Sandbox:Balanitis xerotica obliterans: Difference between revisions
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==Overview== | ==Overview== | ||
Balanitis xerotica obliterans (BXO) is a dermatological (skin) condition affecting the male genitalia. It was first described by Stuhmer in 1928, though earlier reports describe what may have been the same condition.[1] BXO commonly occurs on the foreskin and glans penis.[2] Atrophic white patches appear on the affected area,[3] and commonly, a whitish ring of indurated (hardened) tissue usually forms near the tip that may prevent retraction.[2] | Balanitis xerotica obliterans (BXO) is a dermatological (skin) condition affecting the male genitalia. It was first described by Stuhmer in 1928, though earlier reports describe what may have been the same condition.[1] BXO commonly occurs on the foreskin and glans penis.[2] Atrophic white patches appear on the affected area,[3] and commonly, a whitish ring of indurated (hardened) tissue usually forms near the tip that may prevent retraction.[2] | ||
| Line 9: | Line 9: | ||
==Historical Perspective== | ==Historical Perspective== | ||
==Classification== | ==Classification== | ||
There is no established classification system for | There is no established classification system for BXO. | ||
==Pathophysiology== | ==Pathophysiology== | ||
The exact etiology of BXO is unknown, but multiple factors are considered to play an important in the development of BXO. | |||
{| class="wikitable" | |||
! colspan="2" |Factors associated with pathogenesis of BXO | |||
|- | |||
|Uncircumcised Penis | |||
|Accumulation of secretions and epithelial debris between the foreskin and coronal sulcus leads to chronic irritation, sublincal trauma. accumulated material may also harbor infectious agents, which could play an important role in pathogenesis of BXO | |||
|- | |||
|Autoimmune diseases | |||
| | |||
|- | |||
|human papillomaviruses (HPV) | |||
| | |||
|- | |||
|Hormonal influences | |||
| | |||
|- | |||
|Genetics | |||
| | |||
|} | |||
<section> | |||
The aetiology of male genital lichen sclerosus is unknown, but it is most probably multifactorial. Like most penile inflammatory dermatoses, penile lichen sclerosus occurs most frequently in uncircumcised or late circumcised middle-aged men. The role of the foreskin is unknown, but it most likely contributes to the development of disease through the accumulation of epithelial debris and secretions in the fold between the foreskin and penis proximal to the coronal sulcus. This accumulated material then causes chronic physical irritation, chronic balanitis or subclinical trauma with subsequent Koebner phenomenon, where skin lesions appear along the lines of trauma [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b1 <nowiki>[1,6]</nowiki>]. Alternatively, the accumulated material may harbour an infectious agent which is yet to be identified. ''Borrelia Burgdorferi'', a spirochaete, was implicated by studies in Austria [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b7 <nowiki>[7]</nowiki>], but this organism has not been identified in subsequent studies in America, Britain or Australia. | |||
Penile lichen sclerosus is an inflammatory dermatosis with subsequent fibrosis causing the late complications of the disease. The inflammatory infiltrate is predominantly a T cell infiltrate infiltrating the basal epidermis and superficial dermis. Initially, the T cells are CD4+ T helper cells, but in the active stage of the disease when basal vacuolar change occurs the T cells are predominantly CD8+, CD57+ cytotoxic T cells, which is a profile generally associated with viruses, autoimmune diseases or malignancy [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b8 <nowiki>[8]</nowiki>]. However, the eliciting antigen has not been identified. | |||
In a small number of cases, penile lichen sclerosus has been associated with autoimmune diseases including diabetes mellitus, vitiligo and alopecia areata, and patients have had various autoantibodies, including antinuclear, thyroid antimicrosomal, antigastric parietal cell, anti-adrenal cortex, anti-smooth muscle and antimitochondrial antibodies [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b4 <nowiki>[4,9,10]</nowiki>]. However, Meffert ''et al''. [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b1 <nowiki>[1]</nowiki>] make the comment that the association with these autoimmune diseases is so infrequent that testing for autoimmune diseases is not indicated in patients with penile lichen sclerosus. A study of human leukocyte antigen (HLA) associations showed a predominance of HLA DQ7 with DR11 and DR12 present less commonly [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b9 <nowiki>[9]</nowiki>]. | |||
The presence of human papillomaviruses (HPV) has been reported in some cases of childhood penile lichen sclerosus, with HPV identified by PCR in 52% of cases in one study of 23 cases and 64% of 11 cases [http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#b2 <nowiki>[2,11]</nowiki>]. The HPV serotypes include HPV 6, 16 and 18, as well as HPV 8, 23, 36, 38 and DL285. Whether the lichen sclerosus is directly attributable to HPV infection or whether lichen sclerosus merely promotes HPV infection is unclear. Adults with penile lichen sclerosus have not been demonstrated to have a higher incidence of HPV infection. | |||
