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REVISTA DERMATOLÓGICA MAYO 2004-2024, IMIQUIMOD-ALDARA
En el año 1998 hice dos revisiones del IMIQUIMOD, aprobado por la FDA en 1997, para el tratamiento de la VERRUGAS GENITALES, y te voy a dejar abajo los enlaces a esas revisiones.
En 2004 mayo, hice esta revisión con 22 referencias sobre el uso del imiquimod conocido con el nombre de ALDARA, referentes a tratamiento de: MORFEA, VERRUGAS GENITALES FEMENINAS,, QUELOIDES, QUERATOSIS ACTÍNICA, CARCINOMA BASOCELULAR, QUERATOACANTOMA, METÁSTASIS CUTÁNEAS DE MELANOMA MALIGNO, ENFERMEDAD DE BOWEN (CA IN SITU DE CARCINOMA ESPINOCELULAR) Y MOLUSCO CONTAGIOSO.
Hoy 2024 sigue vigente en el mercado y es utilizado en las patologías descritas con un buen porcentaje de éxito.
Aquí los enlaces, historia y usos: IMIQUIMOD I, USOS (ALDARA).
Descripción del producto: IMIQUIMOD II MONOGRAFÍA DEL PRODUCTO.
Saludos,,,
Dr. José Lapenta.
ENGLISH
In 1998 I did two reviews of IMIQUIMOD, approved by the FDA in 1997, for the treatment of GENITAL WART, and I will leave you the links to those reviews below.
In May 2004, I did this review with 22 references on the use of imiquimod known as ALDARA, referring to the treatment of: MORPHEA, FEMALE GENITAL WARTS, KELOIDS, ACTINIC KERATOSIS, BASAL CELL CARCINOMA, KERATOACANTHOMA, CUTANEOUS METASTASIS OF MALIGNANT MELANOMA, BOWEN'S DISEASE (CA IN SITU OF SQUALANIC CELL CARCINOMA) and CONTAGIOUS MOLLUSCUM.
Today, 2024, it is still on the market and is used in the pathologies described with a good percentage of success.
Here are the links, history and uses: IMIQUIMOD I USES (ALDARA).
Product description: IMIQUIMOD II PRODUCT MONOGRAPH.
Greetings...
Dr. José Lapenta R.
2.) Efficacy of imiquimod 5% cream for basal cell carcinoma in transplant patients.
3.) Using imiquimod for genital warts in female patients.
4.) Medical and surgical therapies for keloids.
6.) Amelanotic lentigo maligna managed with topical imiquimod as immunotherapy.
11.) Imiquimod as a possible treatment for keratoacanthoma.
12.) Imiquimod for the treatment of Bowen's disease and invasive squamous cell carcinoma.
14.) [Standard and experimental therapy of cutaneous T-cell lymphoma].
15.) Topically applied imiquimod inhibits vascular tumor growth in vivo.
16.) Therapeutic response of a brother and sister with xeroderma pigmentosum to imiquimod.
21.) Bowenoid papulosis of the vulva-immunotherapeutical approach with topical imiquimod.
22.) Imiquimod is highly effective for extensive, hyperproliferative condyloma in children.
1.) Use of Imiquimod Cream 5% in the Treatment of Localized Morphea.
J Cutan Med Surg. 2004 May 3 [Epub ahead of print]
Man J, Dytoc MT.
Division of Dermatology, University of Alberta, T6G 2G3, Edmonton,
Alberta, Canada.
Fibrosis is characterized by the increased deposition of collagen and
other matrix components by fibroblasts. This process occurs as a
reaction to inflammation and is mediated by numerous cytokines
including transforming growth factor beta (TGF-beta). Localized
cutaneous scleroderma or morphea is characterized by fibrosis. Current
treatment for morphea includes topical, intralesional, or systemic
corticosteroids, vitamin D analog (calcitriol and calcipotriol),
photochemotherapy, laser therapy, antimalarials, phenytoin,
D-penicillamine, and colchicine, all with varying degrees of success.
In this case report, imiquimod cream 5% (Aldara(R)), which induces
interferon and in turn inhibits TGF-beta, was employed to treat
morphea.
2.) Efficacy of imiquimod 5% cream for basal cell carcinoma in transplant patients.
