scholarly journals Design of an Auxiliary Artificial Lymphatic Vessel in Treatment of Secondary Lymphedema Due to Breast Cancer

Healthcare ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 68
Author(s):  
Gabriela Durán-Aguilar ◽  
Alberto Rossa-Sierra ◽  
Rita Q. Fuentes-Aguilar

Breast cancer is the most common malignant tumor that affects women in the United States, Europe, and Mexico. As an adverse effect when performing treatments for this condition, secondary lymphedema associated with breast cancer occurs in some cases. This complication occurs due to the interruption of lymphatic flow in the upper extremities in conjunction with other factors such as radiation, sedentary lifestyle, removal of lymph nodes, damage to lymphatic vessels, and others. This article reviews breast cancer incidence, mortality, and survival patterns, confirming that, specifically, lymphedema has high health, social, and economic impacts. Research demonstrates that it fundamentally affects women at an early age. In approximately a third of the cases, it becomes a chronic disease. Therefore, physical therapy is essential for a better quality of life in patients who survive this disease. Surgeries and manual and pharmacological treatments are the current procedures done to reduce to reduce the alterations suffered by patients with lymphedema; however, the success of the treatments depends on each patient’s characteristics. To face this problem, the design of a lymphatic vessel has been proposed to assist the mechanical failure of the damaged lymphatic system. In this work, the design methodology used for the blueprint of the lymphatic vessel is presented, as well as the computer analysis of fluid simulation and the selection of the proposed material, resulting in the production of a micrometric design. In the future, it is expected that a surgeon will be able to implant the design of the vessel to restore lymph flow through the lymphatic system, thus helping to combat lymphedema.

2003 ◽  
Vol 21 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Christopher I. Li ◽  
Janet R. Daling ◽  
Kathleen E. Malone

Purpose: Between 1987 and 1998, breast cancer incidence rates rose 0.5%/yr in the United States. A question of potential etiologic and clinical importance is whether the hormone receptor status of breast tumors is also changing over time. This is because hormone receptor status may reflect different etiologic pathways and is useful in predicting response to adjuvant therapy and prognosis. Methods: Age-adjusted, age-specific breast cancer incidence rates by estrogen receptor (ER) and progesterone receptor (PR) status from 1992 to 1998 were obtained and compared from 11 population-based cancer registries in the United States that participate in the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) Program. Results: From 1992 to1998, the overall proportion of breast cancers that were ER-positive and PR-positive increased from 75.4% to 77.5% (P = .0002) and from 65.0% to 67.7% (P < .0001), respectively, continuing trends observed before 1992. These increases were limited to women 40 to 69 years of age. The proportions of ER-positive/PR-positive tumors increased from 56.7% to 62.3% (P = .0010) among 40- to 49-year-olds, from 58.0% to 63.2% (P = .0002) among 50- to 59-year-olds, and from 63.2% to 67.9% (P = .0020) among 60- to 69-year-olds. Conclusion: From 1992 to 1998, the proportion of tumors that are hormone receptor–positive rose as the proportion of hormone receptor–negative tumors declined. Because the incidence rates of hormone receptor–negative tumors remained fairly constant over these years, the overall rise in breast cancer incidence rates in the United States seems to be primarily a result of the increase in the incidence of hormone receptor–positive tumors. Hormonal factors may account for this trend.


2018 ◽  
Author(s):  
Nancy E Davidson

Invasive breast cancer, the most common nonskin cancer in women in the United States, will be diagnosed in 266,120 In 2018, along with 63,960 new cases of non-invasive (in situ) breast cancer. Incidence and mortality reached a plateau and appear to be dropping in both the United States and parts of western Europe. This decline has been attributed to several factors, such as early detection through the use of screening mammography and appropriate use of systemic adjuvant therapy, as well as decreased use of hormone replacement therapy. However, the global burden of breast cancer remains great, and global breast cancer incidence increased from 641,000 in 1980 to 1,643,000 in 2010, an annual rate of increase of 3.1%. This chapter examines the etiology, epidemiology, prevention, screening, staging, and prognosis of breast cancer. The diagnoses and treatments of the four stages of breast cancer are also included. Figures include algorithms used for the systemic treatment of stage IV breast cancer and hormone therapy for women with stage IV breast cancer. Tables describe selected outcomes from the National Surgical Adjuvant Breast and Bowel Project (NSABP) P-1 and P-2 chemoprevention trials, tamoxifen chemoprevention trials for breast cancer, the TNM staging system and stage groupings for breast cancer, some commonly used adjuvant chemotherapy regimens, an algorithm for suggested treatment for patients with operable breast cancer from the 2011 St. Gallen consensus conference, guidelines for surveillance of asymptomatic early breast cancer survivors from the American Society of Clinical Oncology, and newer agents for metastatic breast cancer commercially available in the United States. This review contains 2 highly rendered figures, 8 tables, and 108 references.


