Tunneled island pedicle flap reconstruction for upper lateral cutaneous lip defects.

BACKGROUND: Esthetic upper lateral cutaneous lip reconstruction preserves the apical triangle, nasolabial fold symmetry, and free margin position. The tunneled island pedicle flap (IPF) is a novel single-stage reconstruction to achieve these goals. OBJECTIVES: Describe the technique and patient and surgeon-reported outcomes for the tunneled IPF reconstruction of upper lateral cutaneous lip defects. METHODS: Retrospective chart review of consecutive tunneled IPF reconstruction following Mohs micrographic surgery (MMS) at a tertiary care center between 2014 and 2020. Patients rated their scars using the validated Patient Scar Assessment Scale (PSAS), and independent surgeons rated scars using the validated Observer Scar Assessment Scale (OSAS). Descriptive statistics were generated for patient demographics and tumor defect characteristics. RESULTS: Twenty upper lateral cutaneous lip defects were repaired with the tunneled IPF. Surgeons rated scars with a composite OSAS score of 11.83 ± 4.29 (mean, SD) [scale of 5 (normal skin) to 50 (worst scar imaginable)] and an overall scar score of 2.81 ± 1.11 [scale of 1 (normal skin) to 10 (worst scar imaginable)]. Patients rated their scars with a composite PSAS score of 10 ± 5.39 [scale of 6 (best possible score) to 60 (worst)] and with an overall score of 2.2 ± 1.78 [scale of 1 (normal skin) and 10 (very different from normal skin)]. One flap was surgically revised for pincushioning, but none experienced necrosis, hematoma, or infection. CONCLUSIONS: The tunneled IPF is a single-stage reconstruction for upper lateral cutaneous lip defects with favorable scar ratings by patients and observers.

Development of a core outcome set for cutaneous squamous cell carcinoma trials: identification of core domains and outcomes.

BACKGROUND: The lack of uniformity in the outcomes reported in clinical studies of the treatment of cutaneous squamous cell carcinoma (cSCC) complicates efforts to compare treatment effectiveness across trials. OBJECTIVES: To develop a core outcome set (COS), a minimum set of agreed-upon outcomes to be measured in all clinical trials of a given disease or outcome, for the treatment of cSCC. METHODS: One hundred and nine outcomes were identified via a systematic literature review and interviews with 28 stakeholders. After consolidation of this long list, 55 candidate outcomes were rated by 19 physician and 10 patient stakeholders, in two rounds of Delphi exercises. Outcomes scored 'critically important' (score of 7, 8 or 9) by ≥ 70% of patients and ≥ 70% of physicians were provisionally included. At the consensus meeting, after discussion and voting of 44 international experts and patients, the provisional list was reduced to a final core set, for which consensus was achieved among all meeting participants. RESULTS: A core set of seven outcomes was finalized at the consensus meeting: (i) serious or persistent adverse events, (ii) patient-reported quality of life, (iii) complete response, (iv) partial response, (v) recurrence-free survival, (vi) progression-free survival and (vii) disease-specific survival. CONCLUSIONS: In order to increase the comparability of results across trials and to reduce selective reporting bias, cSCC researchers should consider reporting these core outcomes. Further work needs to be performed to identify the measures that should be reported for each of these outcomes.

Oncogenic osteomalacia. A case report.

Oncogenic osteomalacia is a rare condition characterized by the development of pain and fractures in a patient with specific laboratory abnormalities consisting of hypophosphatemia, hyperphosphaturia, and decreased 1,25-OH vitamin D levels. The clinical scenario is completed by the association of this osteomalacic state with the finding of a neoplastic process in the afflicted patient. The authors report a patient in whom the diagnosis of oncogenic osteomalacia was established and treatment begun despite the fact that the associated tumor (benign undifferentiated tumor of meschymal origin) escaped detection for many months. Following discovery of the tumor and identification by magnetic resonance imaging, the patient was cured by surgical resection.

A four generation study of familial dysalbuminemic hyperthyroxinemia: diagnosis in the presence of an acquired excess of thyroxine-binding globulin.

We have studied the largest kindred with familial dysalbuminemic hyperthyroxinemia (FDH) thus far reported, comprising thirty-three blood relations in four generations and three of their spouses. Our objective was to complement previous evidence concerning the precise mode of inheritance of FDH and to detect any other features of the disorder that had not yet been noted. Among the thirty three, there were thirteen patients with FDH, eight males and five females, in all of whom the abnormality appeared to be fully expressed. Within the kindred, no affected female has borne a female child, but transmission from female to male, male to male, and male to female has been observed. Among the offspring of individuals with FDH, the overall observed frequency of FDH in three filial generations was 12/22, or 54.5 per cent, yielding a computed penetrance ratio of 1.09. Four of the patients with FDH had been investigated for hyperthyroidism, and two of them had mistakenly been treated. Of particular interest were two women with FDH who were receiving oral contraceptives and whose serum thyroxine-binding globulin (TBG) concentrations were increased. The results of their thyroid function tests differed from those of patients with FDH whose TBG concentrations were normal and mainly suggested the presence of only a high TBG state. The diagnosis of FDH in these two patients was obscured, and probably would not have been made were it not for the present investigation, which led to the electrophoretic demonstration of increased binding of T4 by serum albumin.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement by glucocorticoid deficiency of the increase in cycloleucine accumulation induced in rat thymocytes by triiodothyronine.

In previous studies, we have demonstrated that 3,5,3'-triiodothyronine (T3), either added to suspended media in vitro or injected acutely in vivo, increases the in vitro accumulation of the non-metabolized amino acid cycloleucine (CLE) by thymocytes harvested from weanling rats. We now report that this reponse is greatly enhanced by prior adrenalectomy of the donor rat. In vitro, a significant increase in CLE accumulation in thymocytes from adrenalectomized rats was induced by T3 at a concentration of 1 x 10-10 M, while a concentration of 1 x 10-6 M was required to produce a similar and significant effect in thymocytes from intact animals. In adrenalectomized animals, a single iv dose of T3 (0.5 microgram/100 G bw) significantly increased the in vitro accumulation of CLE in thymocytes harvested two hours later. In contrast, ten-times that dose was ineffective in control animals. Increased sensitivity to T3 was abolished by physiological replacement doses of hydrocortisone. The data are consistent with the well-known opposing effects of physiological levels of thyroid and glucocorticoid hormones on the growth and function of lymphoid tissue in vivo and, together with other findings, suggest that thyroid hormones modulate the cellular accumulation of amino acids in the intact animal.