Biomedical subjects
Publications and source records attributed to D V Kazakov.
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In an eleven part series published in Pathologica, we have presented various tumoral, quasitumoral and pseudotumoral lesions of the superficial and somatic soft tissue (ST), which emerged as new entities or as variants of established entities during the last quarter of a century. Detailed clinicomorphological and differential diagnostic features of approximately sixty entities were chosen on the basis of their clinical significance and morphologic distinctiveness. The series included fibrous and myofibroblastic tumors (e.g. solitary fibrous tumor, high grade classic and pigmented dermatofibrosarcoma protuberans, inflammatory myofibroblastic tumor and myofibrosarcomas), fibromyxoid and fibrohistiocytic neoplasms (e.g., Evans' tumor, phosphaturic mesenchymal tumor, inflammatory myxohyaline tumor), special adipocytic/vascular/and smooth muscle lesions (e.g., chondroid lipoma, Dabska's tumor, ST hemangioblastoma, lipoleiomyosarcoma), epithelioid mesenchymal malignancies of diverse lineages (e.g., epithelioid liposarcoma, proximal-type epithelioid sarcoma, neuroendocrine extraskeletal chondromyxoid sarcoma), ST Ewing's tumor and peripheral nerve sheath tumors (perineuriomas and pigmented and rosetting tumors of the schwannoma/neurofibroma group), extranodal dendritic or histiocytic proliferative processes (follicular dendritic cell sarcoma, Rosai-Dorfman disease, Castleman's disease, and plexiform xanthomatous tumor), and tumors with myoepithelial differentiation. The section devoted to selected pseudotumoral entities considered representatives of the hamartoma group (neural fibrolipomatous hamartoma, ectopic hamartomatous thymoma, rudimentary meningocele), metabolic diseases (amyloid tumor, nephrogenic fibrosing dermopathy, tophaceous pseudogout, pseudoinfiltrative parathyromatosis), stromal tissue reactions to trauma (fibroosseous pseudotumors of digits) and infections (bacillary angiomatosis), and normal organs (glomus coccygeum). To conclude the descriptive phase, supplementary material has now been collected and appended in an attempt to provide a quick digest of essential knowledge both for comparison and differential diagnosis. The data have been tailored to synthesize diverse sources, integrating clinical elements and references to articles that previously appeared in Part I ("Introduction"), Part II ("The List and Review of New Entities") and Parts III to XI ("Excerpta"). At the very least we hope this final part ("Appendix") will provide the reader with a useful tabular organization of ST lesions and a reference resource.
Clinical, pathological, and molecular-genetic features as well as etiology of cutaneous pseudolymphoma (CPL, cutaneous lymphoid hyperplasia, lymphocytoma cutis) of the breast nipple are summarized. CPL presents as a nipple induration and it is often suspected to be Paget carcinoma pre-operatively. Histologically, atypical microscopic features of a dense lymhoid infiltrate with follicles often mislead to the diagnosis of a malignant lymphoma. However, CPL runs a benign course. Rare cases of CPL contain a clonal lymphoid population. A substantial number of CPL in the breast nipple is caused by antigenic stimulation by Borrelia burgdorferi. In some patients a tick bite is documented. CPL of the breast is commonly treated by excision, but some patients may be cured by antibiotic therapy. The presence of Borrelia burgdorferi should be detected using methods of serology, culture, and molecular biology. Beside CPL, the differential diagnosis of the breast nipple lesions further includes Paget carcinoma, eczema, and florid papillomatosis.
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Cutaneous lymphomas represent a heterogeneous group of T-, NK- and B-cell neoplasms, with mycosis fungoides (MF) being the most common subtype. MF has a plethora of clinicopathological manifestations. Many variants of this lymphoma differ substantially from the 'classical' Alibert-Bazin disease and are therefore sometimes referred to as 'atypical' forms of the disease. This review addresses the whole clinicopathological spectrum of mycosis fungoides with respect to epidemiology, clinical, histopathological, immunophenotypic and genotypic features and the clinical course and prognosis of its variants: classical, erythrodermic, follicular, syringotropic, bullous/vesicular, granulomatous, poikilodermic, hypo- and hyperpigmented, unilesional, palmoplantar, hyperkeratotic/verrucous, vegetating/papillomatous, ichthyosiform, pigmented purpura-like, pustular and mucosal involvement in MF.
