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol,1999:69(2):148-153
Por el Dr. Rubén José Larrondo Muguercia.
Especialista de Primer Grado en Medicina General Integral y
Especialista de Primero y Segundo Grado en Dermatología.
Dermatólogo del centro de Histoterapia Placentaria.
Ciudad de la Habana. Cuba

25 julio 2016

Guías de manejo para dermatitis atópica

Filed under: Debates interesantes,Interesante — dermatologia @ 10:10

Lawrence F. Eichenfield, MDa, Mark Boguniewicz, MDb, Eric L. Simpson, MDc, John J. Russell, MDd, Julie K. Block, BAe, Steven R. Feldman, MD, PhDf,g, Adele R. Clark, PA-Cf, Susan Tofte, BSN, MS, FNP-Ch Fuente: Pediatrics. 2015 Sep;136(3):554-65. doi: 10.1542/peds.2014-3678. Epub 2015 Aug 3.

Se estima que en  2009 -2011, la dermatitis atópica (DA) afectó al 12,5% de los niños (0-17 años de edad) en los Estados Unidos, con un aumento de poco más de 5% desde 1997 hasta 1999. 1Entre estos pacientes, la gran mayoría (~67%) presentaron 2enfermedad  leve y como tal pudo ser manejada adecuadamente por el pediatra u otros prestadores de atención primaria (PAP)/ médico de cabecera. Sin embargo, la mayoría de los pediatras derivan incluso a sus pacientes con patología leve a los dermatólogos (~ 85%) y proporcionan una atención inicial única y limitada (81%).

Sean o no pacientes derivados a dermatología3, pediatras y médicos de familia seguirán desempeñando un papel central en el manejo para un seguimiento regular, el tratamiento de mantenimiento, la educación continua en pacientes internados y cuidadores, y el contacto de primera línea para los brotes y las complicaciones, como la infección estafilocócica secundaria.

El 6 de septiembre de 2013, se convocó una mesa redonda para discutir los retos en el manejo de la DA junto con las oportunidades de mejorarla a través de una variedad de disciplinas. Esta mesa redonda fue la única que incluyó un paciente abogado, así como representantes de la dermatología (general y pediátrica), alergia-inmunología pediátrica, medicina familiar, cuidado administrado, y de enfermería. Durante el debate, se hizo evidente que las guías de manejo de la DA actuales carecen de ciertos elementos que pueden mejorar su utilidad práctica, especialmente para los prestadores de atención primaria incluyendo los pediatras.


25 junio 2016

Respuesta de acitretin oral en el liquen amiloide

Filed under: Clinica y Terapeutica,Propuesta del editor — dermatologia @ 13:44


12 junio 2016

Manejo de cicatrices en pediatría

Filed under: Clinica y Terapeutica,Debates interesantes — dermatologia @ 6:54

Andrew C. Krakowski, Christine R. Totri, Matthias B. Donelan, Peter R. Shumaker Pediatrics. 2016; 137(2):e20142065

Cualquier lesión significativa a la dermis profunda, tales como quemaduras y otros traumas, inflamación, o cirugía, puede llevar a la cicatrización de heridas que se presentan clínicamente con la formación de una cicatriz. Se gastó mucho tiempo y energía en intentar clasificar a las cicatrices en base a la histopatología o morfología clínica. Aunque hacerlo es útil para la documentación y las decisiones de manejo, contradice la realidad de que una cicatriz por sí misma no es ni “buena” ni “mala”.

Las cicatrices son simplemente el punto final clínico de una confluencia de factores genéticos y ambientales que afectan el proceso de cicatrización de heridas después de una agresión cutánea. Desde la perspectiva de la historia humana, la mayoría de las heridas graves han sido traumáticas (por ejemplo, “uñas y dientes”, caídas, quemaduras, combates), involucrando extensas áreas de daños que necesitaban ser contenidas rápida y eficientemente para controlar el sangrado y la infección.


17 marzo 2016

Eritema anular eosinofílico

Filed under: Clinica y Terapeutica — dermatologia @ 12:20

Thomas L, Fatah S, Nagarajan S, Natarajan S. Clin Exp Dermatol. 2015 Dec;40(8):883-6.

El eritema anular eosinofílico (EAE) es una dermatosis rara, rica en eosinófilos descripta en adultos por Kahofer y col en el 2000. Clínicamente se caracteriza por pápulas y placas urticarianas no escamosas de configuración anular, predominantemente localizada en tronco y extremidades proximales.

Histológicamente, se observa generalmente un infiltrado denso perivascular e intersticial con abundantes eosinófilos en dermis.

Existe debate si el EAE es un subtipo de síndrome de Wells (WS) o una entidad separada, y se ha descripto una condición casi idéntica en infantes (AEI) por Peterson y col en 1981. EL EAE tiene generalmente un curso crónico con recaídas con resistencia a numerosos tratamientos.

Se ha reportado una respuesta anecdótica a esteroides sistémicos y antimaláricos. La terapia UVB no se ha utilizado previamente como terapia de EAE; este caso destaca la respuesta favorable a dicha terapia.


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