[Multiple erythema].
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Administration, Oral↗
Biomedical subjects
C A Sander
Publications and source records attributed to C A Sander.
[Long term results of total skin electron beam therapy (TSEBT) in the treatment of mycosis fungoides].
BACKGROUND AND OBJECTIVE: Total skin electron beam therapy (TSEBT) is an important therapeutic option for the treatment of mycosis fungoides. The aim of this study was to find out long term results in 10 patients with the clinical and histological diagnosis of mycosis fungoides. PATIENTS AND METHODS: Between 1982 and 1997 we performed a total skin electron beam therapy in 10 patients. One patient was in stage I A; 5, in stage I B; 3, in stage II B; and one, in stage IV A. The indication for TSEBT was disease progression in spite of PUVA therapy. The doses of electron beam therapy were 30- 36 Gy at 5-6 MeV. In 7 of 10 cases additional local electron beam therapy was given, because individual lesions persisted or recurred after a short time. RESULTS: Complete remission was achieved in 5 patients. The follow- up has been up to 10 years. One patient died of systemic lymphoma 10 years after electron beam therapy. Three patients died of illnesses unrelated to mycosis fungoides. One patient developed a high grade T-cell lymphoma. CONCLUSIONS: Total skin electron beam therapy is a very effective, but technically difficult therapy for mycosis fungoides, especially in stage I B and II B. Particularly interesting has been the long duration of complete response of three patients, who had follicular mucinosis preceding their mycosis fungoides.
Adult↗
Disease progression in patients with thin cutaneous melanomas (tumour thickness < or = 0.75 mm): clinical and epidemiological data from the Tumour Center Munich 1977-98.
BACKGROUND: Although survival in patients with thin melanomas (tumour thickness < or = 0.75 mm) is usually excellent, thin melanomas have the potential to metastasize. OBJECTIVES: To determine risk factors for the development of disease progression in patients with thin cutaneous melanomas. METHODS: A retrospective study was performed between 1977 and 1998 to identify risk factors for the development of disease progression in 2302 patients with cutaneous melanoma with tumour thickness < or = 0.75 mm, diagnosed and treated at the Department of Dermatology and Allergology, Ludwig-Maximilians University, Munich, Germany. The Kaplan-Meier method was used to estimate the influence of different clinical characteristics for the occurrence of first progression during 10 years of follow-up. RESULTS: An analysis of the data from 6298 patients with cutaneous melanoma identified 2302 patients (37%) who presented with cutaneous melanoma with a tumour thickness < or = 0.75 mm, without clinical signs of metastasis at initial diagnosis (clinical stage Ia). A small subgroup of our patients (77 of 2302) developed metastatic disease during the follow-up period. The estimated rate of occurrence of metastasis after 10 years of follow-up was 4.7%. The mean follow-up time was 62 months (median 46). Of these 77 patients, 16 experienced progression at the primary tumour site and 32 presented with regional lymph node metastases. Twenty-eight patients primarily developed systemic metastases (seven patients with and 20 without regional lymph node metastases, one patient with regional lymph node metastases and local recurrence). In one patient the primary site of metastatic disease was not reported. Clinical characteristics included age, sex of the patient and different subtypes of cutaneous melanoma: superficial spreading melanoma, nodular melanoma, acrolentiginous melanoma (ALM) and lentigo maligna melanoma (LMM). Male patients and patients with LMM or ALM were significantly over-represented (P = 0.02 and P = 0.002). In the group of 77 patients with thin melanomas (< or = 0.75 mm), local recurrence was over-represented as compared with those with melanomas > 0.75 mm. No difference in group was found for overall survival after the occurrence of lymph node metastasis as the first manifestation of disease progression. CONCLUSIONS: Thorough follow-up and skin examination is recommended for a subgroup of patients with thin tumours, which consists of male patients with LMM or ALM located in the head and neck region.
Adult↗
Atrophodermia vermiculata: case report and review of the literature.
A 21-year-old woman with an 11-year history of symmetric reticular atrophy on both cheeks, pre-auricular areas, and forehead is presented. The depressions gave a worm-eaten appearance to the skin. Histopathological findings from a biopsy specimen of lesional skin revealed an atrophic follicle. The connective tissue showed mild inflammation in perifollicular and perivascular distribution. The hair follicle was widely dilated and was filled with a keratotic plug. This case points out many of the outstanding clinical and histopathological features of atrophodermia vermiculata as described previously. Atrophodermia vermiculata appears to be one of a group of closely related conditions characterized by keratosis pilaris and atrophy of the skin.
Adult↗
Kaposi's sarcoma associated with tumour necrosis factor alpha neutralising therapy.
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Aged↗
[Kossard frontal fibrosing alopecia in a man].
