Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2745_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
29 Мб
Скачать
Device Description Total
Body Weight Loss (%)
FDA Approval
AspireAssist
87
Endoscopically placed percutaneous gastrostomy aspiration tube
12.1 Lifestyle alone:
3.5 12 mo
88
2016 BMI 35­55 kg/m
2
vBloc Therapy/Maestro Rechargeable System
89
Laparoscopically implanted device providing intermittent vagal
blockade
9.2 Sham:
6.0 12 mo
90
2015 BMI 40­45 kg/m
2
or 35­40 kg/m2 + at least one weight- ­related comorbid condition
Adapted by permission from Springer: Saunders KH, Igel LI, Saumoy M, Sharaiha RZ, Aronne LJ. Devices and endoscopic bariatric therapies for obesity. Curr Obes Rep. 2018;7(2):162-171. Copyright © 2018 Springer Science+Business Media, LLC, part of Springer Nature. BMI, body mass index; lifestyle, lifestyle counseling (diet + exercise).
Intragastric Balloons
Intragastric balloons (Orbera; Apollo Endosurgery, Austin, TX, ReShape; ReShape Lifesciences, San Clemente, CA, Obalon; Obalon Theraputics, Inc., Carlsbad, CA) are space­occupying devices, which are deployed in the stomach and expand, thus reducing functional gastric volume. Proposed mechanisms of action include delayed gastric emptying and hormonal alterations affecting appetite and satiety. The balloons were approved in 2015-2016 for patients with a BMI of 30 to 40 kg/m2.
78-80
Balloons are swallowed or placed
endoscopically, filled with gas or fluid, and removed endoscopically after 6 months. Serial balloon placement has demonstrated additional weight loss; however, these protocols are not currently approved. Total body weight loss ranges from
6.6% to 10.2% compared with 3.3% to 3.4% with sham.
Contraindications include history of gastrointestinal surgery, clotting/bleeding disorders, large hiatal hernia or other
https://t.me/medicina_free
structural abnormality, gastric mass and pregnancy. The most common TEAEs include abdominal pain, nausea, vomiting, intolerance, and early explantation. Migration, deflation, perforation, and gastric ulcers have also been reported.
Aspiration Therapy
The AspireAssist device (Aspire Bariatrics, King of Prussia, PA) is a percutaneous gastrostomy tube that facilitates partial aspiration of each meal after ingestion. It was approved in 2016 for patients with a BMI of 35 to 55 kg/m2. 87 After the tube is placed endoscopically, an external aspiration port is created at the abdominal surface. After meal ingestion, patients attach an aspiration device to the port for infusion of
water followed by aspiration of 30% of the meal. AspireAssist leads to weight loss not only by direct calorie
loss but also by smaller meal portions. Food particles can flow through the tube only if they are 5 mm or less in diameter and in a slurry, so patients must take time to chew thoroughly and drink sufficient liquid with each meal. AspireAssist is associated with 12.1% total body weight loss compared with
3.5% with lifestyle counseling alone. 88 There has been no evidence of eating disorder development or device overuse and no reported increase in food intake during or between meals to compensate for the aspirated calories. The most frequently reported TEAEs included postoperative abdominal pain, nausea, vomiting, peristomal irritation, and peristomal granulation tissue.
88
Vagal Blockade
The Maestro Rechargeable System or vBloc (ReShape Lifesciences, San Clemente, CA) is a device that provides intermittent electrical blockade to the vagus nerve. It was approved in 2015 for patients with a BMI of 40 to 45 kg/m2 or 35 to 40 kg/m2 with at least one weight-related comorbidity.
89
vBloc is implanted laparoscopically. Two leads are placed around the vagal trunks near the gastroesophageal junction, and a rechargeable neuroregulator is placed subcutaneously on
https://t.me/medicina_free
the thoracic wall. The device is recharged transcutaneously. The vagus nerve plays a role in weight regulation via effects on appetite, metabolism, and autonomic control of the upper gastrointestinal track. vBloc is associated with 9.2% total body weight loss compared with 6.0% with a sham intervention as well as reductions in hunger and improved food-related cognitive restraint. 90 The most frequently reported TEAEs are dyspepsia, heartburn, and implant site pain.
