Kristen Dammeyer

All Publications

• Synchronous disease onset and flares in siblings with PFAPA PEDIATRIC RHEUMATOLOGY Dammeyer, K. L., Schneider, A., April, M. M., Kahn, P. J. 2022; 20 (1): 87

  Abstract

  Periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) is a clinical syndrome of unclear etiology. PFAPA has generally been considered a non-hereditary fever syndrome; however, this has been called into question with recent reports of family clustering. Few reports have been published describing siblings with PFAPA. To our knowledge, this is the first report of siblings with near simultaneous onset of disease followed by synchronous disease flares.We describe the case of near simultaneous onset of periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis in siblings followed by synchronous disease flares of clear frequency and nearly identical character. Flares were characterized predominantly by fever, aphthous ulceration, cervical lymphadenitis, and the absence of infection. The fever episodes demonstrated a robust response to glucocorticoids and recurred in the same staggered manner every four weeks, with complete absence of symptoms and normal growth and development between episodes. Nine months after onset, the older sibling, a 5-year-old female, underwent tonsillectomy resulting in dramatic resolution of episodes. At the same time, her 2-year-old sister experienced resolution of her fever episodes, though she did not undergo tonsillectomy herself.This is an unusual case of simultaneous onset PFAPA followed by synchronous disease flares. PFAPA is an uncommon clinical syndrome, and it is rarely diagnosed in siblings. The etiology of PFAPA remains unclear. Though the disease is classically considered sporadic, there is a growing body of evidence to suggest that PFAPA may be heritable.

  View details for DOI 10.1186/s12969-022-00744-0

  View details for Web of Science ID 000864100900001

  View details for PubMedID 36199113

  View details for PubMedCentralID PMC9532809

• Predicting postoperative complications following mastectomy in the elderly: Evidence for the 5-factor frailty index BREAST JOURNAL Dammeyer, K., Alfonso, A. R., Diep, G. K., Kantar, R. S., Berman, Z. P., Daar, D. A., Ramly, E. P., Sosin, M., Ceradini, D. J. 2021; 27 (6): 509-513

  Abstract

  Understanding the risk factors that contribute to post-mastectomy complications can better inform preoperative discussions. Here, we assess the impact of the 5-Factor Frailty Index Score (mFI-5) in predicting 30-day postoperative complications in patients undergoing mastectomy. A retrospective review of the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) data base was conducted for patients older than 65 undergoing mastectomy between 2010 and 2015. We assessed each patient's Frailty Index Score using the mFI-5. Primary outcomes included wound complications and overall complications. Multivariate logistic and linear regression analyses were used to determine the ability of the mFI-5 to predict postoperative outcomes. A total of 13,783 patients were analyzed. The rate of wound complications was 3.0%, while the rate of overall complications was 6.0%. An mFI-5 score greater than 2 was an independent risk factor for wound complications and overall complications. Overall, patients undergoing mastectomy with an mFI-5 of 2 or greater experienced higher rates of postoperative complications. The mFI-5 is an accessible tool that can be used to risk-stratify patients undergoing mastectomy and can positively contribute to the informed consent and shared decision-making process.

  View details for DOI 10.1111/tbj.14208

  View details for Web of Science ID 000623772800001

  View details for PubMedID 33650221

• Keratinocyte- Macrophage Crosstalk by the Nrf2/Ccl2/EGF Signaling Axis Orchestrates Tissue Repair CELL REPORTS Villarreal-Ponce, A., Tiruneh, M., Lee, J., Guerrero-Juarez, C. F., Kuhn, J., David, J. A., Dammeyer, K., Mc Kell, R., Kwong, J., Rabbani, P. S., Nie, Q., Ceradini, D. J. 2020; 33 (8): 108417

  Abstract

  Unveiling the molecular mechanisms underlying tissue regeneration provides new opportunities to develop treatments for diabetic ulcers and other chronic skin lesions. Here, we show that Ccl2 secretion by epidermal keratinocytes is directly orchestrated by Nrf2, a prominent transcriptional regulator of tissue regeneration that is activated early after cutaneous injury. Through a unique feedback mechanism, we find that Ccl2 from epidermal keratinocytes not only drives chemotaxis of macrophages into the wound but also triggers macrophage expression of EGF, which in turn activates basal epidermal keratinocyte proliferation. Notably, we find dysfunctional activation of Nrf2 in epidermal keratinocytes of diabetic mice after wounding, which partly explains regenerative impairments associated with diabetes. These findings provide mechanistic insight into the critical relationship between keratinocyte and macrophage signaling during tissue repair, providing the basis for continued investigation of the therapeutic value of Nrf2.

  View details for DOI 10.1016/j.celrep.2020.108417

  View details for Web of Science ID 000593108100007

  View details for PubMedID 33238115

  View details for PubMedCentralID PMC8122853

• Endothelial cell-induced cytoglobin expression in vascular smooth muscle cells contributes to modulation of nitric oxide VASCULAR PHARMACOLOGY Lilly, B., Dammeyer, K., Marosis, S., McCallinhart, P. E., Trask, A. J., Lowe, M., Sawant, D. 2018; 110: 7-15

  Abstract

  Cytoglobin is a widely expressed heme protein that binds oxygen, carbon monoxide and nitric oxide. Recent examination of cytoglobin in the vasculature indicates that it contributes to nitric oxide availability, which is central to normal blood vessel function through regulation of smooth muscle cell tone and physiological response. Given the potential implications of cytoglobin in vascular function, we examined how cytoglobin might be uniquely regulated in vascular smooth muscle cells. Our data demonstrate that endothelial cells can increase the expression of cytoglobin in vascular smooth muscle cells, and the induction of cytoglobin is cell contact-dependent. We show that Notch signaling is necessary for endothelial cell-induced cytoglobin expression and Notch2 and Notch3 are sufficient to drive its expression in aortic smooth muscle cells. We further reveal that in cytoglobin-depleted smooth muscle cells there is increased cellular nitric oxide. These data demonstrate that, in addition to being the main producer of vascular nitric oxide, endothelial cells facilitate the ability of smooth muscle cells to metabolize nitric oxide through upregulation of cytoglobin. Our results reveal a novel mechanism by which Notch signaling contributes to vascular function through regulation of a gene that controls nitric oxide levels.

  View details for DOI 10.1016/j.vph.2018.06.016

  View details for Web of Science ID 000445321600002

  View details for PubMedID 29969687

  View details for PubMedCentralID PMC6135703