ABSTRACT
Milia are benign, superficial keratinaceous cysts that present as fine, small white papules. Milia en plaque is a rare, challenging-to-treat variant most often seen in the posterior auricular region. A total of 9 cases of milia en plaque have been reported in the pediatric literature to date. We report a case of milia en plaque of the nose in a 7-year-old boy, a novel site of involvement in the pediatric population, and successful treatment with the use of topical tretinoin. Topical retinoids offer an effective treatment option for the management of milia en plaque in the pediatric population.
Subject(s)
Miliaria/drug therapy , Nose Diseases/drug therapy , Tretinoin/administration & dosage , Administration, Topical , Child , Dermoscopy , Drug Administration Schedule , Humans , Keratosis , Male , Miliaria/diagnosis , Nose Diseases/diagnosis , Treatment OutcomeSubject(s)
Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Inhibitor of Apoptosis Proteins/blood , Pemphigus/blood , Pemphigus/drug therapy , Adaptor Proteins, Signal Transducing/blood , Aged , Dose-Response Relationship, Drug , Humans , Middle Aged , Neoplasm Proteins/blood , Severity of Illness Index , Survivin , Treatment Outcome , X-Linked Inhibitor of Apoptosis Protein/bloodABSTRACT
BACKGROUND: Aphthous stomatitis, a common mucocutaneous disorder, is a well accepted complication of sirolimus therapy. This association has been reported less frequently with tacrolimus. CASE: We present an 11-year old male with Budd-Chiari syndrome who experienced profound worsening of chronic aphthous ulcers after immunosuppressive therapy was changed from tacrolimus to sirolimus. CONCLUSION: Since these drugs are used widely in the pediatric transplantation population, this report serves to heighten awareness of this debilitating phenomenon, and to stress the importance of exercising caution when sirolimus and tacrolimus are administered in combination to pediatric patients.
Subject(s)
Budd-Chiari Syndrome/drug therapy , Calcineurin Inhibitors , Immunosuppressive Agents/adverse effects , Intracellular Signaling Peptides and Proteins/antagonists & inhibitors , Protein Serine-Threonine Kinases/antagonists & inhibitors , Sirolimus/adverse effects , Stomatitis, Aphthous/chemically induced , Administration, Oral , Child , Humans , Male , Severity of Illness Index , TOR Serine-Threonine Kinases , Tongue Diseases/chemically inducedSubject(s)
Immunoglobulin G/blood , Immunoglobulins, Intravenous/administration & dosage , Immunologic Factors/administration & dosage , Pemphigus/blood , Pemphigus/therapy , Plasmapheresis , Combined Modality Therapy , Humans , Immunoglobulin G/immunology , Male , Middle Aged , Pemphigus/immunology , Remission Induction , Severity of Illness IndexABSTRACT
Habitual marijuana smoking is associated with inflammation and atypia of airway epithelium accompanied by symptoms of chronic bronchitis. We hypothesized that Delta(9)-tetrahydrocannabinol (THC), the primary psychoactive component of marijuana, might contribute to these findings by impairing cellular energetics and mitochondrial function. To test this hypothesis, we examined particulate smoke extracts from marijuana cigarettes, tobacco cigarettes, and placebo marijuana (0% THC) cigarettes for their effects on the mitochondrial function of A549 cells in vitro. Only extracts prepared from marijuana cigarettes altered mitochondrial staining by the potentiometric probe JC-1. With the use of a cross-flow, nose-only inhalation system, rats were then exposed for 20 min to whole marijuana smoke and examined for its effects on airway epithelial cells. Inhalation of marijuana smoke produced lung tissue concentrations of THC that were 8-10 times higher than those measured in blood (75 +/- 38 ng/g wet wt tissue vs. 9.2 +/- 2.0 ng/ml), suggesting high local exposure. Intratracheal infusion of JC-1 immediately following marijuana smoke exposure revealed a diffuse decrease in lung cell JC-1 red fluorescence compared with tissue from unexposed or placebo smoke-exposed rats. Exposure to marijuana smoke in vivo also decreased JC-1 red fluorescence (54% decrease, P < 0.01) and ATP levels (75% decrease, P < 0.01) in single-cell preparations of tracheal epithelial cells. These results suggest that inhalation of marijuana smoke has deleterious effects on airway epithelial cell energetics that may contribute to the adverse pulmonary consequences of marijuana smoking.
Subject(s)
Marijuana Smoking/adverse effects , Mitochondria/physiology , Respiratory Mucosa/physiopathology , Animals , Cell Line , Dronabinol/pharmacology , Energy Metabolism , Humans , Intracellular Membranes/drug effects , Intracellular Membranes/physiology , Male , Membrane Potentials/drug effects , Membrane Potentials/physiology , Mitochondria/drug effects , Rats , Rats, Sprague-Dawley , Respiratory Mucosa/drug effects , Respiratory Mucosa/physiology , SmokingABSTRACT
Marijuana smoking is associated with inflammation, cellular atypia, and molecular dysregulation of the tracheobronchial epithelium. While marijuana smoke shares many components in common with tobacco, it also contains a high concentration of Delta9-tetrahydrocannabinol (THC). The potential contribution of THC to airway injury was assessed by exposing primary cultures of human small airway epithelial (SAE) cells to THC (0.1-10.0 microg/ml) for either 1 day or 7 days. THC induced a time- and concentration-dependent decrease in cell viability, ATP level, and mitochondrial membrane potential. Using a targeted gene expression array, we observed acute changes (24 h) in the expression of mRNA for caspase-8, catalase, Bax, early growth response-1, cytochrome P4501A1 (CYP1A1), metallothionein 1A, PLAB, and heat shock factor 1 (HSF1). After 7 days of exposure, decrease in expression of mRNA for heat shock proteins (HSPs) and the pro-apoptotic protein Bax was observed, while expression of GADD45A, IL-1A, CYP1A1, and PTGS-2 increased significantly. These findings suggest a contribution of THC to DNA damage, inflammation, and alterations in apoptosis. Treatment with selected prototypical toxicants, 2,3,7,8-tetrachlorodibenznzo-p-dioxin (TCDD) and carbonyl cyanide-p-(trifluoramethoxy)-phenyl hydrazone (FCCP), produced partially overlapping gene expression profiles suggesting some similarity in mechanism of action with THC. THC, delivered as a component of marijuana smoke, may induce a profile of gene expression that contributes to the pulmonary pathology associated with marijuana use.