Clin Exp Dermatol. 2004 May;29(3):237-9. Related Articles, Links
Vidal D, Alomar A.
Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Summary Imiquimod 5% cream has proven to be effective in superficial and nodular basal cell carcinomas in nonimmunosuppressed patients and treating squamous cell carcinomas in situ in transplant patients. The objective of this open-label study was to determine the efficacy of imiquimod 5% cream in treating basal cell carcinoma in transplant patients. At our unit, four renal transplant patients and one cardiac transplant patient were diagnosed with 10 basal cell carcinomas in 2001. Four tumours were superficial, three nodular and three infiltrative. Five basal cell carcinomas received imiquimod 5% cream at night four times weekly for 6 weeks, without occlusion, and the other five tumours were treated on 5 nights per week for 5 weeks. Biopsies taken 6 weeks after the end of treatment showed no tumour in seven of 10 of the cases. Notably, all four superficial basal cell carcinomas, two of the three of nodular lesions and one of the three of infiltrative cases had completely cleared.
3.) Using imiquimod for genital warts in female patients.
J Womens Health (Larchmt). 2004 Apr;13(3):265-71.Cox JT, Petry KU, Rylander E, Roy M.
Student Health Service, University of California, Santa Barbara, California 93106, USA. cox-t@sa.ucsb.edu
Genital warts (GW) are the manifestation of infection with specific types of human papillomavirus (HPV), one of the most common sexually transmitted viral infections in the world. Genital warts can be either raised (exophytic) or flat. Exophytic genital warts are most commonly secondary to inoculation of the basal epithelium with nononcogenic HPV types 6 and 11, whereas flat warts are usually secondary to potentially oncogenic HPV types 16 and 31. Genital warts can occasionally cause irritation and discomfort, particularly during intercourse, although most cases are asymptomatic. It is the psychosocial effects of infection, such as a sense of shame, depression, and anxiety, that represent the more significant toll for most patients with GW. Current therapies for GW are mainly ablative and do not directly enhance the immune response to HPV. Therefore, recurrence is a problem for many patients. Imiquimod 5% cream is a patient-applied therapy that directly enhances the immune response to HPV and is safe and effective for the treatment of GW. A reduction in viral load is observed following treatment. Low recurrence rates compared to other treatment modalities may be due to the stimulation of the cell-mediated immune response by imiquimod.
4.) Medical and surgical therapies for keloids.
Dermatol Ther. 2004;17(2):212-8.
Kelly AP.
Division of Dermatology, King/Drew Medical Center, Los Angeles,
CA.
Keloids are benign, but sometimes painful and/or pruritic,
proliferative growths of dermal collagen, usually resulting from
excessive tissue response to trauma. Although benign, the social and
psychological impact on affected individuals must be considered.
Keloids often arise secondary to ear piercing and operative
procedures. No single treatment modality is always successful. The
more common ones are discussed. Some of the medical therapies
include corticosteroids, interferon, 5-fluorouracil, and imiquimod.
Primary excision and cryosurgery are among the major surgical
options. Radiation therapies and other physical modalities are also
discussed.
5.) In vivo and in situ modulation of the expression of genes involved in metastasis and angiogenesis in a patient treated with topical imiquimod for melanoma skin metastases.
Br J Dermatol. 2004 Apr;150(4):761-7.
Hesling C, D'Incan M, Mansard S, Franck F, Corbin-Duval A, Chevenet C, Dechelotte P, Madelmont JC, Veyre A, Souteyrand P, Bignon YJ.
Laboratory of Molecular Oncology/UMR 484, Centre Jean Perrin, Clermont-Ferrand, France.