90,91
Impact of Obesity Treatment on Multiple Sclerosis
Recently, it has been hypothesized that weight loss can delay the development of MS, so obesity treatment is particularly important among patients with concurrent MS. 92 Furthermore,
interferon beta is a cornerstone of disease-modifying treatment for MS that can reduce the number of relapses, delay
disability, and limit new disease activity seen on magnetic resonance imaging (MRI). There is a reduction in treatment effect in patients with excess weight, so it is particularly important to treat obesity in patients who would benefit from interferon beta therapy.
93
Lifestyle Modifications
The National Multiple Sclerosis Society recommends a well­balanced and planned diet for patients with MS. 94 Although there is no “MS diet,” it is suggested that patients follow a low-fat, high-fiber diet similar to the diets recommended by the American Heart Association and the American Cancer Society. Sodium is a dietary factor that has been linked to MS. A recent observational study reported that patients who consumed moderate to high amounts of sodium had increased rates of relapse and a greater risk of developing new MRI lesions than patients who consumed a low-sodium diet.
95
Diet may play an important role in risk of MS, disease progression, and symptom management, especially energy level and bladder and bowel function. Possible mechanisms
https://t.me/medicina_free
through which diet can affect MS include direct effect on the immune system or indirectly through changes in a patient’s gut microbiome. Currently there is insufficient evidence to recommend particular dietary interventions; however, there are several ongoing pilot studies investigating the role of the Mediterranean diet and other diets in inflammation associated with MS.
Limited animal studies have led to theories that a ketogenic diet could improve the neurodegenerative (vs. inflammatory) component of MS. 96 Ketogenic diets have been shown to promote mitochondrial biogenesis and thus increase antioxidant levels and decrease oxidative damage, which eventually leads to less neuronal damage. Further studies on ketogenic diets among human patients with MS are needed before broad dietary recommendations can be made.
Although physical activity plays an important role in weight loss, weight loss maintenance, and overall metabolic health, exercise can be difficult for patients with MS because of pain and physical limitations. Pain affects quality of life both physically and emotionally. Patients with pain tend to reduce physical activity and, as a result, suffer from worsening stiffness, reduced flexibility, increasing weakness, and overall deconditioning. 97 A recent systemic review and meta-analysis found that exercise has a small to moderate effect size in reducing pain and thereby improving quality of life in patients with MS. 97 Physical therapy, stretching, and low-impact exercise such as swimming can be reasonable options for patients with MS.
Antiobesity Medications
When prescribing antiobesity medications to patients with MS, it is important to consider potential interactions with MS medications as well as possible adverse events that could exacerbate symptoms of MS. There are limited data on the effect of antiobesity medications in patients with MS specifically; however, there is some evidence that several of the antiobesity drugs (or components of combination
https://t.me/medicina_free
medications) could provide benefit beyond weight loss to patients with MS.
Among the six most widely prescribed antiobesity agents approved by the FDA—phentermine, orlistat, phentermine/topiramate extended release (ER); lorcaserin, naltrexone sustained release (SR)/bupropion SR, and liraglutide 3.0 mg—there are potential benefits associated with phentermine, topiramate, naltrexone, bupropion, and liraglutide. There are no data on orlistat or lorcaserin.
Phentermine and bupropion are both activating medications that can increase energy. Although there are no studies of phentermine in patients with MS, bupropion has been reported to improve fatigue among patients with MS. Over 80% of patients with MS report symptoms of fatigue, which is a poorly understood interplay between disease, physical fatigue, psychological factors, drug-induced/side effect, and sleep dysfunction. 98 Patients with MS treated with bupropion have shown higher fatigue remission rates and improved reward responsive rates thereby enriching quality of life.
98,99
Topiramate has been shown to improve cerebellar tremors and dysesthetic pain, both of which can be symptoms of MS. Cerebellar tremors, which are action-mediated tremors that most frequently affect the arms, and can also involve the head, trunk, and voice, are common in patients with MS.
100
These
tremors affect 25% to 60% of patients with MS and have been historically difficult to treat pharmacologically. Per a single case report, topiramate was shown to improve symptoms of cerebellar ataxia and tremor in a patient with MS who was followed over a 2-year period.
101
Dysesthetic pain is a type of neuropathic pain found commonly in patients with MS. It is a constant, mostly burning pain affecting the legs and feet.
102
First-line treatment
for this pain includes tricyclic antidepressants (such as amitriptyline) and antiepileptic medications (carbamezapine, gabapentin, and pregabalin), many of which can induce significant weight gain. Although topiramate can sometimes lead to paresthesias, it can also improve such neuropathic pain. One case report described resolution of dysesthetic pain in a
https://t.me/medicina_free
patient with MS who had suffered from treatment-resistant pain for over 8 years.