Hormonal influences may contribute to the development of vulvar lichen sclerosus but have not been demonstrated in penile lichen sclerosus to date. Childhood vulvar lichen sclerosus frequently resolves with the onset of menarche when there is an increase in testosterone production in genital skin. | |||
There may be a genetic basis in some cases of lichen sclerosus, including penile lichen sclerosus. However, no well defined genetic association has been identified in the majority of cases of penile lichen sclerosus. | |||
</section><section> | |||
== HISTOPATHOLOGY == | |||
The early stage in the development of penile lichen sclerosus is a moderately heavy lymphocytic infiltrate in the basal epidermis and superficial dermis, associated with basal vacuolar change in the epidermis ([http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#f1 Fig. 1]). In cases with pronounced vacuolar change, the epidermis may detach from the dermis with the formation of haemorrhagic bullae. As the lesion develops, the epidermis becomes atrophic with surface hyperkeratosis. During the development of the lesions, there is loss of elastic fibres in the papillary dermis and the dermal inflammatory infiltrate is displaced downwards by subepidermal oedema, which is subsequently replaced by fibrosis.<section></section>Therefore, the classic lesion associated with penile lichen sclerosus occurs relatively late and is characterized by epidermal atrophy with surface hyperkeratosis, a thickened basement membrane and an underlying broad zone of subepidermal oedema with homogenization of collagen, which becomes more sclerotic over time. At this time, the inflammatory infiltrate is relatively light and located deep to the dermal fibrosis ([http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2011.10699.x/full#f2 Fig. 2]).<section></section></section> | |||
===Pathogenesis=== | ===Pathogenesis=== | ||
The exact pathogenesis is not clearly known, but following theories have been postulated:<ref name="pmid113199702">{{cite journal| author=Porter WM, Bunker CB| title=The dysfunctional foreskin. | journal=Int J STD AIDS | year= 2001 | volume= 12 | issue= 4 | pages= 216-20 | pmid=11319970 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11319970 }}</ref> | The exact pathogenesis is not clearly known, but following theories have been postulated:<ref name="pmid113199702">{{cite journal| author=Porter WM, Bunker CB| title=The dysfunctional foreskin. | journal=Int J STD AIDS | year= 2001 | volume= 12 | issue= 4 | pages= 216-20 | pmid=11319970 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11319970 }}</ref> | ||
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*Dermal vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, is a characteristic feature of ZB. | *Dermal vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, is a characteristic feature of ZB. | ||
*In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates. | *In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates. | ||
Associated conditions: | |||
Patients with BXO, were found to have an other associated autoimmune conditions, which include:<ref name="pmid7868709">{{cite journal| author=Meffert JJ, Davis BM, Grimwood RE| title=Lichen sclerosus. | journal=J Am Acad Dermatol | year= 1995 | volume= 32 | issue= 3 | pages= 393-416; quiz 417-8 | pmid=7868709 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7868709 }}</ref> | |||
* Diabetes Mellitus, | |||
* Vitiligo | |||
* Alopecia aerata | |||
==Causes== | ==Causes== | ||
The etiology of BXO is uncertain. However, some possibilities have been suggested. | The etiology of BXO is uncertain. However, some possibilities have been suggested. | ||
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=== Surgery === | === Surgery === | ||
Prevention | |||
There is no known means of preventing BXO. However, one study reports that the data "suggest that circumcision prevents or protects against common infective penile dermatoses."<ref name="mallon2000" /> | There is no known means of preventing BXO. However, one study reports that the data "suggest that circumcision prevents or protects against common infective penile dermatoses."<ref name="mallon2000" /> | ||
Revision as of 17:09, 20 January 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vishal Devarkonda, M.B.B.S[2]
Synonyms and keywords:BXO, Penile lichen sclerosus
Overview
Balanitis xerotica obliterans (BXO) is a dermatological (skin) condition affecting the male genitalia. It was first described by Stuhmer in 1928, though earlier reports describe what may have been the same condition.[1] BXO commonly occurs on the foreskin and glans penis.[2] Atrophic white patches appear on the affected area,[3] and commonly, a whitish ring of indurated (hardened) tissue usually forms near the tip that may prevent retraction.[2]
Historical Perspective
Classification
There is no established classification system for BXO.