8There is a growing body of evidence to support the efficacy of topical imiquimod in the treatment of primary skin carcinomas. Conflicting data exist concerning the use of imiquimod for the treatment of skin melanoma metastases. To date, only the impact of imiquimod on cytokines involved in immunological processes has been studied extensively. We report a woman successfully treated with imiquimod (once daily for 8 weeks) for skin melanoma metastases in whom we investigated the expression of molecules involved in metastasis and angiogenesis. Before and after treatment, a skin lesion was biopsied and the expression of the following molecules was investigated using real-time reverse transcription-polymerase chain reaction: matrix metalloproteinase (MMP)-1, 2 and 9 and their inhibitors KiSS-1 and tissue inhibitor of metalloproteinase (TIMP)-1, vascular endothelial growth factor (VEGF), fibroblast growth factor-2, and angiogenesis inhibitors (thrombospondin-1 and 2). Interferon (IFN)-alpha was also investigated as an in vivo marker of imiquimod activity. IFN-alpha was upregulated by the treatment. Under imiquimod, the following molecules were upregulated: TIMP-1, KiSS-1 and MMP-1. MMP-2 expression was not modified. MMP-9 expression was dramatically decreased. The expression of angiogenesis inhibitors was slightly increased but VEGF expression remained at a basal level. These results suggest that imiquimod could downregulate metastasis invasion and angiogenesis. However, these data were obtained at a transcriptional level and from a single case, and further investigations should include migration assays and additional cases in order to confirm that imiquimod may be safely used for treatment of melanoma metastases.
6.) Amelanotic lentigo maligna managed with topical imiquimod as
immunotherapy.
J Am Acad Dermatol. 2004 May;50(5):792-6.
Powell AM, Russell-Jones R.
Clinically amelanotic lentigo maligna often resembles an inflammatory lesion rather than a melanoma in situ. We present two cases of extensive amelanotic lentigo maligna presenting as gradually enlarging erythematous patches on the faces of women following incomplete excisions of lentigo maligna. Because of their site and size, therapeutic options were limited; the lesions have, however, resolved (clinically and histologically) following the topical application of 5% imiquimod cream. We discuss the rationale for the use of imiquimod in the treatment of lentigo maligna.
7.) Imiquimod 5% cream for the treatment of superficial basal
cell carcinoma: Results from two phase III, randomized,
vehicle-controlled studies.
J Am Acad Dermatol. 2004 May;50(5):722-33.
Geisse J, Caro I, Lindholm J, Golitz L, Stampone P, Owens M.
BACKGROUND: Imiquimod is an immune response modifier that is a Toll-like
receptor 7 agonist that induces interferon and other cytokines through the
innate immune system and stimulates cell-mediated immunity through T
cells. Imiquimod has been shown to be efficacious as a topical treatment
for basal cell carcinoma (BCC). OBJECTIVE: We sought to evaluate the
efficacy and safety of imiquimod 5% cream compared with vehicle for
treating superficial BCC (sBCC). METHODS: Two identical studies were
conducted. Subjects with one sBCC were dosed with imiquimod or vehicle
cream once daily 5 or 7x/week for 6 weeks in these 2 randomized,
double-blind, vehicle-controlled Phase III studies. The lesion site was
clinically examined 12 weeks posttreatment and then excised for
histological evaluation. RESULTS: Data from both studies were pooled.
Composite clearance rates (combined clinical and histological assessments)
for the 5 and 7x/week imiquimod groups were 75% and 73%, respectively.
Histological clearance rates for the 5 and 7x/week imiquimod groups were
82% and 79%, respectively. Increasing severity of erythema, erosion, and
scabbing/crusting was associated with higher clearance rates. CONCLUSION:
Imiquimod appears to be safe and effective for the treatment of sBCC when
compared with vehicle cream. The difference in clearance rates between the
two imiquimod dosing groups was not significant. The 5x/week regimen is
recommended.
8.) imiquimod 5% cream for the treatment of actinic keratosis: Results from two phase III, randomized, double-blind, parallel group, vehicle-controlled trials.
J Am Acad Dermatol. 2004 May;50(5):714-21.
Lebwohl M, Dinehart S, Whiting D, Lee PK, Tawfik N, Jorizzo J, Lee JH, Fox TL.
