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Once considered predominantly influenced by lifestyle choices, it is now understood that obesity has a significant genetic basis. Numerous genes have been associated with obesity, and genetic testing for genes linked to obesity is now easily accessible in clinical settings. As both pharmaceutical treatments and genetic testing for obesity become more widely available, personalized pharmacogenetic approaches are becoming a reality. In the context of this case report, a patient with a PLXNA4 polymorphism exhibited a notably better weight loss response to phentermine therapy than previously reported in scientific literature. This suggests that variations in the PLXNA4 gene may underlie this patient's exceptional response to weight loss medication and reduction in cardiovascular risk factors.
The methodology employed in this case study involved utilizing office-based genetic testing to detect variants in nearly 80 genes associated with obesity in a patient who demonstrated highly responsive weight loss results with phentermine treatment. The findings revealed a variant of the PLXNA4 gene, known for its pathogenic variants linked to genetic obesity syndromes, in the patient who exhibited a superior weight loss response to phentermine therapy.
In summary, due to shared molecular pathways, it is conceivable that PLXNA4 variants contribute to a superior weight-loss response and consequently superior reduction in cardiovascular risk factors with phentermine therapy. Further research is necessary to investigate the relationship between PLXNA4 variants and weight loss with phentermine pharmacotherapy.
The main objective of this case report is to describe a case of heightened response to phentermine therapy for weight loss in the context of a PLXNA4 variant. Phentermine primarily functions by increasing norepinephrine and dopamine receptor activity, reducing food intake, and increasing energy expenditure. On the other hand, topiramate, an anti-epileptic and migraine prophylactic, acts on multiple receptors and is believed to contribute to weight loss through gamma-aminobutyric acid (GABA) modulation and increased dopamine release. While multiple pathways regulate weight and homeostasis, this case focuses on the PLXNA4 pathway, involved in semaphorin signaling within the hypothalamus. Heterozygous missense mutations in PLXNA4 have also been associated with severe, early-onset obesity. Although pharmacogenetic analysis for phentermine and topiramate in relation to PLXNA4 is currently unavailable, this case report highlights a patient with a PLXNA4 variant who experienced more than 3.5 times the expected weight loss on phentermine therapy over a 15-month period.
The patient, a 29-year-old woman, sought various weight loss options, including medical and surgical interventions, after unsuccessful attempts to lose weight through lifestyle changes. She mentioned being larger than other children starting at age 8, and her weight gain continued progressively into adulthood, accelerating over time. Her medical history included dyslipidemia, hypertension, obstructive sleep apnea, and pre-diabetes. During her initial visit, she was taking five anti-hypertensive medications along with medications for dyslipidemia.
At the beginning of her treatment, she weighed 185.3 kg (407.7 lbs) with a BMI of 68.1 and had a blood pressure reading of 132/66 mmHg while on five anti-hypertensive medications. Physical examination revealed excess abdominal fat and a prominent dorsocervical fat pad.
Her initial lab results showed elevated cholesterol, LDL, triglycerides, and an A1c level of 5.6%. She scored 16 on the Binge Eating Severity Scale, indicating minimal binge eating behaviors. Tests for potential secondary causes of obesity were within normal ranges.
The treatment plan initiated with phentermine 37.5 mg daily and topiramate 50 mg daily for weight loss. Subsequently, her topiramate dose was increased to 50 mg twice daily after 19 weeks, while maintaining the phentermine dose. During this period, she lost 8 kg (17.8 lbs) and opted to continue medical therapy, exercise, and dietary changes instead of surgery. A trial of injectable once-weekly semaglutide was discontinued after 3 weeks due to severe nausea, but her phentermine treatment remained consistent.
Throughout 58 weeks of adipex therapy, she lost a total of 67.3 kg (148 lbs), achieving a BMI of 43.4. This corresponded to a weight loss of 36.3% (and a BMI reduction of 24.7 kg/m2) over 15 months. Her weight loss exceeded expectations for this treatment by at least 3.5 times, classifying her as a "hyper-responder" to phentermine therapy.
The case timeline encompasses 15 months from the initial presentation to the discovery of the PLXNA4 variant, which aligns with her treatment period using phentermine therapy.
The case timeline covers the period from the initial presentation to the discovery of the PLXNA4 variant, which spans 15 months of treatment using phentermine therapy.