Pathophysiology
The exact etiology of BXO is unknown, but multiple factors are considered to play an important in the development of BXO.
| Factors associated with pathogenesis of BXO | |
|---|---|
| Uncircumcised Penis | Accumulation of secretions and epithelial debris between the foreskin and coronal sulcus leads to chronic irritation, sublincal trauma. accumulated material may also harbor infectious agents, which could play an important role in pathogenesis of BXO |
| Autoimmune diseases | |
| human papillomaviruses (HPV) | |
| Hormonal influences | |
| Genetics | |
<section> The aetiology of male genital lichen sclerosus is unknown, but it is most probably multifactorial. Like most penile inflammatory dermatoses, penile lichen sclerosus occurs most frequently in uncircumcised or late circumcised middle-aged men. The role of the foreskin is unknown, but it most likely contributes to the development of disease through the accumulation of epithelial debris and secretions in the fold between the foreskin and penis proximal to the coronal sulcus. This accumulated material then causes chronic physical irritation, chronic balanitis or subclinical trauma with subsequent Koebner phenomenon, where skin lesions appear along the lines of trauma [1,6]. Alternatively, the accumulated material may harbour an infectious agent which is yet to be identified. Borrelia Burgdorferi, a spirochaete, was implicated by studies in Austria [7], but this organism has not been identified in subsequent studies in America, Britain or Australia.
Penile lichen sclerosus is an inflammatory dermatosis with subsequent fibrosis causing the late complications of the disease. The inflammatory infiltrate is predominantly a T cell infiltrate infiltrating the basal epidermis and superficial dermis. Initially, the T cells are CD4+ T helper cells, but in the active stage of the disease when basal vacuolar change occurs the T cells are predominantly CD8+, CD57+ cytotoxic T cells, which is a profile generally associated with viruses, autoimmune diseases or malignancy [8]. However, the eliciting antigen has not been identified.
In a small number of cases, penile lichen sclerosus has been associated with autoimmune diseases including diabetes mellitus, vitiligo and alopecia areata, and patients have had various autoantibodies, including antinuclear, thyroid antimicrosomal, antigastric parietal cell, anti-adrenal cortex, anti-smooth muscle and antimitochondrial antibodies [4,9,10]. However, Meffert et al. [1] make the comment that the association with these autoimmune diseases is so infrequent that testing for autoimmune diseases is not indicated in patients with penile lichen sclerosus. A study of human leukocyte antigen (HLA) associations showed a predominance of HLA DQ7 with DR11 and DR12 present less commonly [9].
The presence of human papillomaviruses (HPV) has been reported in some cases of childhood penile lichen sclerosus, with HPV identified by PCR in 52% of cases in one study of 23 cases and 64% of 11 cases [2,11]. The HPV serotypes include HPV 6, 16 and 18, as well as HPV 8, 23, 36, 38 and DL285. Whether the lichen sclerosus is directly attributable to HPV infection or whether lichen sclerosus merely promotes HPV infection is unclear. Adults with penile lichen sclerosus have not been demonstrated to have a higher incidence of HPV infection.
Hormonal influences may contribute to the development of vulvar lichen sclerosus but have not been demonstrated in penile lichen sclerosus to date. Childhood vulvar lichen sclerosus frequently resolves with the onset of menarche when there is an increase in testosterone production in genital skin.
