Prognostic factors in cutaneous apocrine carcinoma: a single-institution retrospective study of 32 patients.

BACKGROUND: Cutaneous apocrine carcinoma (CAC) is a rare adnexal carcinoma. Limited data exists on the demographics and overall survival (OS) of patients with CAC; thus, there is no consensus on surgical management. This study aimed to examine demographic and survival data of patients with CAC to determine optimal surgical management. METHODS: A single-center retrospective cohort study was conducted at the National Cancer Center Hospital in Tokyo between 2005 and 2022. Patients with a histologically-confirmed CAC diagnosis were identified and data on patient demographics, OS, and lymph node (LN) status were gathered. RESULTS: Thirty-two patients were included (median age, 65.5 years; male-female ratio, 15:1). The most common involvement site was the axilla (87.5%). Of the nine patients in the clinical local stage, pathological LN metastases were found in five patients. Either pathological LN or distant metastases were present in 75% of the patients at initial diagnosis. The most common initial surgical treatments included wide local excision and complete LN dissection. Across cohorts, the median OS was 39 months. Patients with ≥ 4 LN metastases had reduced recurrence-free survival and OS compared to those with ≤ 3 LN metastases (p = 0.042, p = 0.041, respectively). The OS was not remarkably different between patients who did and did not receive postoperative radiation therapy. CONCLUSIONS: Since CAC has a high rate of LN metastasis-and the number of LN metastases is a significant prognostic factor-LN evaluation should be considered for patients with CAC as initial treatment. Nonetheless, ≥ 4 LN metastases can be a poor prognostic factor for CAC.

Arteriosclerosis Derived from Cutaneous Inflammation Is Ameliorated by the Deletion of IL-17A and IL-17F.

The skin is one of the major immune organs producing large amounts of proinflammatory and inflammatory cytokines in response to internal or exogenous stimuli, inducing systemic inflammation in various internal organs. In recent years, organ damage associated with inflammatory skin diseases such as psoriasis and atopic dermatitis has received increasing attention, and vascular disorder such as arteriosclerosis is one of the serious complications of chronic inflammatory skin diseases. However, the detailed mechanism of arteriosclerosis in dermatitis and the role of cytokines have not been clarified so far. In the current study, using a spontaneous dermatitis model, we investigated the pathophysiology of arteriosclerosis and the treatment option for inflammatory skin conditions. We employed spontaneous dermatitis model mice overexpressing human caspase-1 in the epidermal keratinocyte (Kcasp1Tg). The thoracic and abdominal aorta was investigated histologically. GeneChip and RT-PCR analysis were performed to measure the changes in mRNA levels in the aorta. To elucidate the direct effect on the artery by major inflammatory cytokines, endothelial cells, vascular smooth muscle cells, and fibroblast cells were co-cultured with several cytokines, and mRNA expression levels were measured. In order to observe the efficacy of IL-17A/F in arteriosclerosis, cross-mating with IL-17A, IL-17F, and IL-17A/F deficient mice was performed. Finally, we also measured snap tension in the abdominal aorta in WT, Kcasp1Tg, and IL17A/F-deficient mice. Kcasp1Tg showed a decrease in the diameter of the abdominal aorta compared to wild-type mice. mRNA levels for six genes including Apol11b, Camp, Chil3, S100a8, S100a9, and Spta1 were increased in the abdominal aorta of Kcasp1Tg. Some of the above mRNA levels were also increased in the co-culture with major inflammatory cytokines, IL-17A/F, IL-1ß, and TNF-α. Dermatitis improved and mRNA levels were partially ameliorated in Kcasp1Tg with IL-17A/F deletion. Arterial fragility was also evidenced in the inflammatory model, but arterial flexibility was revealed in the IL-17A/F deletion model. Severe dermatitis is closely related to secondary arteriosclerosis caused by the persistent release of inflammatory cytokines. The results also proved that treatment against IL-17A and F may ameliorate arteriosclerosis.

Septic pulmonary embolism and subsequent bilateral pneumothorax in patients undergoing chemoradiotherapy for head angiosarcoma: An autopsy case report and literature review.

RATIONALE: Septic pulmonary embolism (SPE) and subsequent pneumothorax are rare but serious conditions. We report a case of SPE and pneumothorax caused by central venous port (CV port) infection. PATIENT CONCERNS: A 73-year-old woman, who underwent chemoradiotherapy for a head angiosarcoma and a CV port placement, presented with general malaise and myalgia. DIAGNOSIS: A laboratory examination showed high levels of inflammatory markers. Chest computed tomography showed fluid collection around the CV port and multiple ground-glass opacities and nodular shadows in the bilateral lung field. She was admitted with a diagnosis of SPE due to CV port infection. The port was removed, and antibiotic administration was initiated; however, she was intubated because of refractory septic shock. Methicillin-susceptible Staphylococcus aureus was detected in the blood and pus around the port site. INTERVENTIONS: Her respiratory status did not improve despite recovering from septic shock, and radiologic findings showed a left pneumothorax and exacerbation of SPE on day 9. Her condition was judged ineligible for surgery for pneumothorax, and chest tube thoracostomy was continued. OUTCOMES: Air leaks persisted after chest tube thoracostomy, and her respiratory status did not improve despite ventilator management and recruitment maneuvers. Moreover, a right pneumothorax developed on day 19. Her respiratory status gradually worsened, and she died on day 21. Autopsy showed multiple cavitary lesions in the bilateral lungs and emboli containing organization and inflammatory cells that obstructed the pulmonary arterioles. LESSONS: This case indicates that CV port-related infections are infrequent and difficult to diagnose; understanding the clinical features of SPE is important because of its high mortality rate; and pneumothorax secondary to SPE is a rare but serious condition and is difficult to treat during ventilator management.

