1,720,985 research outputs found
Carcinoma of the pancreas with neuroendocrine differentiation and nodular panniculitis
No full textBackground: On rare occasions tumours of the pancreas produce high amounts of pancreatic lipase. The enzyme activity in the blood and in different tissues causes a syndrome called nodular panniculitis by focal necrosis of lipids and a concomittant inflammatory reaction. Case Report: A 72-year-old man was admitted to the dermatology clinic with the diagnosis of erythema nodosum. The patient had been well until 3 months earlier when painful red nodes developed on the skin of both shanks. He complained of profuse night sweating and a weight loss of 10 kg within that time but did not have fever. He also had noticed a painful swelling of his right index finger, left middle finger and the third toe on his left foot. Biopsy of the nodes revealed a focal necrosis of fatty tissue. Laboratory examinations showed a highly elevated concentration of serum pancreatic lipase. Further investigations showed a tumour in the pancreas and several osteolytic lesions. Tumour biopsy revealed a neuroendocrine carcinoma. After tumour resection serum lipase level immediately fell to almost normal values, and all skin and bone manifestations disappeared quickly. Conclusion: Due to its clinical appearance the panniculitis syndrome is most often mistaken for either erythema nodosum or rheumatoid arthritis. A resection of the tumour after correct diagnosis should always be considered because the widespread manifestations in the skin and bones do not represent distant metastasis and have a very good chance to dissolve completely
Two sisters with familial dyskeratotic comedones
No full textFamilial dyskeratotic comedones is a rare autosomal dominant genodermatosis, which presents with disseminated keratotic papules and comedo-like lesions. The disease usually manifests in childhood. The histology of the lesions is characterized by a crater-like invagination of the epidermis filled with parakeratotic keratin. The epidermis usually shows acantholysis. So far the causative gene defect is unknown. We report on a new family with two affected sisters. The more severely affected woman was treated with oral retinoids without any effect. Afterwards some regions were successfully treated by CO2 laser-therapy
Granulocyte colony-stimulating-factor-induced psoriasiform dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation
No full textPsoriasis is a chronic inflammatory skin disorder characterized by accumulation of Th1-type T cells and neutrophils, regenerative keratinocyte proliferation and differentiation, and enhanced epidermal production of antimicrobial peptides. The underlying cause is unknown, but there are some similarities with the immunologic defense program against bacteria. Development of psoriasiform skin lesions has been reported after administration of granulocyte colony-stimulating factor (G-CSF), a cytokine induced in monocytes by bacterial antigens. To further investigate the relation between this type of cytokine-induced dermatitis and psoriasis, we analyzed the cutaneous cytokine profile [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), IL-12p35 and p40, and IL-8] and expression of markers of epidermal activation [Ki-67, cytokeratin-16, major histocompatibility complex (MHC) class II, intercellular adhesion molecule-1 (ICAM-1)] in a patient who developed G-CSF-induced psoriasiform dermatitis by using quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistology. The histologic picture resembled psoriasis with regard to epidermal hyperparakeratosis and the accumulation of lymphocytes in the upper corium. CD8(+) T cells were found to infiltrate the epidermis which was associated with an aberrant expression of Ki-67, cytokeratin-16, MHC class II, and ICAM-1 on adjacent keratinocytes. As compared to normal skin (n = 7), there was an increased expression of TNF-alpha, IL-12p40, and IL-8, a decreased expression of TGF-beta1, and a lack of IL-10, similar to the findings in active psoriasis (n = 8). Therefore, G-CSF may cause a lymphocytic dermatitis that, similar to psoriasis, is characterized by a pro-inflammatory Th1-type cytokine milieu and an epidermal phenotype indicative of aberrant maturation and acquisition of non-professional immune functions
No Chromosomal Imbalances in Seborrheic Keratoses Detectable by Comparative Genomic Hybridization
No full textAberrations of the CDKN2A network components p16, p53 and RB1 in primary cutaneous B-cell lymphoma
No full textIdiopathic calcinosis cutis with extended leg ulcers. Successful therapy with aluminium hydroxide
No full textWe report on a 51-year-old woman with an idiopathic calcinosis cutis. She developed longstanding multiple, extended and very painful ulcers on both lower legs. The ulcerations showed a bizarre configuration surrounded by a livedo racemosa vessel pattern and they were extremely resistant to any therapy. The characteristical histopathological features with occlusion of small and medium-sized blood vessels and massive calcification of the intima, ischemic necrosis and calcifications of subcutanous fat distant from blood vessels led to the diagnosis. Moreover, we detected multiple calcifications in the soft tissue radiologically. We did not find any underlying cause for the calcinosis cutis. Despite serum phosphate levels in the upper normal range therapy with oral aluminium hydroxide was started. There were no adverse effects from therapy. After 12 weeks the lesions showed continious improvement accompanied by a significant pain relief. The ulcers healed completely after covering with split thickness skin grafts, This case supports the efficiency of oral phosphate-binding agents in the therapy of calcinosis cutis
Aberrations of the CDKN2A network components p16, p14, p53 and Rb in primary cutaneous B-cell lymphomas: Rb phosphorylation status is a possible parameter for subgroup differentiation
No full textIdiopathic calcinosis cutis with extended leg ulcers. Successful therapy with aluminium hydroxide
No full textWe report on a 51-year-old woman with an idiopathic calcinosis cutis. She developed longstanding multiple, extended and very painful ulcers on both lower legs. The ulcerations showed a bizarre configuration surrounded by a livedo racemosa vessel pattern and they were extremely resistant to any therapy. The characteristical histopathological features with occlusion of small and medium-sized blood vessels and massive calcification of the intima, ischemic necrosis and calcifications of subcutanous fat distant from blood vessels led to the diagnosis. Moreover, we detected multiple calcifications in the soft tissue radiologically. We did not find any underlying cause for the calcinosis cutis. Despite serum phosphate levels in the upper normal range therapy with oral aluminium hydroxide was started. There were no adverse effects from therapy. After 12 weeks the lesions showed continious improvement accompanied by a significant pain relief. The ulcers healed completely after covering with split thickness skin grafts, This case supports the efficiency of oral phosphate-binding agents in the therapy of calcinosis cutis
CD4+CD56+blastic tumor of the skin: cytogenetic observations and further evidence of an origin from plasmocytoid dendritic cells
No full textWe here report on a case of a blastic tumor, recently described to belong to a new entity sharing phenotypic similarities with blood derived plasmocytoid dendritic cells and formerly regarded as belonging to the group of natural killer cell lymphomas. Besides immunophenotypic characteristics such as the absence of T- cell markers and almost complete absence of markers of the myeloid lineage, these tumors express CD4, CD56 and CD123, the receptor for interleukin-3. Moreover, using the comparative genomic hybridisation technique, CGH, we demonstrate a gain of chromosome 7q, 22 and a loss of chromosome 3p and 13q. Since this type of hematologic disorder often shows its primary manifestation in the skin and often runs a rapidly fatal course, it is important to distinguish this from other types of primary cutaneous lymphomas
Aberrations of the CDKN2A network components p16, p14, p53 and Rb in primary cutaneous B-cell lymphomas: Rb phosphorylation status is a possible parameter for subgroup differentiation
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