There may be a genetic basis in some cases of lichen sclerosus, including penile lichen sclerosus. However, no well defined genetic association has been identified in the majority of cases of penile lichen sclerosus. </section><section>
HISTOPATHOLOGY
The early stage in the development of penile lichen sclerosus is a moderately heavy lymphocytic infiltrate in the basal epidermis and superficial dermis, associated with basal vacuolar change in the epidermis (Fig. 1). In cases with pronounced vacuolar change, the epidermis may detach from the dermis with the formation of haemorrhagic bullae. As the lesion develops, the epidermis becomes atrophic with surface hyperkeratosis. During the development of the lesions, there is loss of elastic fibres in the papillary dermis and the dermal inflammatory infiltrate is displaced downwards by subepidermal oedema, which is subsequently replaced by fibrosis.<section></section>Therefore, the classic lesion associated with penile lichen sclerosus occurs relatively late and is characterized by epidermal atrophy with surface hyperkeratosis, a thickened basement membrane and an underlying broad zone of subepidermal oedema with homogenization of collagen, which becomes more sclerotic over time. At this time, the inflammatory infiltrate is relatively light and located deep to the dermal fibrosis (Fig. 2).<section></section></section>
Pathogenesis
The exact pathogenesis is not clearly known, but following theories have been postulated:[1]
- Accumlation of epithelial debris and secretions between foreskin and penis proximal to coronal sulcus, smegma, poor genital hygiene, repeated local infections, hot and humid weather results in chronic physical irritation or subclinical trauma, which in turn results in skin lesion along the lines of the trauma.
- Chronic infection with Mycobacterium smegmatis and human papillomaviruses (HPV) was found to be associated with development of Zoon balanitis.[2]
- Many theories, which include 1) local disturbance of circulation, 2) hypersensitivity response mediated by IgE class of antibodies, 3) “extramedullary plasmacytic infiltrations that persists are expressions of occult multiple myeloma” have been postulated, no supportive evidence have been found for these hypothesis.[3]
Histopathology
ZB has distinctive histopathological features, which include:[4]
Epidermal
- Epidermal changes include, early thickening, acanthosis and parakeratosis of epidermis, which is followed by atrophy, erosions and spongiosis.
- Scattered neutrophils can be present in superficial erosions of the epidermis.
- Spongiosis accentuation occurs in the lower half of the spinous zone.
- Subepidermal clefts, necrotic keratinocytes, and lozenge keratinocytes can be seen in the late stages of ZB.
Dermal
- Dermal changes include patchy lichenoid infiltrate of lymphocytes and plasma cells in papillary dermis, which are replaced by plasma cells, neutrophils, eosinophils, lymphocytes, and erythrocytes.
- Dermal vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, is a characteristic feature of ZB.
- In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates.
Associated conditions:
Patients with BXO, were found to have an other associated autoimmune conditions, which include:[5]
- Diabetes Mellitus,
- Vitiligo
- Alopecia aerata
Causes
The etiology of BXO is uncertain. However, some possibilities have been suggested.
Some studies have shown that patients with BXO also show signs of suffering from autoimmune disorders.[6][7][8] However, this finding is not repeated in every study.[7]
Infection from "human papilloma virus (serotype 16 in particular), spirochetes and atypical mycobacteria" has also been suggested as a cause.[9] Additional suggestions include "pemphigus vulgaris and chronic nonspecific bacterial balanitis".[10]
Relationship to phimosis
BXO is a common cause of pathological phimosis.[11][12]
Kiss et al. report that 40% of boys with phimosis suffered from BXO.[13] Shankar and Rickwood reported BXO in 84% of phimosis patients.[14] Evans reported BXO in 10.5% of phimosis patients.[15] Clemmensen et al. reported BXO in 14.2% of phimosis patients.[16] Bale reported that BXO was found in 19% of circumcisions performed for diseases of the prepuce and penis.[17] Mattioli observed BXO in 60% of patients with acquired phimosis and 30% of patients with congenital phimosis.[18] Rickwood reported BXO in 20 of 21 patients circumcised for pathological phimosis.[19]
Relationship to lichen sclerosus
Many researchers regard BXO as lichen sclerosus et atrophicus (LSA) of the penis, LSA is also known as lichen sclerosus (LS). Lately BXO was coded as part of LSA by Medical literature search tool Medline.[20][21][22] However, Mallon et al. suggest that BXO "may be a consequence of other fibrosing dermatoses, such as lichen planus and cicatricial pemphigoid."[23] When occurring on the male genitals, the term 'BXO' is traditionally used.[11]
Epidemiology and Demographics
The true prevalence of BXO is controversial and unclear. One study calculated a rate of 0.6% of boys affected by their 15th birthday.[14] Another reported a rate of 0.07%.[9] However, a review noted that "with a high degree of suspicion and histologic examination, the condition will prove to be much more frequent than one generally believes."[24] Another suggested that "more cases would be diagnosed during infancy if all dried foreskin were examined systematically."[25] Another remarked that the condition "may be misdiagnosed or ignored in the young boy."[26] Yet another commented that "its true incidence is not appreciated because most cases are cured by circumcision, and unfortunately many surgeons still fail to send their circumcision specimens for histology."[27] Another remarked that the "extent of asymptomatic disease in this series would suggest the true prevalence of LS in men might be much higher than published work suggests."[28]
According to some authors, the disease most frequently affects middle-aged men.[11] However, a large study reported that the age distribution was similar from 2 to 90 years of age, except for men in their twenties, who were at twice the risk.[9] The same study found that black and Hispanic men had approximately twice the risk of white men. The authors suggested possible reasons for this, including access to health care, differences in neonatal circumcision rates, and climate differences.
