Chronic Opioid Use after Laryngeal Cancer Treatment: A VA Study.

OBJECTIVE: To investigate opioid utilization in veterans undergoing laryngeal cancer treatment and describe the risk of chronic use after treatment cessation. STUDY DESIGN: A retrospective cohort study. SETTING: A single Veterans Health Administration site. SUBJECTS AND METHODS: Veterans with newly diagnosed and treated laryngeal cancer with attributable opioid use from 2005 to 2015. Milligram morphine equivalents (MMEs) were calculated from 90 days prior to diagnosis for up to 1 year. Adjuvant pain medications filled 30 days prior to and up to a year from the date of diagnosis were assessed. RESULTS: Of 74 veterans with biopsy-proven laryngeal carcinoma, 73 (98.6%) were male and 71 (96%) were white. Forty-three (58%) patients were stage 0/I/II; 31 (42%) were III/IV. Eleven (14.9%) were treated with surgery alone, 35 (47.3%) with radiation alone, and 28 (38%) with multimodal therapy. Twenty-four (32.4%) patients had preexisting opioid use prior to cancer diagnosis. Patients who used opioids more than 30 days prior to date of diagnosis were found to be 10 times more likely to have persistent opioid use at 90 days (P = .0024) and 8 times more likely to have chronic use at 360 days (P = .0041). Maximum MMEs within 1 year of diagnosis were significantly associated with chronic use at 90 days (P = .00045) and chronic use at 360 days (P = .0006). CONCLUSION: Preexisting opioid use and maximum MMEs are strongly associated with chronic opioid use among veterans treated for laryngeal carcinoma independent of stage and treatment type.

Identification of Helicobacter pylori in skin biopsy of prurigo pigmentosa.

A 23-year-old Chinese man presented with a 3-year history of a pruritic eruption. On examination, pink urticarial papules associated with hyperpigmented reticulated patches were noted on his neck, back, and upper chest. Histopathology revealed vacuolar interface dermatitis and numerous gram-negative rods within a dilated hair follicle. The organisms were reactive with anti-Helicobacter pylori immunohistochemisty. The histologic findings and clinical presentation support the diagnosis of prurigo pigmentosa. Additional testing demonstrated a positive urease breath test and serum H. pylori IgG antibodies. The patient was referred to gastroenterology and treated with appropriate antibiotics. After treatment, esophagogastroduodenoscopy revealed chronic gastritis without evidence of H. pylori infection and his skin showed reticulated hyperpigmented patches without evidence of active inflammatory papules. Although previous reports have associated prurigo pigmentosa to H. Pylori gastritis, this is the first report of H. pylori organisms identified in a skin biopsy of prurigo pigmentosa.

Cutaneous collagenous vasculopathy: report of the first pediatric case.

We describe a 16-year-old girl who presented with a 3-year history of telangiectatic patches on the extremities and trunk. Skin biopsies demonstrated dilated vessels with thickened walls containing hyaline material in the papillary dermis, resembling those seen in systemic amyloidosis, porphyrias, or lipoid proteinosis. A diagnosis of cutaneous collagenous vasculopathy was made. To our knowledge, cutaneous collagenous vasculopathy has previously only been described in adults aged 50 and older.

Expression of TGF-beta type II receptors in the olfactory epithelium and their regulation in TGF-alpha transgenic mice.

Numerous in vitro studies of neurogenesis of olfactory receptor neurons (ORNs) suggest that transforming growth factor (TGF)-beta promotes the maturation/differentiation of olfactory progenitors. We demonstrate that in vivo both mature and immature ORNs, and possibly a basal neuronal progenitor cell, express the TGF-beta type II receptor (TGF-betaRII), suggesting that these cells are targets for TGF-beta signaling. In a previous study of neurogenesis in the OE of TGF-alpha overexpressing transgenic (T) mice, we observed an apparent reduction in the expression of olfactory marker protein (OMP), a marker of terminal differentiation in ORNs in T mice compared to nontransgenic (NT) littermate controls; this was confirmed by Western blotting and immunohistochemistry. In contrast, there was no apparent difference between T and NT mice in the intensity of immunoreactivity for a neuronal marker, protein gene product 9.5. Because TGF-alpha overexpression has been reported to affect TGF-beta signaling in other epithelia, we compared the expression of the TGF-beta type II receptor (TGF-betaRII) in T and NT mice. The intensity of TGF-betaRII immunoreactivity on ORNs was substantially reduced in T compared to NT mice. Similar reductions in TGF-betaRII expression in vomeronasal receptor neurons and in other epithelia in the nasal cavity of T mice were also observed. Taken together, these results indicate that TGF-beta signaling regulates terminal differentiation of ORNs in vivo and suggest ways in which interactions between TGF-alpha and TGF-beta signaling pathways may interact in the OE.