Browsing by Author "Snyder, Alyssa"
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Item Hypercholesterolemia Induced by a High-Fat, Low-Carbohydrate Diet in a 16-year-old Male and 6-year-old Female.(2024-03-21) Snyder, Alyssa; Hamilton, Luke; Wilson, DonBackground: The ketogenic diet is a high-fat, low-carbohydrate (HFLC) diet that has been linked to hypercholesterolemia. There are ongoing studies on the connection between hypercholesterolemia and adherence to the ketogenic diet. Medically supervised HFLC ketogenic diets with up to 90% fat have been used successfully in children as an alternative treatment for epilepsy. Although safety and efficacy data are limited in children, this high-fat diet has also been used for weight loss. Case information: Patient 1:A 16-year-old previously healthy African American male was concerned about his weight and his mother started him on a ketogenic diet. Before diet implementation, he weighed 93.2 kg (BMI of 31.6 kg/m2; 99%) and had a low-density lipoprotein cholesterol (LDL-C) of 114 mg/dL (normal LDL-C is below 110 mg/dL). During the following months, the patient lost weight and his LDL-C levels continuously increased and peaked at 348 mg/dL after losing 59lbs on the ketogenic diet. The patient was offered pharmacotherapy but the parents declined. During his most recent follow-up appointment, the patient stopped adhering to the ketogenic diet and increased his weight to 79.2 kg (BMI of 26.2 kg/m2; 87.5%), and his LDL-C level dropped to 182 mg/dL. Throughout appointments, triglycerides remained normal. No pathological variants for APOB, LDLR, LDLRAP1, and PCSK9were found on genetic testing. Patient 2: A 6-year-old female with a history of idiopathic ketotic hypoglycemia and growth hormone deficiency was started on the ketogenic diet as a way to help control hypoglycemic episodes. The diet helped keep her blood glucose levels stable but she demonstrated severe hypercholesterolemia on her lipid screening. Her LDL-C levels were significantly elevated at 310 mg/dL 37 months after her first appointment. She was taken off the ketogenic diet for 6-8 weeks with significant improvement in her LDL-C dropping down to 116 mg/dL. At 42 months, the patient was admitted to the hospital for hypoglycemia. It was noted that the mother had started the patient on the ketogenic diet again due to recurrent episodes of hypoglycemia. On lipid screening, her LDL-C was back up to 397 mg/dL. Genetic testing for APOB, LDLR, LDLRAP1, and PCSK9 were all negative. Conclusions: Several mechanisms have been proposed to explain the adverse effect of hypercholesterolemia in individuals participating in the ketogenic diet. This includes increased saturated fatty acid intake causing downregulation of LDL receptors, genetic polymorphisms, and cholesterol mobilization associated with weight loss. Although there is ongoing research regarding the mechanism behind hypercholesterolemia associated with HFLC diets, there is no clear, definitive explanation yet. Our case study and other case series in adults on the ketogenic diet for weight loss show the importance of ruling out HFLC diets when patients present with hypercholesterolemia and have no known genetic mutations suggesting familial hypercholesterolemia (FH).Item A Qualitative Histological Comparison of Collagen Deposition Between a Diseased and Healthy Cadaveric Heart(2023) Shah, Krusha; Snyder, Alyssa; Markgraf, Jon Michael; Sarathy, Swathi; Kronser, Leo; Crowe, NicolePurpose: Fibrosis is a pathological process characterized by the overproduction of extracellular matrix (ECM), especially collagen. Type I collagen is the most abundant structural protein found in ECM and serves as an indicator for fibrosis. Although increased collagen accumulation is considered a normal aspect of aging, excessive collagen accumulation is also a notable hallmark observed in chronic cardiovascular disease. Numerous studies have examined collagen deposition using animal models and pathologic human cardiac tissue. However, few studies have investigated the normal accumulation of collagen in healthy human hearts. This study aims to perform a qualitative comparison of collagen deposition between a diseased and healthy human heart. Methods and Results: This study utilized two hearts from cadaveric donors, one designated "diseased” and the other "healthy”. Each heart originated from a female in their 6th decade of life and had a body mass index within the normal range (18.5-24.9 kg/m2). The donor with the "diseased” heart had a known history of heart disease. Furthermore, gross examination revealed the "diseased” heart was enlarged (mass: 458.5 g; normal range: 230-290 g), had severe coronary artery disease, contained two implanted coronary artery grafts, and demonstrated left ventricular wall hypertrophy (thickness: 2.0 cm; normal thickness: ≤1.5 cm). In contrast, the donor with the "healthy” heart had no known history of heart disease and showed no visible signs of disease. Tissue samples were collected from the right ventricle, interventricular septum, and left ventricle from each heart and underwent routine histological preparation with Masson’s trichrome staining. Microscopic observation was performed to determine the pattern of collagen deposition within each section, classified as interstitial-perimyocyte, replacement, or mixed. Additionally, the location of collagen in each section of the ventricular wall was noted as being primarily within the inner 50% (endocardial side), outer 50% (epicardial side), or diffuse. To assess the reliability and repeatability of this study, an analysis of intra- and interobserver error will be conducted by the authors. Preliminary findings suggest the amount and patterns of collagen differs between the two hearts. Conclusion: In this study, histology was used to qualitatively analyze the differences in collagen deposition between a diseased and healthy human heart. These findings highlight the importance of conducting a comprehensive study that examines the normal accumulation of collagen in healthy human hearts. Gaining an in-depth understanding of how collagen accumulates normally is critical for recognizing disease related changes.