Mallon et al. found that BXO was related to circumcision status. Adjusting for age, lack of circumcision was associated with an odds ratio of 53.55. The finding was statistically significant.[23] However, BXO has also been noted to occur after late circumcision, especially when performed for phimosis.[29][23][9]
Screening
There is no established screening guidelines for Zoon balanitis
Natural History, Complications, and Prognosis
Natural history
If left untreated, there is risk for malignant transformation.[30]
Complications
Complications of Zoon balanitis include:
- Phimosis
- Paraphimosis
Prognosis
BXO is chronic and often progressive.[11] Please see the following section on treatment.
The condition may cause pain, irritation, and disturbance of sexual function.[10]
In later stages, a meatal stricture may occur, causing urinary retention.[29][11] This may result in bladder or kidney damage.[11]
The coronal sulcus and frenulum may be destroyed.[11]
Phimosis or paraphimosis may occur.[11]
Several studies indicate that BXO may play a pre-cancerous role,[31][32][33][34][35] resulting in squamous cell carcinoma of the penis, a form of penile cancer.
Prognosis is good with treatment.[36]
Diagnosis
Neuhaus and Skidmore report that "Tzanck smear and cutaneous biopsy, along with a rapid protein reagin test, will provide a definitive diagnosis."[37]
Depasquale et al. note that many surgeons do not send circumcision specimens for histology. They caution that this practice "is becoming medicolegally indefensible in a litigation-conscious society, where the clinical sequelae of BXO are often misinterpreted by the patient as surgical errors."[27]
History and symptoms
Patients with Zoon balanitits could be asymptomatic or present with:[38]
- Itching (pruritus) of the genitalia.
- Discomfort in urination(dysuria)
- Pain in the gential region
- blood stain discharge
- Difficult or painful sexual intercourse
Physical examination
Physical examination findings include:[2][39]
- Well circumscribed single or multiple, orange-red in colour with a characteristic glazed appearance and multiple pinpoint redder spots-"cayenne pepper spots"(please click here to view the image) most commonly involving the glans penis, but inner surface of prepuce and coronal sulcus may be involved.
- Though uncommon, lesions of Zoon balanitis can involve other sites which include labia minora in females, oral mucosa, conjunctiva, urethra, cheeks, and epiglottis have been described in literature.[40]
| Clinical criteria in diagnosing Zoon balanitis [39] |
|---|
| Shiny, erythematous patches on the glans, prepuce, or both |
| Lesion present for > 3months |
| Absence of lesion suggestive of Lichen planus, psoriasis elsewhere on the body |
| Poor response to topical therapies |
| Absence of concurrent infections which are ruled out after performing tzanck, potassium hydroxide, gram stain, and VDRL test. |
Laboratory findings
| Reflectance confocal microscopy | A nucleated honeycomb pattern and vermicular vessels is a clue for benign inflammatory genital skin disease[41] |
| Dermoscopy | Focal/diffuse orange-yellowish structure, less areas representing hemosiderin deposition, curved vessels due to epidermal thinning helps in distinguishing ZB from carcinoma in situ.[42] |
Treatment
Therapy focuses on prevention of disease progression.[30]
Shelley reported some success with long-term antibiotic therapy. However, relapses were seen upon stopping treatment.[31]
Some success has been reported with topical steroids,[32] when scarring is minimal,[33] though some have found this ineffectual.[34]
Moderate therapeutic results have been reported using etretinate.[35]
Some success has been reported in the use of carbon dioxide laser therapy.[36][37]
Many authors report that circumcision is the treatment of choice,[9][2][38] with modifications if necessary.[39] Pasieczny suggests testosterone ointment, however.[40]
Glansectomy may be required.[9]
Currently, topical steriods are the most commonly used and most effective medication for the treatment of the adverse skin changes associated with BXO. Patients with urethral stricture disease associated with BXO are generally best managed with surgery to relieve the obstruction. Although urethral dilation is a treatment option, this treatment generally offers only temporary relief of the blockage and a complication of dilations can be stricture progression. The best treatment of urethral stricture treatment options are extended meatotomy (an open incision of the urethra) for short strictures and staged tissue transfer urethroplasty, a surgery to reconstruct the urethra using grafts such as buccal mucosa from inside the cheek.