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Systemic anaplastic large-cell lymphoma (ALCL) in human immunodeficiency virus (HIV)-infected individuals showing an extensive infiltrate of neutrophils has been reported and referred to as 'neutrophil-rich' CD30+ ALCL. Secondary cutaneous involvement has been found in a subset of these cases. We report the clinicopathological features of four immunocompetent patients with primary cutaneous neutrophil-rich ALCL and present a new histological subtype with a dissolute growth pattern of CD30+ tumour cells. Four HIV-negative patients presented with rapidly growing solitary or multiple tumours located on the face. Ulceration of the lesions with purulent discharge was a typical finding. Various inflammatory dermatoses were considered clinically in all cases. The histological hallmark was a large number of neutrophils in the infiltrate that masked neoplastic CD30+ anaplastic cells. In two cases, a dissolute growth pattern of anaplastic tumour cells was observed. In two cases, a strong correlation between tumour growth and interleukin (IL)-8 cytokine pattern as well as the production of IL-8 by tumour cells was demonstrated. The diagnosis of neutrophil-rich ALCL is challenging clinically and histologically as the tumour cell compartment is masked by an extensive inflammatory infiltrate of neutrophils and other reactive cells such as histiocytes which may be mainly due to release of IL-8 by tumour cells. The term 'pyogenic' designates the typical feature of this distinct neutrophil-rich ALCL, namely abscess formation ('pyo-') by cytokines (IL-8) produced by tumour cells ('-genic'). The clinical behaviour of this type is the same as in primary cutaneous CD30+ ALCL with classical histological presentation.
We report three patients with blastic natural killer (NK)-cell lymphoma of the skin associated with myelodysplastic syndrome (MDS) (two patients) or subacute myelomonocytic leukaemia (one patient). In two patients MDS was diagnosed before skin lesions; the patient with leukaemia initially presented with skin lesions. Our patients had several clinical features in common, namely multiple skin lesions with a bruise-like appearance, involvement of the oral mucosa, and good general status at presentation but very rapid deterioration in the course of the disease. All patients died of disease 4-14 months after the diagnosis. Histopathologically, there were cutaneous infiltrates of slightly pleomorphic medium-sized cells expressing CD4, CD56, terminal deoxynucleotidyl transferase (focally) and being negative for surface CD3, cytotoxic molecules, B-cell-associated markers and myelomonocytic markers. Erythrocyte extravasation was seen in all patients. T-cell receptor genes were in germline configuration. MDS was classified as refractory cytopenia with multilineage dysplasia and ring sideroblasts and refractory anaemia with transition to refractory anaemia with excess of blasts. We reviewed similar cases reported in the literature showing coexistence of blastic NK-cell lymphoma/leukaemia and MDS or myelogenous leukaemia. We conclude that given an overall limited number of reported cases of blastic NK-cell lymphoma/leukaemia, its association with various myelodysplastic/myeloproliferative disorders seen in a subset of patients ( approximately 15-20%) is more than coincidental and may indicate their common origin.
BACKGROUND: Multiple eruptive dermatofibroma (MEDF) is a rare disorder seen in immunocompromised patients, simulating Kaposi's sarcoma (KS). Whereas KS is strongly associated with human herpesvirus 8 (HHV-8), the virus has never been detected in MEDF until now. OBJECTIVE: To present a patient with MEDF who showed no signs of immunodeficiency but was seropositive for HHV-8 antibodies and demonstrated HHV-8 DNA both in the peripheral blood and lesional skin of MEDF. METHODS: Clinical, histological and serological investigations were performed as well as polymerase chain reaction (PCR) studies and in situ hybridization (ISH). RESULTS: A 35-year-old white man with suspected KS was referred for evaluation of multiple pigmented nodules and patches. Biopsies revealed features of dermatofibroma, superficial fibrosing dermatitis and scar. One of the nodular lesions harbored HHV-8 DNA sequences. A faint amplification product was detected in the superficial fibrosing dermatitis lesion, while no HHV-8 sequences were found in normal skin and scar. Whole-blood samples and serum were positive for HHV-8. None of the skin lesions shown to harbor HHV-8 DNA sequences by nested PCR displayed a signal for HHV-8 RNA by ISH. Repetitive peripheral blood examinations did not reveal any serum antibodies against or antigens of HIV. Serum antibodies against the HHV-8 capsid antigen orf 65.2 were detected. CONCLUSION: Results of PCR studies and ISH indicate that the presence of HHV-8 in the lesional tissue was probably blood-borne due to viremia and not due to viral replication in tumor cells. The presence of HHV-8 is not fully restricted to KS. The differential diagnosis of KS and its simulators should be based on an integrative analysis of all available clinicopathological and molecular data and should not rely exclusively or predominantly on the presence or absence of HHV-8.