Successful Treatment of Ulcerative-Type Pyoderma Gangrenosum with a Combination Therapy of Oral Prednisolone, Vacuum-Assisted Closure, and Skin Grafting.

Pyoderma gangrenosum (PG) is a relatively rare inflammatory skin disease that progressively causes necrotic ulceration mainly on the lower extremities and trunk. Systemic corticosteroid is considered a first-line treatment for PG as it facilitates wound healing; however, several cases where tumor necrosis factor-α inhibitors, adalimumab and infliximab, were administered showed good response. For intractable PG with a large ulcer or problematic epithelization, chemical or mechanical debridement of necrotic tissue in combination with skin grafting may be necessary to promote wound healing. Our report presents a case of intractable ulcerative PG requiring oral prednisolone and skin grafting. Although mechanical debridement was performed, granulation was poor; therefore, after the PG activity became quiescent, we utilized a vacuum-assisted closure (VAC) system to promote granulation and adaptation of the grafted skin. Although more cases are required for a definitive conclusion, the VAC system may be a choice for PG with large ulcers.

Whether to maintain or strengthen the treatment for pyoderma gangrenosum ulcerative type may depend on the response after two to four-week treatment intervention: The outcome of three cases with details clinical course.

Determining whether the treatment intensity needs to be increased or can be maintained at a constant level may be suggested after 2-4 weeks of treatment. The use of TNF-α inhibitor, removal of necrotic tissue, and skin grafting may promote epithelialization.

Psychometric examination of the Japanese translation of the Satter eating competence Inventory-2.0™ for parents of fifth and sixth grade students.

AIM: To verify the reliability and validity of a Japanese translation of the Satter eating competence Inventory-2.0™ (ecSI-2.0™) for parents of fifth and sixth grade elementary school students. METHODS: Participants were parents who prepared meals for their children aged 10-12 years. A preliminary study was conducted with 11 parents using semi-structured interviews and questionnaires, followed by a main study of 2,825 parents. Internal consistency and test-retest methods were used to verify reliability. Face and content validity were confirmed in the preliminary study, and feasibility was examined by the valid response rate and response time. Construct validity was verified using factor validity and known population validity. RESULTS: Of the 2,825 persons surveyed, 626 returned valid responses, and among the 60 persons who received the re-survey, 48 returned valid responses. The average score of the Japanese translation of the ecSI-2.0™ was 33.1 (SD ± 7.8) points. Cronbach's alpha coefficient for the whole scale was .87 and ranged from .67-.79 for the four subscales. The test-retest method confirmed the scale's stability. Factor analysis confirmed that reproducibility of the four factors was similar to the original version. In the examination of known population validity, the same correlation as the original edition was confirmed. CONCLUSIONS: The Japanese translation of the ecSI-2.0™ may be reliable and valid for understanding eating competence related to behavior of parents of school-age children.

Amino- and carboxyl-terminal domains of Filamin-A interact with CRMP1 to mediate Sema3A signalling.

Reorganization of the actin cytoskeleton is an early cellular response to various extracellular signals. Sema3A, a repulsive axon guidance molecule, induces the reorganization of actin cytoskeleton in the growth cones. Collapsin response mediator protein 1 (CRMP1) mediates the intracellular Sema3A signalling through its Ser522 phosphorylation. Here we show that UNC-33, CRMP1 C. elegans homologue, interacts with FLN-1, an actin-binding Filamin-A orthologue. In nematodes, this interaction participates in the projection of DD/VD motor neurons. CRMP1 binds both the actin-binding domain and the last immunoglobulin-like repeat of Filamin-A. The alanine mutants of Filamin-A or CRMP1 in their interacting residues suppress the Sema3A repulsion in neurons. Conversely, a phosphor-mimicking mutant CRMP1(Ser522Asp) enhances the Sema3A response. Atomic-force microscopy analysis reveals that the V-shaped Filamin-A changes to a condensed form with CRMP1(Ser522Asp). CRMP1(Ser522Asp) weakens the F-actin gelation crosslinked by Filamin-A. Thus, phosphorylated CRMP1 may remove Filamin-A from the actin cytoskeleton to facilitate its remodelling.