General measures
Good hygiene which include retracting the foreskin regularly and gentle cleansing of entire glans, preputial sac, and foreskin were found effective in treating the diseases.[43]
Medical Therapy
| Various medical managements for Zoons balanitis | |||
|---|---|---|---|
| Drug dosage | Effectiveness | ||
| Topical steroids | Saline compresses containing 1% hydrocortisone/0.02% betamethason+/-17-valerate/0.05% betamethasone dipropionate | 3 out of 6 patients responded | |
| Oxytetracycline 3%, nystatin 100,00(units/g), and clobetasone butyrate 0.05% applied until complete resolution was observed | All patients responded, but 3 out of 10 patients had recurrences | ||
| Topical calineurin | Tacrolimus ointment 0.1% twice daily | Complete remission after 4 weeks of treatment was observed in 9 patients , with no relapse observed after 3 months of follow up | |
| Topical Pimecrolimus | Pimecrolimus cream 1% twice daily | Improvement is observed after 2 months of treatment with no relapse observed | |
| Topical Imiquimod | 5% imiquimod cream, 3 times a week for 4 months with multiple periods without treatment | Complete resolution can be found after 4-12 weeks of treatment, with no cases of relapse observed | |
| 5% imiquimod cream, 3 times a week for 12 months without any interruption | |||
Surgery
Prevention
There is no known means of preventing BXO. However, one study reports that the data "suggest that circumcision prevents or protects against common infective penile dermatoses."[23]
Primary Prevention
Circumcision in males can help in reducing risk of having ZB.[44]
Secondary prevention
There is no secondary prevention measures.
References
- ↑ Porter WM, Bunker CB (2001). "The dysfunctional foreskin". Int J STD AIDS. 12 (4): 216–20. PMID 11319970.
- ↑ 2.0 2.1 Pastar Z, Rados J, Lipozencić J, Skerlev M, Loncarić D (2004). "Zoon plasma cell balanitis: an overview and role of histopathology". Acta Dermatovenerol Croat. 12 (4): 268–73. PMID 15588560.
- ↑ Weyers W, Ende Y, Schalla W, Diaz-Cascajo C (2002). "Balanitis of Zoon: a clinicopathologic study of 45 cases". Am J Dermatopathol. 24 (6): 459–67. PMID 12454596.
- ↑ Weyers W, Ende Y, Schalla W, Diaz-Cascajo C (2002). "Balanitis of Zoon: a clinicopathologic study of 45 cases". Am J Dermatopathol. 24 (6): 459–67. PMID 12454596.
- ↑ Meffert JJ, Davis BM, Grimwood RE (1995). "Lichen sclerosus". J Am Acad Dermatol. 32 (3): 393–416, quiz 417-8. PMID 7868709.
- ↑ Azurdia R, Luzzi G, Byren I, Welsh K, Wojnarowska F, Marren P, Edwards A (1999). "Lichen sclerosus in adult men: a study of HLA associations and susceptibility to autoimmune disease". Br J Dermatol. 140 (1): 79–83. PMID 10215772. Unknown parameter
|month=ignored (help) - ↑ 7.0 7.1 Meyrick Thomas R, Ridley C, Black M (1983). "The association of lichen sclerosus et atrophicus and autoimmune-related disease in males". Br J Dermatol. 109 (6): 661–4. PMID 6652042. Unknown parameter
|month=ignored (help) - ↑ Harrington C, Dunsmore I (1981). "An investigation into the incidence of auto-immune disorders in patients with lichen sclerosus and atrophicus". Br J Dermatol. 104 (5): 563–6. PMID 7236515. Unknown parameter
|month=ignored (help) - ↑ 9.0 9.1 9.2 9.3 Kizer W, Prarie T, Morey A (2003). "Balanitis xerotica obliterans: epidemiologic distribution in an equal access health care system". South Med J. 96 (1): 9–11. PMID 12602705. Unknown parameter
|month=ignored (help) - ↑ 10.0 10.1 Edwards S. (1996). "Balanitis and balanoposthitis: a review" (Reprint:The CIRP Circumcision Reference Library). Genitourin Med. 72 (3): 155–9.
- ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7
- ↑
- ↑ Kiss A, Király L, Kutasy B, Merksz M (2005). "High incidence of balanitis xerotica obliterans in boys with phimosis: prospective 10-year study". Pediatr Dermatol. 22 (4): 305–8. PMID 16060864. Unknown parameter
|month=ignored (help) - ↑ 14.0 14.1 Shankar K, Rickwood A (1999). "The incidence of phimosis in boys". BJU Int. 84 (1): 101–2. PMID 10444134. Unknown parameter
|month=ignored (help) - ↑ Evans D (2000). "Retrospective study of male lichen sclerosus and outcome in Leicester: 1995-9 inclusive: experience of a genitourinary medicine clinic". Sex Transm Infect. 76 (6): 495. PMID 11221136.
- ↑ Clemmensen O, Krogh J, Petri M (1988). "The histologic spectrum of prepuces from patients with phimosis". Am J Dermatopathol. 10 (2): 104–8. PMID 3239715. Unknown parameter
|month=ignored (help) - ↑ Bale P, Lochhead A, Martin H, Gollow I (1987). "Balanitis xerotica obliterans in children". Pediatr Pathol. 7 (5–6): 617–27. PMID 3449818.
- ↑ Mattioli G, Repetto P, Carlini C, Granata C, Gambini C, Jasonni V (2002). "Lichen sclerosus et atrophicus in children with phimosis and hypospadias". Pediatr Surg Int. 18 (4): 273–5. PMID 12021978. Unknown parameter
|month=ignored (help) - ↑ Rickwood AMK, Hemalatha V, Batcup G, Spitz L. (1980). "Phimosis in boys" (Reprint:The CIRP Circumcision Reference Library). Brit J Urol. 52: 147–50.
- ↑ Finkbeiner A (2003). "Balanitis xerotica obliterans: a form of lichen sclerosus". South Med J. 96 (1): 7–8. PMID 12602704. Unknown parameter
|month=ignored (help) - ↑ Laymon CW, Freeman C. (1944). "Relationship of balanitis xerotica obliterans to lichen sclerosus et atrophicus" (Reprint:The CIRP Circumcision Reference Library). Arch Dermat Syph. 49: 57–9.
- ↑ Neill S, Tatnall F, Cox N (2002). "Guidelines for the management of lichen sclerosus". Br J Dermatol. 147 (4): 640–9. PMID 12366407. Unknown parameter
|month=ignored (help) - ↑ 23.0 23.1 23.2 23.3 Mallon E, Hawkins D, Dinneen M, Francics N, Fearfield L, Newson R, Bunker C (2000). "Circumcision and genital dermatoses". Arch Dermatol. 136 (3): 350–4. PMID 10724196. Unknown parameter
|month=ignored (help) - ↑ Das S, Tunuguntla H (2000). "Balanitis xerotica obliterans--a review". World J Urol. 18 (6): 382–7. PMID 11204255. Unknown parameter
|month=ignored (help) - ↑ Garat J, Chéchile G, Algaba F, Santaularia J (1986). "Balanitis xerotica obliterans in children". J Urol. 136 (2): 436–7. PMID 3735511. Unknown parameter
|month=ignored (help) - ↑ McKay D, Fuqua F, Weinberg A (1975). "Balanitis xerotica obliterans in children". J Urol. 114 (5): 773–5. PMID 1237636. Unknown parameter
|month=ignored (help) - ↑ 27.0 27.1 Depasquale I, Park AJ, Bracka A. (2000). "The treatment of balanitis xerotica obliterans" (Reprint:The CIRP Circumcision Reference Library). BJU Int. 86 (4): 459–65. Retrieved 2006-10-01.
- ↑ Riddell I, Edwards A, Sherrard J. (2000). "Clinical features of lichen sclerosus in men attending a department of genitourinary medicine". Sex Trans Infect. 76 (4): 311–3. Unknown parameter
|month=ignored (help) - ↑ 29.0 29.1
- ↑ Dayal S, Sahu P (2016). "Zoon balanitis: A comprehensive review". Indian J Sex Transm Dis. 37 (2): 129–138. doi:10.4103/0253-7184.192128. PMC 5111296. PMID 27890945.