BACKGROUND: The immune system plays a critical role in the development and pathogenesis of actinic keratosis (AK). Imiquimod has been shown to stimulate the cutaneous immune response and be effective for the treatment of nonmelanoma skin cancers. OBJECTIVE: Two phase III, randomized, double-blind, vehicle-controlled studies evaluated the efficacy of imiquimod 5% cream compared with vehicle in the treatment of AK lesions on the face and balding scalp. METHODS: A total of 436 participants at 24 centers in the United States and Canada were randomized to either imiquimod 5% or vehicle cream. Study cream was applied one time per day, 2 days per week for 16 weeks. Clearance of AK lesions was clinically assessed at an 8-week posttreatment visit. RESULTS: The complete clearance rate was 45.1% for the imiquimod group and 3.2% for the vehicle group. The difference in complete clearance rates (imiquimod minus vehicle) was 41.9% with a 95% confidence interval of 34.9% to 49%. The partial (>/=75%) clearance rate was 59.1% for the imiquimod group and 11.8% for the vehicle group. The difference in partial clearance rates (imiquimod minus vehicle) was 47.3% with a 95% confidence interval of 39.5% to 55.1%. The median percent reduction in AK lesions was 83.3% for the imiquimod group and 0% for the vehicle group. Local skin reactions were common. Severe erythema was reported by 17.7% of participants who received imiquimod and 2.3% of participants who received vehicle. Overall, imiquimod was very well tolerated. CONCLUSION: Imiquimod 5% cream used 2 times per week for 16 weeks is an effective and well-tolerated treatment for AK.
9.) Pharmacokinetics and safety of imiquimod 5% cream in the treatment of actinic keratoses of the face, scalp, or hands and arms.
Arch Dermatol Res. 2004 Apr 9 [Epub ahead of print]
Harrison LI, Skinner SL, Marbury TC, Owens ML, Kurup S, McKane S, Greene
RJ.
Department of Pharmacokinetics and Drug Metabolism, 3 M Pharmaceuticals,
3 M Center 270-3S-05, MN 55144, St. Paul, USA.
The safety and efficacy of imiquimod 5% cream is being evaluated for the
treatment of dysplastic lesions of the epidermis (actinic keratoses,
AK). The objective of this clinical study was to describe the
pharmacokinetics and safety of topical imiquimod during multiple dosing
of AK subjects. A total of 58 adult subjects with 5 to 20 AK lesions at
the treatment site applied imiquimod cream three times per week for up
to 16 weeks as follows: 12 males and 11 females applied 12.5 mg
imiquimod to the face; 11 males applied 25 mg to the entire balding area
of the scalp; and 12 males and 12 females applied 75 mg to both hands
and forearms. Pharmacokinetics and safety were assessed after the first
and last doses, as well as biweekly. Imiquimod and its metabolites were
measured in the serum and urine using sensitive liquid
chromatography/mass spectrometry methods. Less than 0.6% of the applied
doses was recovered in the urine of all subjects. Serum imiquimod levels
were low, reflecting minimal dermal absorption, and increased with dose,
although not proportionally. Peak levels at the end of dosing were 0.1,
0.2, and 1.6 ng/ml for the face, scalp, and hands/arms groups,
respectively. A two- to fourfold accumulation was seen at the end of
dosing. Local application site reactions were the most common adverse
event, reported by approximately 50% of the subjects in each treatment
group. The small number of systemic adverse events, including 'flu-like
symptoms, were mostly mild and did not show a dose response. Thus,
minimal systemic absorption and good safety margins for topical
imiquimod were seen in AK subjects with doses as high as 75 mg three
times per week for 16 weeks.
10.) Combination topical treatment of molluscum contagiosum with
cantharidin and imiquimod 5% in children: A case series of 16
patients.
.
Australas J Dermatol. 2004 May;45(2):100-2.
Ross GL, Orchard DC.
Dermatology Department, Royal Children's Hospital, Melbourne, Victoria,
Australia.
SUMMARY The objective of this study was to assess the efficacy and
tolerability of combination therapy for molluscum contagiosum (MC) with
topical cantharidin and imiquimod 5%. A prospective case series of 16
paediatric patients with a mean age of 4.8 years had cantharidin applied
to lesions by a dermatologist, followed by home treatment with imiquimod
5% cream nightly for an average of 5 weeks. This regimen resulted in
>90% of lesions clearing in 12 patients, with half of these being
totally clear. Two patients had 80-90% of lesions resolve. Two patients
had 30-50% clearance of lesions at the end of the treatment period. One
patient found the cantharidin reaction too strong. The mean number of
imiquimod 250 mg sachets used was 4.25. In conclusion, this study suggests
that combination therapy using cantharidin and imiquimod for treatment of
MC in children is effective and well tolerated.
11.) Imiquimod as a possible treatment
for keratoacanthoma.
J Drugs Dermatol. 2004 Jan-Feb;3(1):71-4.
Bhatia N.
