Related Experiment Videos
Value-based healthcare in Lynch syndrome
Simone D Hennink1, Nandy Hofland, Jessica P Gopie
1Department of Gastroenterology and Hepatology, Leiden University Medical Centre, Leiden, The Netherlands.
Familial Cancer
|May 18, 2013
Summary
Value-based care models for Lynch syndrome (LS) prioritize cancer prevention and early detection. This study developed a model focusing on patient-identified outcomes like rapid testing and psychological support, improving hereditary colorectal cancer care.
Area of Science:
- Oncology
- Healthcare Management
- Genetics
Background:
- Lynch syndrome (LS) is a frequent hereditary colorectal cancer (CRC) cause due to mismatch repair (MMR) gene defects.
- LS carriers face significantly increased risks for CRC and endometrial cancer.
- Value-based healthcare emphasizes cost-effective delivery of measurable patient value.
Purpose of the Study:
- To develop a value-based care model for Lynch syndrome.
- To determine patient value and associated costs for LS management.
- To design a coordinated care pathway integrating existing guidelines.
Main Methods:
- Multidisciplinary specialist evaluation of current LS patient care.
- Formulation of patient value outcome measures by specialists.
- Patient questionnaire assessing the importance of identified outcome measures (scale 1-10).
Main Results:
- Six high-value outcomes identified: cancer prevention/early detection, rapid MMR gene testing, prompt colon/uterine investigation, pain minimization, psychological support, and registry enrollment.
- Patient validation confirmed the relevance of all outcomes, with mean scores from 7.2 to 9.9.
- Patients emphasized the importance of education and efficient surveillance.
Conclusions:
- Value-based care for LS necessitates implementing six key parameters focusing on prevention, early detection, efficiency, and continuity of care.
- Estimated costs: €3320 for the first care cycle, €720 for subsequent annual cycles.
- The developed model provides a framework for optimizing LS patient management and resource allocation.
Related Concept Videos
01:19Cushing Syndrome II: Pathophysiology
Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:26Cushing Syndrome I: Introduction
Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
02:57Targeted Cancer Therapies
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
There are several types of targeted therapies against specific...
01:12Loss of Tumor Suppressor Gene Functions
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
02:56Treatment Resistant Cancers
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...