ABSTRACT
Impetigo herpetiformis, first described by Hebra, is a rare pustular disorder that primarily affects pregnant women and it is often complicated by an increased risk of spontaneous abortion. A commonly associated hypocalcemia often appears with hypoparathyroidism. Here we report a case of complicated impetigo herpetiformis without hypocalcemia paired with a compensatory hyperparathyroidism.
Subject(s)
Dermatitis Herpetiformis/complications , Hyperparathyroidism/complications , Hypocalcemia/complications , Impetigo/complications , Pregnancy Complications/diagnosis , Adult , Female , Humans , PregnancyABSTRACT
BACKGROUND: Actinic keratoses (AKs) are premalignant lesions that can progress into squamous cell carcinoma. Imiquimod, which belongs to the new class of immune-response modifiers, was recently shown to be effective in the treatment of AKs. The underlying mechanisms are not fully understood. OBJECTIVES: To study the expression of individual genes in uninvolved skin and AKs before therapy and to elucidate the way in which the expression of these genes is influenced by imiquimod therapy. METHODS: We treated 13 patients with AK with imiquimod and compared gene expression before, during (five patients) and after (eight patients) therapy with that in uninvolved skin. We analysed genes coding for inflammatory cytokines or their receptors, adhesion molecules, anti-apoptotic proteins, p53 and toll-like receptors (TLRs) by reverse-transcriptase polymerase chain reaction. RESULTS: Comparing uninvolved skin and untreated AK, we found significant differences in the expression of interleukin (IL)-6, hurpin, TLR7 and TLR8. During imiquimod therapy, we detected a further upregulation of interferon-alpha, IL-6, IL-10 receptor 1 and TLR7. In contrast, two anti-apoptotic genes, hurpin and HAX-1, were downregulated. We did not detect significant differences in gene expression for p53, tumour necrosis factor-alpha and alpha- and beta-catenins. Clinically, the upregulated expression of the proinflammatory cytokines correlated with the local inflammation induced by imiquimod. CONCLUSIONS: Our results indicate that specific differences in gene expression are detectable between AK and uninvolved skin. Imiquimod influenced the expression of most genes analysed in this study. This work extends previous findings on the effects of imiquimod on gene regulation in AKs.
Subject(s)
Aminoquinolines/pharmacology , Antineoplastic Agents/pharmacology , Gene Expression Regulation/drug effects , Interferon Inducers/pharmacology , Keratosis/drug therapy , Aged , Aminoquinolines/therapeutic use , Antineoplastic Agents/therapeutic use , Apoptosis/genetics , Cell Adhesion Molecules/metabolism , Cytokines/genetics , Cytokines/metabolism , Genes, p53 , Humans , Imiquimod , Interferon Inducers/therapeutic use , Keratosis/genetics , Keratosis/metabolism , Male , Membrane Glycoproteins/metabolism , Middle Aged , Neoplasms, Radiation-Induced/drug therapy , Neoplasms, Radiation-Induced/genetics , Neoplasms, Radiation-Induced/metabolism , Precancerous Conditions/drug therapy , Precancerous Conditions/genetics , Precancerous Conditions/metabolism , Receptors, Cell Surface/metabolism , Reverse Transcriptase Polymerase Chain Reaction/methods , Skin Neoplasms/drug therapy , Skin Neoplasms/genetics , Skin Neoplasms/metabolism , Toll-Like Receptor 7 , Toll-Like Receptor 8 , Toll-Like ReceptorsABSTRACT
A 36-year-old man presented with a giant congenital melanocytic nevus and multiple disseminated melanocytic nevi. After he had developed neurological symptoms (grand mal seizures), a cerebral metastasis of a malignant melanoma without a primary melanoma was found. The patient was diagnosed as having a neurocutaneous melanosis with a cerebral metastasis. In spite of a variety of therapeutic attempts (surgery, radiation therapy and chemotherapy) he followed a rapidly progressive, lethal course with increased intracranial pressure, hydrocephalus and spinal metastases.
Subject(s)
Melanoma/diagnosis , Melanosis/diagnosis , Neurocutaneous Syndromes/diagnosis , Skin Neoplasms/diagnosis , Adult , Brain/pathology , Brain Neoplasms/diagnosis , Brain Neoplasms/pathology , Brain Neoplasms/secondary , Brain Neoplasms/therapy , Diagnosis, Differential , Fatal Outcome , Humans , Male , Melanoma/pathology , Melanoma/secondary , Melanoma/therapy , Melanosis/pathology , Melanosis/therapy , Neoplasms, Multiple Primary/diagnosis , Neoplasms, Multiple Primary/pathology , Neoplasms, Multiple Primary/therapy , Neurocutaneous Syndromes/pathology , Neurocutaneous Syndromes/therapy , Nevus, Pigmented/diagnosis , Nevus, Pigmented/pathology , Nevus, Pigmented/therapy , Skin/pathology , Skin Neoplasms/pathology , Skin Neoplasms/therapy , Spinal Neoplasms/diagnosis , Spinal Neoplasms/pathology , Spinal Neoplasms/secondary , Spinal Neoplasms/therapyABSTRACT
Zinc is crucial for the biosynthesis, storage, and secretion of insulin in pancreatic islet cells. We have previously presented evidence that NO interferes with cellular Zn(2+) homeostasis and we therefore investigated the influence of chronic NO exposure on the labile islet cell Zn(2+) content. A strong fluorescence activity in a large islet cell subpopulation was found after staining with the Zn(2+)-specific fluorophore Zinquin. Culture for 24 h in the presence of nontoxic concentrations of the slow-releasing NO donor DETA/NO resulted in a significantly reduced Zn(2+)-dependent fluorescence. This appears to be islet specific as in endothelial cells DETA/NO exposure enhanced the Zn(2+)-dependent fluorescence activity in a concentration-dependent manner. These results suggest that NO interferes with cellular Zn(2+) homeostasis, which in islet cells is crucial for proper hormone delivery and thus special cell function.