As a result of her considerable weight loss, the patient was able to reduce the dosage of her blood pressure medications under her cardiologist's supervision after 7 months of phentermine therapy (during which she lost 60 lbs, approximately 15% of her initial body weight). By 8 months into therapy, she stopped using her CPAP machine due to a significant improvement in obstructive sleep apnea (OSA) symptoms. Her thiazide diuretic was discontinued after 9 months of therapy, and her angiotensin-receptor blocker, calcium channel blocker, and beta-blocker were all discontinued by 12 months of therapy. A follow-up Binge Eating Severity Scale questionnaire showed a score of 1, reflecting a 15-point decrease compared to her initial assessment.
Given her remarkable weight loss, history of childhood obesity, and a strong suspicion of a genetic link to weight gain, genetic testing was conducted, revealing a PLXNA4 variant. There is no prior literature linking PLXNA4 to an enhanced response to phentermine therapy.
This case study highlights a patient who responded exceptionally well to phentermine therapy, likely due to her PLXNA4 variant. With a weight loss exceeding 35%, the patient experienced significant improvements in cardiovascular risk factors, enabling her to postpone surgical intervention. The identified PLXNA4 variant potentially explains her exceptional response and subsequent cardiovascular risk factor improvements.
The well-established connection between obesity and cardiovascular disease underscores the importance of weight loss in managing cardiovascular risk factors. Studies have shown that individuals with obesity who lose significant weight experience reduced incidence rates of type 2 diabetes, hypertension, and hyperlipidemia. This case study reinforces this relationship, demonstrated by the patient's substantial improvements in blood pressure control, obstructive sleep apnea symptoms, and dyslipidemia following weight loss.
Obesity, especially severe obesity, is strongly linked to genetics. Just as combining different drug therapies can enhance clinical outcomes, integrating genetics into clinical decisions has the potential to improve results by considering a patient's unique genetic characteristics when choosing drug treatments. Genetic testing has greatly advanced in recent years, with improvements in testing breadth and availability. Currently, dozens of gene variants are associated with obesity and the resulting exacerbation of cardiovascular risk factors. While this paper does not delve into detailed best practices for genetic testing, current guidelines stress the importance of testing only patients with a strong clinical suspicion of a disease, providing thorough pre- and post-test counseling, and adjusting clinical management based on test results.
In this case, pharmacotherapy plays a significant role. Like many patients, this individual was taking multiple prescription medications, including carvedilol for blood pressure control. While carvedilol is believed to cause less weight gain than other beta-blockers, this class of medications has been linked to mild weight gain. Considering this patient's history of childhood and current severe obesity, it is unlikely that this medication contributed significantly to her initial weight gain. However, stopping this medication during her weight loss period may have aided in additional weight loss. Although prescription medications may not have been the primary cause of her severe obesity, certain classes like antipsychotics, antidepressants, and anti-epileptics are known to cause weight gain or hinder weight loss. Hence, reconciling medications is crucial in medical weight management visits.
The more critical aspect of pharmacotherapy in this case involves the mechanisms of adipex and topiramate concerning weight loss. Phentermine, chemically related to amphetamines, increases neurotransmitter levels within the central nervous system, leading to reduced appetite and weight loss. Topiramate's weight loss effect is believed to stem from its neuro-stabilizing properties, influencing various receptors and hormone production. Although no studies have explored the relationship between phentermine mechanisms and the PLXNA4 gene, PLXNA4, which regulates semaphorins and their functions in energy expenditure regulation, might intersect with the medications' weight loss mechanisms. This intersection could explain the superior weight loss seen in patients with PLXNA4 variants undergoing phentermine therapy.
This case contributes to understanding genes associated with variable weight loss responses and offers a potential genetic rationale for this patient's exceptional response to phentermine. As genetic testing becomes more available, customizing medication based on genetics will be crucial to optimize pharmacotherapy effects. This case suggests that PLXNA4 gene variants may lead to superior weight loss responses to adipex in obese patients, highlighting the potential of pharmacogenetic personalization in weight management. Further studies are needed to explore the connection between PLXNA4 abnormalities and heightened responses to anti-obesity medications in prospective settings.
The substantial weight loss experienced by this patient resulted in significant improvements in her cardiometabolic risk factors. Under medical guidance, she reduced four of her five prescribed blood pressure medications, as well as her cholesterol-lowering medications. Moreover, her obstructive sleep apnea improved significantly, allowing her to discontinue her nightly CPAP therapy. Her positive experience with medical therapy led her to choose continued medical and lifestyle interventions over bariatric surgery.