- ↑ Velazquez E, Cubilla A (2003). "Lichen sclerosus in 68 patients with squamous cell carcinoma of the penis: frequent atypias and correlation with special carcinoma variants suggests a precancerous role". Am J Surg Pathol. 27 (11): 1448–53. PMID 14576478. Unknown parameter
|month=ignored (help) - ↑ Cubilla A, Velazquez E, Young R (2004). "Pseudohyperplastic squamous cell carcinoma of the penis associated with lichen sclerosus. An extremely well-differentiated, nonverruciform neoplasm that preferentially affects the foreskin and is frequently misdiagnosed: a report of 10 cases of a distinctive clinicopathologic entity". Am J Surg Pathol. 28 (7): 895–900. PMID 15223959. Unknown parameter
|month=ignored (help) - ↑ Perceau G, Derancourt C, Clavel C, Durlach A, Pluot M, Lardennois B, Bernard P (2003). "Lichen sclerosus is frequently present in penile squamous cell carcinomas but is not always associated with oncogenic human papillomavirus". Br J Dermatol. 148 (5): 934–8. PMID 12786823. Unknown parameter
|month=ignored (help) - ↑ Powell J, Robson A, Cranston D, Wojnarowska F, Turner R (2001). "High incidence of lichen sclerosus in patients with squamous cell carcinoma of the penis". Br J Dermatol. 145 (1): 85–9. PMID 11453912. Unknown parameter
|month=ignored (help) - ↑ Micali G, Nasca M, Innocenzi D (2001). "Lichen sclerosus of the glans is significantly associated with penile carcinoma". Sex Transm Infect. 77 (3): 226. PMID 11402247. Unknown parameter
|month=ignored (help) - ↑ Dayal S, Sahu P (2016). "Zoon balanitis: A comprehensive review". Indian J Sex Transm Dis. 37 (2): 129–138. doi:10.4103/0253-7184.192128. PMC 5111296. PMID 27890945.
- ↑ Neuhaus I, Skidmore R (1999). "Balanitis xerotica obliterans and its differential diagnosis". J Am Board Fam Pract. 12 (6): 473–6. PMID 10612365. Unknown parameter
|month=ignored (help) - ↑ Edwards SK, Bunker CB, Ziller F, van der Meijden WI (2014). "2013 European guideline for the management of balanoposthitis". Int J STD AIDS. 25 (9): 615–26. doi:10.1177/0956462414533099. PMID 24828553.
- ↑ 39.0 39.1 Kumar B, Narang T, Dass Radotra B, Gupta S (2006). "Plasma cell balanitis: clinicopathologic study of 112 cases and treatment modalities". J Cutan Med Surg. 10 (1): 11–5. PMID 17241566.
- ↑ Adégbidi H, Atadokpèdé F, Dégboé B, Saka B, Akpadjan F, Yédomon H; et al. (2014). "[Zoon's balanitis in circumcised and HIV infected man, at Cotonou (Benin)]". Bull Soc Pathol Exot. 107 (3): 139–41. doi:10.1007/s13149-014-0359-4. PMID 24792459.
- ↑ Arzberger E, Komericki P, Ahlgrimm-Siess V, Massone C, Chubisov D, Hofmann-Wellenhof R (2013). "Differentiation between balanitis and carcinoma in situ using reflectance confocal microscopy". JAMA Dermatol. 149 (4): 440–5. doi:10.1001/jamadermatol.2013.2440. PMID 23325422.
- ↑ Errichetti E, Lacarrubba F, Micali G, Stinco G (2016). "Dermoscopy of Zoon's plasma cell balanitis". J Eur Acad Dermatol Venereol. 30 (12): e209–e210. doi:10.1111/jdv.13538. PMID 26670716.
- ↑ Edwards SK, Bunker CB, Ziller F, van der Meijden WI (2014). "2013 European guideline for the management of balanoposthitis". Int J STD AIDS. 25 (9): 615–26. doi:10.1177/0956462414533099. PMID 24828553.
- ↑ Dayal S, Sahu P (2016). "Zoon balanitis: A comprehensive review". Indian J Sex Transm Dis. 37 (2): 129–138. doi:10.4103/0253-7184.192128. PMC 5111296. PMID 27890945.