In 1994 Steven Kossard described a new and peculiar type of hair loss that he named postmenopausal frontal fibrosing alopecia. In 6 elderly women he observed a symmetric regression of the frontal hair line. Often the eyebrows were also affected. Histology showed lichen planopilaris. There were no clinical signs of lichen planus on the rest of the body. Since the original description by Kossard, several cases of frontal fibrosing alopecia have been described--almost all of them in elderly women. We report a man with frontal fibrosing alopecia of the Kossard type.
Aged↗
Lymphadenopathy detected by ultrasound examination as first diagnostic hint of chronic lymphocytic leukaemia in a patient with melanoma.
Recent reports indicate that patients with malignant melanoma might be at higher risk for developing a non-cutaneous unrelated second malignancy. We describe the case of a 46-year-old woman who had a malignant melanoma on her right shoulder that was treated in 1998 by surgical excision combined with axillary lymph node dissection. In 1999, ultrasound examination of peripheral lymph nodes revealed one suspicious echopoor structure in the woman's right axilla that was not palpable. Diagnostic excision and histopathological examination revealed a small B-cell lymphocytic lymphoma, and further investigations led to a diagnosis of chronic lymphocytic B-cell leukaemia (B-CLL). We would like to point out the value of high-resolution ultrasound examination in the follow-up of patients with malignant melanoma; this examination can detect early metastasis as well as other unrelated malignancies.
Axilla↗
Parotid sarcoidosis mimicking Sjögren's syndrome: report of a case.
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Adult↗
[Adult T-cell lymphoma/leukemia: a very rare disease in Europe].
HISTORY AND CLINICAL FINDINGS: A 45-year-old man was admitted with generalized itchy papules. He was originally from the Carribean island of Grenada. The disease had started two years before and was diagnosed as lupus erythematosus, polymorphic light eruption and atopic eczema. Physical examination showed skin-colored papules all over the integument, sebostasis and enlarged supraclavicular and inguinal lymph nodes. INVESTIGATIONS: Lymphocyte count was elevated with 58% as well as LDH (322 U/l) and gamma GT (133 U/l). In a blood smear characteristic pleomorphic lymphoid cells (flower cells) could be obtained. Histopathologic evaluation demonstrated a subepidermally located infiltrate of pleomorphic lymphocytes with epidermal involvement. HTLV-I/II serology (ELISA-screening test) was positive. Polymerase chain reaction analysis revealed HTLV-specific sequences. DIAGNOSIS, TREATMENT AND COURSE: Diagnosis of adult T-cell lymphoma/leukemia was obtained. Treatment consisted of interferon alpha 2b and zidovudine which resulted in a rapid response. However, as a result of an increased loss of weight (12 kg) this therapy was stopped. Two weeks later generalized lymphadenopathy and disseminated skin lesions were observed. Chemotherapy (CHOP-scheme) was initiated. The patient deceased with signs of an acute leukemia after a short period. CONCLUSIONS: Adult T-cell lymphoma/leukemia is a rare disease in Europe. However, in patients with skin rashes, and lymphadenopathy, which are originally from HTLV-I endemic areas, adult T-cell lymphoma/leukemia should be considered.
Antibodies, Viral↗
[Figurated plaque on actinically damaged skin. Actinic O'Brien granuloma].
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Aged↗
Molecular analysis of T-cell clonality with concomitant specific T-cell proliferation in vitro in nickel-allergic individuals.
BACKGROUND: The peripheral blood mononuclear cells (PBMC) of individuals with nickel contact allergy are reported to proliferate to a varying degree upon nickel stimulation in vitro. Different phenotypes of the T cells involved are described. With regard to preferential use of the T-cell receptor (TCR), analysis of the several families of the TCR-gamma gene allows rearrangement evaluation of all T cells regardless of predominant surface expression of TCR alpha/beta. METHODS: The PBMC of 10 nickel-allergic and five nonallergic individuals were cultured for 4 days in the presence of either medium, PHA, NiSO4, or tetanus toxoid (TT). Proliferation was measured by radioactive thymidine uptake and expressed as stimulation index (SI). T-cell clonality was assessed by analysis of the TCR-gamma chain gene, including the use of PCR with a primer combination covering the four main groups (Vgamma1-8, Vgamma9, Vgamma10, and Vgamma11) of the variable region of the TCR-beta chain gene. RESULTS: In the allergic individuals, proliferation to NiSO4 was significantly (P<0.05) higher than in nonallergics (mean SI: 18.05/17.87 vs 0.67/2.27). In unstimulated and PHA-stimulated cultures, there was a random TCR spectrum in both groups. In contrast, in nickel-allergic individuals or individuals with recent TT-booster, oligoclonality could be observed in the correspondingly stimulated cultures. CONCLUSION: In addition to proliferation assay, analysis of T-cell clonality may be a further means to characterize clinical hypersensitivity reactions on the basis of antigen-dependent oligoclonal T-cell expansion, as in the case of tissue-infiltrating lymphocytes.