UCSD School of Medicine, San Diego, CA, USA. ndbhatia@juno.com
Imiquimod is an immune-response modifier that has the potential to be
useful in many dermatological indications (Table 1). To date, the
approved use is for condyloma acuminata; approval for use in treating
basal cell carcinoma (BCC) has been filed with the FDA and is expected
to be approved in the coming months. In the interim, the expansion of
the horizons for this immunomodulator depends on the application of the
science and immunology behind the drug to the appropriate disease
states. Recent investigations have presented explanations on the
possible mechanisms behind the anti-tumor activity of imiquimod, more
specifically for its use in treating superficial BCC. There are studies
currently underway as well as anecdotal data published for its possible
use in treating squamous cell carcinoma (SCC), although this is not as
widely accepted for off-label use as BCC among many dermatologists.
However, many patients who may not be surgical candidates that present
with tumors other than BCC have been successfully treated with
imiquimod. This is a case of an elderly patient who could not undergo
surgery that presented with a large keratoacanthoma and was clear of her
tumor after five months using imiquimod 5% cream on a daily basis.
12.) Imiquimod for the treatment of Bowen's disease and
invasive squamous cell carcinoma.
J Drugs Dermatol. 2003 Dec;2(6):669-73.
Nouri K, O'Connell C, Rivas MP.
Department of Dermatology and Otolaryngology, University of Miami School
of Medicine, USA. KNouri@med.miami.edu
Topical imiquimod is an immune response modifier FDA approved for the
treatment of anogenital warts. Recent studies have reported its
effectiveness in the treatment of some types of basal cell carcinomas.
There have also been some case reports and case series reporting success
treating of squamous cell carcinoma in situ with imiquimod. We report
two patients with squamous cell carcinoma in situ and one with invasive
squamous cell carcinoma treated with 5% imiquimod cream. Lesions were
located on shin, posterior shoulder, and nasal tip. 5% imiquimod cream
was applied at night for six weeks. Side effects included erythema and
crusting in one patient. Biopsies taken four weeks after treatment
revealed no residual squamous cell carcinoma in situ or squamous cell
carcinoma. Topical 5% imiquimod cream is becoming established as a
promising treatment for squamous cell carcinoma in situ. It also seems
to be an alternative treatment for some cases of squamous cell
carcinoma.
13.) An open label evaluation of the
efficacy of imiquimod 5% cream in the treatment of recalcitrant
subungual and periungual cutaneous warts.
J Dermatolog Treat. 2003 Dec;14(4):233-6.
Micali G, Dall'Oglio F, Nasca MR.
Dermatology Clinic, University of Catania, Piazza S. Agata La Vetere
6, 95124 Catania, Italy. cldermct@nti.it
BACKGROUND: Periungual and subungual warts are very difficult to
eradicate with current therapies. Most are destructive in nature
(liquid nitrogen, cantharidin, vascular lesion laser) and
inflammation, pain and pigment dyschromia are common side effects.
Furthermore, failure to respond or appearance of new lesions often
leads to even more destructive treatments (CO(2) laser, excisional
surgery) and can lead to more pain and scarring. METHODS: In an open
trial, the efficacy, safety, and tolerability of topical imiquimod 5%
cream was assessed in 15 patients with resistant and recurrent
periungual and subungual warts over a 16 week period. RESULTS: Twelve
patients (80%) completed therapy, showing complete resolution after a
mean time of three weeks (range 1-6 weeks), with the remaining three
patients (20%) being classified as non-responders. Local side effects
(erythema, pruritus, burning and pain) were generally mild and
well-tolerated. No relapses occurred during a 6-month follow-up.
CONCLUSION: Topical imiquimod is an interesting novel treatment for
multiple periungual and subungual warts. Tolerability is excellent
when compared to other commonly used modalities and there are few side
effects. This trial suggests a high clinical response rate. This
treatment is applicable to patients who have failed conventional
therapies before embarking on potentially scarring approaches such as
excisional surgery.
14.) [Standard and experimental therapy of cutaneous T-cell lymphoma]
Hautarzt. 2003 Dec;54(12):1177-84.
[Article in German]
Beyeler M, Dummer R.
Dermatologische Klinik Universitatsspital Zurich, Zurich.