Author(s):  
Mary C. White ◽  
Marion (Mhel) H. E. Kavanaugh-Lynch ◽  
Shauntay Davis-Patterson ◽  
Nancy Buermeyer

Advances in breast cancer science, early detection, and treatment have resulted in improvements in breast cancer survival but not in breast cancer incidence. After skin cancer, breast cancer is the most common cancer diagnosis in the United States. Each year, nearly a quarter million U.S. women receive a breast cancer diagnosis, and the number continues to rise each year with the growth in the population of older women. Although much remains to be understood about breast cancer origins and prevention, action can be taken on the existing scientific knowledge to address the systemic factors that drive breast cancer risk at the population level. The California Breast Cancer Research Program funded a team at Breast Cancer Prevention Partners (BCPP) to convene leaders in advocacy, policy, and research related to breast cancer prevention from across the state of California. The objective was the development of a strategic plan to direct collective efforts toward specific and measurable objectives to reduce the incidence of breast cancer. The structured, innovative approach used by BCPP to integrate scientific evidence with community perspectives provides a model for other states to consider, to potentially change the future trajectory of breast cancer incidence in the United States.


Author(s):  
Louise A. Brinton ◽  
Mia M. Gaudet ◽  
Gretchen L. Gierach

Breast cancer is the most frequently diagnosed cancer in women worldwide, with annual estimates of 1.7 million newly diagnosed cases and 522,000 deaths. Although more breast cancers are diagnosed in economically developed than in developing countries, the reverse is true for mortality, reflecting limited screening and less effective treatments in the latter. Breast cancer incidence has been on the rise in the United States for many years, but in recent years this is restricted to certain subgroups, while internationally there have been continued generalized increases, likely reflecting adoption of more Westernized lifestyles. Breast cancer is widely recognized as being hormonally influenced, with most of the established risk factors believed to reflect the influence of cumulative exposure of the breast to stimulatory effects of ovarian hormones—leading to increased cellular proliferation, which in turn can result in genetic errors during cell division.


2019 ◽  
Vol 316 (1) ◽  
pp. G217-G227 ◽  
Author(s):  
Olga Y. Gasheva ◽  
Irina Tsoy Nizamutdinova ◽  
Laura Hargrove ◽  
Cassidy Gobbell ◽  
Maria Troyanova-Wood ◽  
...  

This study aimed to establish mechanistic links between the prolonged intake of desloratadine, a common H1 receptor blocker (i.e., antihistamine), and development of obesity and metabolic syndrome. Male Sprague-Dawley rats were treated for 16 wk with desloratadine. We analyzed the dynamics of body weight gain, tissue fat accumulation/density, contractility of isolated mesenteric lymphatic vessels, and levels of blood lipids, glucose, and insulin, together with parameters of liver function. Prolonged intake of desloratadine induced development of an obesity-like phenotype and signs of metabolic syndrome. These alterations in the body included excessive weight gain, increased density of abdominal subcutaneous fat and intracapsular brown fat, high blood triglycerides with an indication of their rerouting toward portal blood, high HDL, high fasting blood glucose with normal fasting and nonfasting insulin levels (insulin resistance), high liver/body weight ratio, and liver steatosis (fatty liver). These changes were associated with dysfunction of mesenteric lymphatic vessels, specifically high lymphatic tone and resistance to flow together with diminished tonic and abolished phasic responses to increases in flow, (i.e., greatly diminished adaptive reserves to respond to postprandial increases in lymph flow). The role of nitric oxide in this flow-dependent adaptation was abolished, with remnants of these responses controlled by lymphatic vessel-derived histamine. Our current data, considered together with reports in the literature, support the notion that millions of the United States population are highly likely affected by underevaluated, lymphatic-related side effects of antihistamines and may develop obesity and metabolic syndrome due to the prolonged intake of this medication. NEW & NOTEWORTHY Prolonged intake of desloratadine induced development of obesity and metabolic syndrome associated with dysfunction of mesenteric lymphatic vessels, high lymphatic tone, and resistance to flow together with greatly diminished adaptive reserves to respond to postprandial increases in lymph flow. Data support the notion that millions of the USA population are highly likely affected by underevaluated, lymphatic-related side effects of antihistamines and may develop obesity and metabolic syndrome due to the prolonged intake of this medication.


