Molecular detection of clone-specific DNA in hypopigmented lesions of a patient with early evolving mycosis fungoides

A specific molecular probe for the malignant lymphoid clone of lesions of a patient with mycosis fungoides was developed. As a clone-specific marker the junctional region of rearranged T-cell-receptor-gamma (TCR-γ) genes was used. An oligonucleotide primer complementary to these sequences was designed. Using this primer and polymerase chain-reaction technology, early hypopigmented lesions of the patient, which were previously unclassifiable by conventional microscopy, were analysed. The study demonstrates, on the molecular level, that these hypopigmented lesions contain tumour clone-specific DNA and may represent early manifestations of mycosis fungoides.     

Recurrent post-herpetic erythema multiforme mimicking polymorphic light and juvenile spring eruption: report of two cases in young boys

We report two young boys with a variant of recurrent post-herpetic erythema multiforme which clinically mimicked polymorphic light eruption and juvenile spring eruption.     

NK cell density in malignant skin tumours—a stereological study

We determined the density of natural killer (NK) cells in frozen sections of malignant melanoma (nine cases), squamous cell carcinoma (six cases) and non-neoplastic tonsil (five cases) by immunohistological and stereological methods. The mean density of NK cells in malignant melanoma (5.0 +/- 1.5 X 10(3)/mm3) and in squamous cell carcinoma (5.1 +/- 2.7 X 10(3)/mm3) was significantly lower than in germinal centres of normal human tonsils (5.0 +/- 0.8 X 10(4)/mm3). The NK cell/tumour cell ratio (0.03 +/- 0.015 in malignant melanoma and 0.02 +/- 0.015 in squamous cell carcinoma) is 10(2)-10(4) times lower than that commonly used for in vitro assays. The possible role of NK cells in malignant skin tumours should be viewed with caution.     

CLINICAL AND HISTOPATHOLOGIC SPECTRUM OF PILOMATRICOMAS IN ADULTS

Background. Pilomatricomas are benign cutaneous neoplasms with differentiation toward hair matrix. Although previously reported to occur mostly in children and young adults, Taaffe et al. recently observed a second onset peak in adults and the elderly. Methods. To study the clinical and histopathologic features of pilomatricomas in adults we analyzed files and histologic sections of all cases of pilomatricomas seen at the Department of Dermatology, University of Graz, Graz, Austria, between January 1980 and December 1990. Results. A total of 118 patients were identified, 58 of whom were >45 years of age. The clinical features of patients >45 years of age were generally similar to those of patients <45 years of age. Differential diagnoses in both groups were also comparable except in some cases of the older study-group where differential diagnoses included basal cell carcinoma, keratoacanthoma, and metastasis. Recurrence of the lesions after simple excision was observed in one patient >45 years of age. Histopathologically, lesions in both age groups showed similar features except in four lesions of the older patients where “atypical” features were present. The histopathologic differential diagnosis of the lesions with “atypical” features included pilomatrical carcinoma, basal cell carcinoma with matrical differentiation, and matricoma. Conclusions. Our study reveals the relatively frequent occurrence of pilomatricomas in adults and the elderly. Pilomatricoma should be considered along with other benign and malignant conditions in the clinical differential diagnosis of solitary, firm skin nodules presenting in adults and the elderly, especially on the head and neck.     

A subepidermal blistering disease with histopathological features of dermatitis herpetiformis and immunofluorescence characteristcs of bullous pemphigoid: a novel subepidermal blistering disease or a variant of bullous pemphigoid?

A 64-year-old man presented with a bullous eruption which clinically and histopathologically resembled dermatitis herpetiformis. However, direct immunofluorescence analysis showed IgG deposits at the basement membrane zone, indicating a relationship with bullous pemphigoid or epidermolysis bullosa acquisita. Indirect immunofluorescence studies on salt-split skin showed binding of IgG mainly on the dermal side of the blister. Immunoblot analysis revealed a novel 200 kDa dermal antigen that could be associated with a major pathogen in this blistering a disease. The histopathological similarity to dermatitis herpetiformis and the immunofluorescence findings indicating bullous pemphigoid or epidermolysis bullosa acquisita seem typical of a distinct subepidermal blistering disease characterized by this 200 kDa antigen. However, the pathogenetic role of autoantibodies against this antigen should be further elucidated before confirming whether this case represents a novel subepidermal blistering disease or a special variant of bullous pemphigoid.     

Regression of Atypical Nevus: An Anecdotal Dermoscopic Observation

BACKGROUND: Clark nevi (atypical melanocytic nevi) can be considered as risk markers and potential precursors of melanoma. The authors report on the morphologic changes of an atypical nevus by dermoscopic follow-up examination over a 7-year period. CASE REPORT: A 43-year-old man had a brown macule on his back, sized 5 mm, with an irregular shape, clinically and dermoscopically diagnosed as an equivocal melanocytic lesion. Dermoscopically during the initial examination, a predominant reticular pattern with peripheral eccentric hyperpigmentation in the lower portion of the lesion could be seen. After 7 months, the area of peripheral eccentric hyperpigmentation had regressed, and after 4.5 years the atypical pigment network had almost disappeared. After 7 years of follow-up, a diffuse area of hypopigmentation and a residual light brown pigmentation were detectable. The histopathologic diagnosis was consistent with an atypical junctional nevus with regression with features of a Clark nevus. CONCLUSION: Based on our observation, even a dermoscopically atypical nevus may undergo regression as documented by long-term dermoscopic follow-up.     

Molecular detection of Treponema pallidum in secondary and tertiary syphilis

Treponema pallidum can be detected by conventional techniques such as dark-field microscopy, immunofluorescence or the rabbit infectivity test, in large numbers in the skin lesions of primary and early secondary syphilis. In the skin lesions of late secondary and tertiary syphilis, conventional techniques fail to detect spirochaetes in general, perhaps due to increasing degeneration and the disappearance of treponemal spirochaetes in late syphilitic skin lesions. We used the highly sensitive technique of polymerase chain reaction (PCR) to prove the presence of Treponema pallidum -specific DNA in six lesions of late secondary syphilis and seven lesions of tertiary syphilis, including one syphilitic gumma. A Whartin-Starry stain was carried out in all 13 specimens and did not reveal any treponemal structures. Treponema pallidum-specific DNA was amplified by PCR in four of six cases of secondary syphilis and in the syphilitic gumma. These results are in favour of a direct cell-mediated immune reaction directed against treponemal antigen rather than the concept of an Id-reaction. Beside the usefulness of a PCR-based assay for understanding the aetiology of lesions of late syphilis, the assay described can be of clinical importance in various situations where traditional methods fail to detect Treponema pallidum because of lack of sensitivity.