Cutaneous T-cell lymphoma represent a heterogeneous group of diseases
characterized by skin invasion of monoclonal T-lymphocytes. These
cutaneous T-cell lymphomas are divided into 3 groups based on clinical,
histological and immunohistological characteristics: Indolent with a
survival time of over 10 years, aggressive with a survival time less
than 10 years and provisional (EORTC classification). Standard
treatments such as PUVA, total skin electron beam, methotrexate,
polychemotherapy regimens, retinoids and photopheresis have been used
for years. Bexarotene is a newly registered drug. To achieve better
response rates, several new drugs are being evaluated in clinical
trails, including imiquimod, denileukon-diftitox, liposomal doxorubicin,
adeno-interferon-gamma and various combination approaches.
15.) Topically applied imiquimod inhibits vascular tumor growth in vivo.
J Invest Dermatol. 2003 Nov;121(5):1205-9.
Sidbury R, Neuschler N, Neuschler E, Sun P, Wang XQ, Miller R, Tomai M, Puscasiu E, Gugneja S, Paller AS.
Department of Pediatrics, Children's Memorial Hospital, Northwestern University Medical School, Chicago, Illinois 60614, USA.
Vascular tumors occur in approximately 10% of all infants and may be associated with significant morbidity. Available therapies for vascular tumors, such as systemic corticosteroids, vincristine, and interferon-alpha, may cause toxicity, limiting their use to complicated cases. Using a mouse hemangioendothelioma model, we investigated the efficacy and mechanism of action of imiquimod, a topically applied inducer of cytokines. Application of imiquimod cream, whether initiated at the time of cell inoculation or when tumors became visible, significantly decreased tumor growth and increased animal survival in comparison with control mice. Imiquimod-treated tumors showed decreased tumor cell proliferation, increased tumor apoptosis, and increased expression of tissue inhibitor of matrix metalloproteinase-1 with decreased activity of matrix metalloproteinase-9. The demonstration that local application of imiquimod inhibits vascular tumor enlargement in the mouse vascular tumor model suggests a novel, less toxic means of treating infantile hemangioendotheliomas and perhaps other cutaneous vascular tumors.
16.) Therapeutic response of a brother and sister with xeroderma pigmentosum to imiquimod.
Dermatol Surg. 2002 Jun;28(6):518-23.
Weisberg NK, Varghese M.
Department of Dermatology, Weill Cornell Medical School, New York, New
York 10021, USA.
BACKGROUND: Xeroderma pigmentosum (XP) is an autosomal recessive disease
marked by solar sensitivity, photophobia, early onset of freckling, and
solar-induced cutaneous neoplastic changes. These patients can often
develop hundreds of cutaneous tumors, making surgical therapy difficult.
Imiquimod 5% cream has been shown to have activity in treating various
cutaneous malignancies. OBJECTIVE: To examine the effectiveness and
tolerability of imiquimod 5% cream in treating facial basal cell
carcinomas (BCCs) in a brother and sister with XP. These patients were
developing skin cancers faster than could be managed surgically and had
failed 6 months of chemoprophylaxis with isotretinoin. METHODS:
Imiquimod 5% cream was applied to the faces of these two patients as
frequently as tolerated, with the goal of gaining control over the many
clinically evident BCCs present on the faces of these siblings. We also
examined whether we could reduce the rate of new neoplasm development.
RESULTS: The brother in our study tolerated imiquimod 5% cream twice a
day every day with minimal inflammatory response. He had clinical
resolution of many of the BCCs present within the treatment area as well
as shrinking of many of the remaining lesions. He has continued to
produce new tumors at a substantially reduced rate relative to his
pretreatment baseline. The sister in our study exhibited a severe
inflammatory response to imiquimod 5% cream, with facial swelling and
erosion of the treated area with application as infrequent as three
times a week. In spite of the vastly different inflammatory response,
her cutaneous tumors responded favorably to therapy as well. CONCLUSION:
Imiquimod 5% cream was effective in treating facial BCCs in these
siblings with XP. As well, we have noted a significant reduction in the
development of new tumors within the imiquimod-treated area. The
inflammatory response to this medicine was at opposite extremes among
these two siblings. However, this did not appear to alter the
therapeutic benefit of this therapy.
17.) Imiquimod, a topical immune response modifier, in the treatment of cutaneous metastases of malignant melanoma.
Dermatology. 2002;205(2):135-8.
Bong AB, Bonnekoh B, Franke I, Schon MP, Ulrich J, Gollnick H.