Adult↗
Loss of tuberin, the tuberous-sclerosis-complex-2 gene product is associated with angiogenesis.
BACKGROUND: Tuberous sclerosis complex (TSC) is an autosomal dominantly inherited disorder associated with an alteration of the TSC2 tumor suppressor gene which encodes for the protein product tuberin. The disease is characterized by the development of hamartomas, e.g. cutaneous angiofibromas which consist of vascular cells, interstitial cells, and normal components of the skin. The Eker rat model, an animal model of inherited cancer, has been shown to carry a mutation of TSC2. METHODS: Immunohistochemical analyses of human angiofibromas were performed using antibodies directed against tuberin and angiogenic growth factors. Proliferation of human dermal microvascular endothelial cells (HDMEC) was determined after incubation with the supernatants of TSC2 (+/+) and TSC2 (-/-) rat embryonic fibroblasts (REF) that were derived from the Eker strain. RESULTS: Loss of the expression of tuberin was observed in the interstitial cells of 13 of 39 angiofibromas. The expression of tuberin was retained in the vascular cells. In all analyzed angiofibromas, the angiogenic factors bFGF, PD-ECGF, VEGF and angiogenin were detected in the interstitial cells and/or vascular cells. Expression of PDGF-B and TGF-beta1 was weak. Tissue culture supernatants from TSC2 (-/-) REF stimulated the growth of HDMEC significantly more than supernatants from TSC2 (+/+) REF. CONCLUSION: A functional loss of tuberin may stimulate vascular growth.
Angiofibroma↗
Follicular mycosis fungoides. A histopathologic analysis of nine cases.
BACKGROUND: The spectrum of mycosis fungoides is exceedingly broad. Many different variants have been described, based on both clinical appearance and histological pattern. A rare form which shows preferential infiltration of hair follicles by malignant lymphocytes is follicular mycosis fungoides. METHODS: We reviewed our experience with nine cases of follicular mycosis fungoides. RESULTS: The unifying feature was infiltration of the hair follicle epithelium by atypical lymphocytes causing varying degrees of damage to the hair follicles. In some specimens the lymphocytes displayed only minor atypia leading to a misinterpretation as pseudolymphoma. Gene rearrangement studies were particularly helpful for establishing a diagnosis of malignant lymphoma. Additionally, epidermotropism of lymphocytes, eosinophils and mucin deposition were present to varying degrees. Mucin makes the distinction from mycosis fungoides-associated follicular mucinosis difficult. We found both dermal mucin and a follicular mucinosis pattern present at different stages of disease in the same patient. CONCLUSIONS: We suggest the term mycosis fungoides-associated follicular mucinosis should be replaced by follicular mycosis fungoides in future lymphoma classification schemes.
Aged↗
Hidden scabies: diagnosis by polymerase chain reaction.
Diagnosis of scabies infection can be difficult as in many cases only few mites are present on an infected person, and in some cases the skin manifestations can be subtle or atypical. We describe the use of polymerase chain reaction (PCR) to amplify Sarcoptes scabiei DNA in a patient presenting with clinically atypical eczema. Cutaneous scales were PCR positive for S. scabiei DNA before, and negative 2 weeks after, therapy. This method facilitates fast and very sensitive diagnosis of clinically atypical or inapparent scabies infection and therapy control in severely affected patients and may help to identify previously unrecognized scabies cases.
Animals↗
Evidence of a leading role for VEGF in Bartonella henselae-induced endothelial cell proliferations.
Bartonella henselae causes the vasculoproliferative disorders bacillary angiomatosis (BA) and bacillary peliosis (BP). The pathomechanisms of these tumorous proliferations are unknown. Our results suggest a novel bacterial two-step pathogenicity strategy, in which the pathogen triggers growth factor production for subsequent proliferation of its own host cells. In fact, B. henselae induces host cell production of the angiogenic factor vascular endothelial growth factor (VEGF), leading to proliferation of endothelial cells. The presence of B. henselae pili was associated with host cell VEGF production, as a Pil- mutant of B. henselae was unable to induce VEGF production. In turn, VEGF-stimulated endothelial cells promoted the growth of B. henselae. Immunohistochemistry for VEGF in specimens from patients with BA or BP revealed increased VEGF expression in vivo. These findings suggest a novel bacteria-dependent mechanism of tumour growth.