Author(s):  
Victor G. Vogel

Risk for breast cancer can be easily and rapidly assessed using validated, quantitative models. Multiple randomized studies show that the selective estrogen response modifiers (SERMs) tamoxifen and raloxifene can safely reduce the risk of invasive breast cancer in both pre- and postmenopausal women. Treatment resulted in a 38% reduction in breast cancer incidence, and 42 women would need to be treated to prevent one breast cancer event in the first 10 years of follow-up. Reduction was larger in the first 5 years of follow-up than in years 5 to 10, but no studies treated patients for longer than 5 years. Thromboembolic events were significantly increased with all SERMs, whereas vertebral fractures were reduced. Tamoxifen provides net benefit to all premenopausal women who are at increased risk, whereas raloxifene reduces risk nearly as much in postmenopausal women and offers increased safety. Both tamoxifen and raloxifene reduce the incidence of in situ cancers. Lasofoxifene reduced the risk of breast cancer by 79% in postmenopausal women with osteoporosis. The MAP3 trial showed a 65% reduction in the annual incidence of invasive breast cancer in postmenopausal women who were at moderately increased risk for breast cancer who took the aromatase inhibitor exemestane. The IBIS-II trial showed a 53% reduction in the risk of invasive breast cancer in postmenopausal women aged 40 to 70 who took the aromatase inhibitor anastrozole. Of the 50 million white women in the United States aged 35 to 79, 2.4 million would have a positive benefit/risk index for chemoprevention.


2021 ◽  
Vol 18 (3) ◽  
pp. 336-344
Author(s):  
V. V. Klimontov ◽  
D. M. Bulumbaeva

The lymphatic system (LS) is one of the main integrative systems of the body, providing protective and transport functions. In recent years, interactions between LS and adipose tissue (AT) have been of particular interest. Lymphatic vessels play an important role in metabolic and regulatory functions of AT, acting as a collector of lipolysis products and adipokines. In its turn, hormones and adipocytokines that produced in adipocytes (including leptin, adiponectin, IL-6, TNF-α, etc.) affect the function of lymphatic endothelial cells and control the growth of lymphatic vessels. Cooperation between LS and AT becomes pathogenetically and clinically important in lymphedema and obesity. It is known that both primary and secondary lymphedema are characterized by increased fat accumulation which is associated with the severity of lymphostasis and inflammation. Similarly, in obesity, the drainage function of LS is impaired, which is accompanied by perilymphatic mononuclear infiltration in the AT. The development of these changes is facilitated by endocrine dysfunction of adipocytes and impaired production of adipocytokines. The increase in the production of inflammatory mediators and the disruption of the traffic of inflammatory cells causes a further deterioration in the outflow of interstitial fluid and exacerbates the inflammation of the AT, thereby forming a vicious circle. The role of lymphangiogenesis in AT remodeling in obesity needs further research. Another promising area of research is the study of the role of intestinal LS in the development of obesity and related disorders. It has been shown that the transport of chylomicrons from the intestine depends on the expression of a number of molecular mediators (VEGF-C, DLL-4, neuropilin-1, VEGFR-1, CD36/FAT, etc.)in the endotheliocytes of the intestinal lymphatic vessels, as well as the functioning of «push-button» and “zippering” junctions between endothelial cells. New approach to the treatment of obesity based on blockade of lymphatic chylomicrontransport has been experimentally substantiated. Further identification of the molecular mechanisms and signaling pathways that determine the remodeling of AT in lymphedema and obesity are likely to provide new approaches to the treatment of these diseases.


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