Department of Dermatology and Venereology, Otto von Guericke University,
Magdeburg, Germany.
BACKGROUND: Imiquimod 5% cream (Aldara, a novel topical immune response
modifier, has been approved for the topical treatment of anogenital
HPV-induced warts. In addition, several studies have demonstrated
antitumoral activity in solar keratoses, superficial basal cell
carcinomas and Bowen's disease. AIM: Given the convincing therapeutic
results of imiquimod when used for treating selected types of epithelial
skin cancer, we became interested to study imiquimod as an adjuvant for
treating cutaneous metastases of malignant melanoma. METHODS: Three
patients with multiple, i.e. more than 15, cutaneous in-transit
metastases of malignant melanoma in unilateral localization on the leg
were treated topically with imiquimod 5% cream. RESULTS: Twice daily
application under occlusive conditions for a period of 21-28 weeks
resulted in >90% regression of cutaneous metastases in 2 patients.
The third patient showed marked response only when topical imiquimod was
intermittently supplemented by intralesional interleukin (IL)-2 for 2
weeks. Unwanted side effects were mild in all patients. CONCLUSION:
Overall, imiquimod as a single agent or in combination with
intralesional IL-2 may be a promising immunomodulatory compound for the
adjuvant topical treatment of patients with multiple cutaneous
metastases of malignant melanoma.
18.) The use of imiquimod 5% cream for the treatment of superficial basal cell carcinomas in a basal cell nevus syndrome patient.
Dermatol Surg. 2000 Jun;26(6):577-8; discussion 578-9.
Kagy MK, Amonette R.
University of Tennessee-Memphis, Memphis, Tennessee, USA.
BACKGROUND: Imiquimod 5% cream has been used effectively to treat
superficial basal cell carcinomas (BCCs). OBJECTIVE: The purpose of this
study is to examine the effectiveness, tolerability, and desirability of
imiquimod 5% cream in treating superficial non-facial basal cell
carcinomas in a patient with basal cell nevus syndrome. METHODS: Three
biopsy-proven nonfacial BCCs were treated for 18 weeks with once daily
application of 5% imiquimod cream. The lesions were then removed to
search histologically for residual tumor. RESULTS: The two adequately
treated tumors revealed no residual BCC upon removal. Our patient
reported that he tolerated the treatment but he would not desire this
treatment again based on the length of treatment time and the degree of
local inflammation at the treatment sites. CONCLUSION: Imiquimod 5%
cream appears to be effective in eradicating superficial nonfacial BCCs.
The degree of local inflammatory response may affect the patients'
tolerability of treatment and therefore patient compliance.
Curr Opin Infect Dis. 2003 Apr;16(2):85-9.
Garland SM.
Department of Microbiology and Infectious Diseases, The Royal Women's
Hospital, Carlton, Victoria, Australia. suzanne.garland@wch.org.au
PURPOSE OF REVIEW: Imiquimod is the first member of a new class of
immune response modifiers; it was first approved in 1997 for the topical
treatment of external genital and perianal warts. It is an
imidazoquinoline, a novel synthetic compound which is an immune response
stimulator, enhancing both the innate and acquired immune pathways
(particularly T helper cell type 1-mediated immune responses) resulting
in antiviral, antitumour and immunoregulatory activities. The mechanism
of action of imiquimod involves cytokine induction in the skin, which
then triggers the host's immune system to recognize the presence of a
viral infection or tumour, ultimately to eradicate the associated
lesion. RECENT FINDINGS: Imiquimod, a patient-applied topical 5% cream
is clinically efficacious and safe in the management of condylomata
acuminata and other warty manifestations of human papillomavirus
infections. Although not licensed for use against other viral skin
infections, preliminary data suggest imiquimod's success against
molluscum contagiosum, caused by a poxvirus. Initial studies with
imiquimod for the management of HPV-related intraepithelial dysplasias
(bowenoid papulosis/vulvar intraepithelial neoplasia) as well as for
ultraviolet-induced skin lesions such as actinic keratoses, Bowen's
disease, and basal cell carcinomas show great promise in immunocompetent
and immunosuppressed patients. SUMMARY: In the future, imiquimod and
newer generations of imidazoquinolines (resiquimod) require further
investigation for potential clinical utility in treating other cutaneous
and mucosal viral infections, dysplasias and neoplasia, as well as
potential vaccine adjuvants.