Angiomatosis, Bacillary↗
Expression of killer cell inhibitory receptors is restricted to true NK cell lymphomas and a subset of intestinal enteropathy-type T cell lymphomas with a cytotoxic phenotype.
BACKGROUND/AIMS: Killer inhibitory receptors (KIR) have a modulating effect on the cytotoxic functions of natural killer (NK) cells and T cells. Because lymphoma cells often have the same receptors as their non-neoplastic counterparts, this study investigated the expression of KIR on well defined groups of NK and T cell lymphomas, with and without a cytotoxic phenotype, from different sites of origin. METHODS: Nine CD56+/CD3- NK cell lymphomas, 29 CD3+/CD56- T cell lymphomas with a cytotoxic phenotype, and 19 T cell lymphomas without a cytotoxic phenotype were stained for KIR using monoclonal antibodies specific for CD94, CD158a, and CD158b. In addition, the expression of KIR was studied on normal lymphoid tissues. RESULTS: KIR expression was seen in five of nine true NK cell lymphomas including three of four nasal, one of four cutaneous, and one of one intestinal lymphoma nasal type. Double staining for CD56 and CD94 in normal lymphoid tissues revealed that KIR was predominantly expressed by CD56+ NK cells and sporadically on CD8+ T cells. Moreover, enteropathy-type T cell lymphomas with a cytotoxic phenotype showed KIR expression (three cases expressing CD94 and one case expressing CD158a). All nodal and extranodal nonintestinal T cell lymphomas with or without a cytotoxic phenotype lacked expression of KIR. CONCLUSIONS: These results show that KIR expression is restricted to CD56+/CD3- true NK cell lymphomas originating from the nose, gut, and skin, as well as in a subset of extranodal T cell lymphomas originating from the small intestine, which possessed a cytotoxic phenotype. Thus, the presence of KIR on NK/T cell lymphomas seems to mimic the distribution of KIR found on NK and T cells in normal lymphoid tissue.
CD3 Complex↗
Cutaneous manifestations of lymphoma: a clinical guide based on the WHO classification. World Health Organization.
Cutaneous lymphomas are a heterogeneous group of lymphomas that show variations in histology, immunophenotype, and prognosis. At the time of presentation, cutaneous lymphomas may be primary or may involve the skin as a secondary site of involvement. Primary cutaneous lymphomas, in many instances, are distinct from morphologically similar lymphomas arising in lymph nodes. Their natural history is often more indolent than nodal lymphomas, and for that reason, they often require different therapeutic approaches. A classification scheme should recognize those lymphomas that are unique to the skin, as well as those arising in other sites. The mode of presentation of a lymphoma is often an indication of underlying biological distinctions. However, organ-specific classification systems undermine communication among medical specialists. The World Health Organization classification of hematopoietic and lymphoid malignancies offers a comprehensive approach and proposes that lymphomas should be viewed as a list of individual diseases and that each disease can be defined by a constellation of morphological, biological, and clinical features. The current review will focus on the spectrum of primary and secondary cutaneous lymphomas, emphasizing those features of importance to the clinical oncologist.
Female↗
Mast cells control neutrophil recruitment during T cell-mediated delayed-type hypersensitivity reactions through tumor necrosis factor and macrophage inflammatory protein 2.
Polymorphonuclear leukocytes (PMNs) characterize the pathology of T cell-mediated autoimmune diseases and delayed-type hypersensitivity reactions (DTHRs) in the skin, joints, and gut, but are absent in T cell-mediated autoimmune diseases of the brain or pancreas. All of these reactions are mediated by interferon gamma-producing type 1 T cells and produce a similar pattern of cytokines. Thus, the cells and mediators responsible for the PMN recruitment into skin, joints, or gut during DTHRs remain unknown. Analyzing hapten-induced DTHRs of the skin, we found that mast cells determine the T cell-dependent PMN recruitment through two mediators, tumor necrosis factor (TNF) and the CXC chemokine macrophage inflammatory protein 2 (MIP-2), the functional analogue of human interleukin 8. Extractable MIP-2 protein was abundant during DTHRs in and around mast cells of wild-type (WT) mice but absent in mast cell-deficient WBB6F(1)-Kit(W)/Kit(W-)(v) (Kit(W)/Kit(W)(-v)) mice. T cell-dependent PMN recruitment was reduced >60% by anti-MIP-2 antibodies and >80% in mast cell-deficient Kit(W)/Kit(W)(-v) mice. Mast cells from WT mice efficiently restored DTHRs and MIP-2-dependent PMN recruitment in Kit(W)/Kit(W)-(v) mice, whereas mast cells from TNF(-/)- mice did not. Thus, mast cell-derived TNF and MIP-2 ultimately determine the pattern of infiltrating cells during T cell-mediated DTHRs.
Animals↗