20.) Detection of CD8+ T cell
responses to human papillomavirus type 16 antigens in women using
imiquimod as a treatment for high-grade vulval intraepithelial
neoplasia.
Todd RW, Steele JC, Etherington I, Luesley DM.
Department of Gynaecologic Oncology, Birmingham Women's NHS Trust, Birmingham B15 2TG, UK. rick@todd38.freeserve.co.uk
OBJECTIVES: To investigate CD8+ T cell reactivity to human papillomavirus (HPV) 16 antigens in patients with high-grade vulval intraepithelial neoplasia (VIN) before, during and after treatment with 5% imiquimod cream. METHODS: CD8-enriched responder cell populations were obtained from 10 patients with high-grade VIN using imiquimod cream as a treatment. Overlapping synthetic peptides covering the entire primary sequences of the HPV16 E6, E7 and E4 proteins were used to screen for CD8+ T cell responses using an ELISPOT assay of interferon (IFN)-gamma release. RESULTS: Reactivity to the proteins was detected in all patients on at least one occasion. With the exception of one patient, CD8+ T cell reactivity generally increased at some stage during treatment. The magnitude and specificities of responses changed over the treatment period. This was particularly noticeable in response to peptides derived from the E4 protein. CD8+ T cell reactivity to HPV16 E7 appeared to be dominant amongst women with high-grade VIN. The magnitude and specificity of response had no correlation with clinical response to imiquimod. CONCLUSIONS: HPV16 specific CD8+ T cell activity was detected in patients with high-grade VIN. Imiquimod use appeared to increase the magnitude of the response and broaden the specificity of response in some patients. Despite the presence of these CD8+ T cells, the disease state persisted; therefore, a role for HPV-specific cytotoxic T cells (CTLs) in VIN resolution remains unproven.
21.) Bowenoid papulosis of the
vulva-immunotherapeutical approach with topical imiquimod.
Arch Gynecol Obstet. 2003 Oct;268(4):333-6. Epub 2003 Jan 23.
Richter ON, Petrow W, Wardelmann E, Dorn C, Kupka M, Ulrich U.
Department of Obstetrics and Gynecology, University of Bonn School of Medicine, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. Dr.OliverRichter@t-online.de
INTRODUCTION. Bowenoid papulosis is a characteristic lesion of the ano-genital region and represents a form of squamous cell carcinoma in situ, very often associated to the oncogenic high-risk human papilloma virus (HPV) types 16, 18, 31 and 33. Therapies applied so far, in general, show high rates of relapse, and patients complain of pruritus and pain. Imiquimod cream is a topical immune response modifier with indirect antiviral and antitumor effects through the stimulation of local cytokine production and cell-mediated immune response. CASE REPORT. In the present paper we report on the topical application of imiquimod cream in a woman with a high-risk HPV-associated vulvar intraepithelial neoplasia grade III (VIN III) of the vulva. DISCUSSION. In addition a review of the literature is given.
22.) Imiquimod is highly effective for
extensive, hyperproliferative condyloma in children.
Pediatr Dermatol. 2003 Sep-Oct;20(5):440-2.
Majewski S, Pniewski T, Malejczyk M, Jablonska S.
Department of Dermatology and Venereology, Warsaw School of Medicine,
Warsaw, Poland.
We describe a dramatic response to imiquimod of long-lasting, highly
proliferative extensive perianal condylomas involving the anal canal
in a 19-month-old girl. Her mother was free of condyloma and allegedly
had no human papillomavirus (HPV) infection during pregnancy. There
was no evidence of sexual abuse. Application of 5% imiquimod cream to
the child every other day for 3 weeks resulted in almost complete
resolution of the warts, with total clearance within another 2 weeks.
The inflammatory reaction was moderate. Since there is still
discussion of whether imiquimod may be prescribed for small children,
this case of very extensive condyloma provides evidence that the
compound is safe and highly effective.
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DATA-MEDICOS/DERMAGIC-EXPRESS /MAY JOURNAL 2.004/ DR. JOSE LAPENTA
R.
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Produced by Dr. José Lapenta R. Dermatologist
Venezuela
1.998-2.024
Producido por Dr. José Lapenta R. Dermatólogo Venezuela 1.998-2.0024
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