102
Low-dose naltrexone (LDN) has been used off-label for the treatment of pain and inflammation in many chronic inflammatory diseases, including MS, Crohn disease, and
fibromyalgia.
103
It is hypothesized that lower-than-standard
doses of naltrexone inhibit cellular proliferation of T and B cells and block Toll-like receptor 4, resulting in analgesia and an anti-inflammatory effect. Numerous studies have explored the effects of LDN on MS. It has been shown to reduce fatigue; however, it has not been shown to alter the disease course in MS.
103
In addition to treating diabetes and obesity, GLP-1 agonists have demonstrated a range of other physiological effects in the body. In preclinical trials, a substantial body of evidence has shown that these incretin mimetics have neuroprotective and anti-inflammatory effects.
104
In animal models for other
neurodegenerative diseases, GLP-1 was found to cross the blood-brain barrier and reduce CNS inflammation. The neuroprotective effect is thought to be secondary to neurogenesis and increased neuronal repair, protection against oxidative stress, and reduction in plaque formation.
104,105
A
recent study in animals models of MS found that liraglutide delays disease onset and progression.
105
These preliminary
results in animal models are promising for potentially using GLP-1 receptor agonists to concurrently treat obesity and MS.
Finally, metformin is FDA approved for the treatment of type 2 diabetes but is commonly used off-label for other conditions, including type 2 diabetes prevention in patients with prediabetes or impaired fasting glucose, treatment of polycystic ovarian syndrome, and obesity/overweight.
106
Metformin has been shown to reduce disease severity in animal models of MS by downregulating the proinflammatory response in the CNS.
107,108
These benefits observed in animal
models have been confirmed in human subjects with both metabolic syndrome and MS: metformin reduces disease activity in these patients as evidenced by fewer MRI lesions.
93
https://t.me/medicina_free
Bariatric Surgery
Although there are no studies evaluating antiobesity devices and endoscopic bariatric therapies in patients with MS, there are a few studies examining bariatric surgery outcomes. After bariatric surgery, patients with MS experience weight loss similar to that seen in the general population.
109
Small
retrospective studies and case reports confirm that bariatric surgery is safe in patients with MS. In general, these patients have improved ambulation from the significant weight loss and do not have worsening disease progression or increased relapse rates when compared with patients with MS and obesity who do not undergo bariatric surgery.
30,109
Following
bariatric surgery, patients with MS have improved Patient Health Questionnaire (PHQ-9) depression scores for the first year; however, rates of depression reach the MS control rates after about 3 years post surgery. 16 Although patients with MS are often at higher risk for surgery, preliminary studies show good outcomes in this patient population. Larger studies are necessary to further optimize treatment.
As rates of obesity and MS increase, bariatric surgery may play an important role in a multidimensional treatment plan. It is important that practitioners who follow these patients post surgery have a heightened awareness of nutritional deficiencies. Bariatric patients in the general population are at risk for neurological complications due to deficiencies in vitamin B12, thiamine, and copper. In patients with underlying MS, these deficiencies could lead to more severe symptoms, so long-term monitoring of vitamin levels is necessary. Vitamin D deficiency is also of particular concern for patients following bariatric surgery, as it may be an independent risk factor for the development of MS as well as increased relapse rate, severity of disease, and degree of disease-related disability.
Conclusion
Not only is obesity a risk factor for MS, but obesity can also worsen symptoms of MS and complicate treatment. As a result, it is important to treat obesity in patients with MS.
https://t.me/medicina_free
Lifestyle modifications are the cornerstones of weight management; however, such interventions are insufficient for clinically significant weight loss in the majority of patients. Health care providers who treat patients with MS should be familiar with more advanced options for patients with obesity, including antiobesity pharmacotherapy, devices, endoscopic bariatric procedures, and bariatric surgery. The future of obesity treatment is a multidisciplinary approach, as combinations of strategies can lead to additive or synergistic weight loss. This is an area that requires further investigation.
Case Study
A 56-year-old woman presented to our center 2 years ago for weight management. Her BMI was 39 kg/m2. She had undergone a Roux-en-Y gastric bypass in 1999 and exceeded her expectations losing 147 lbs (297 → 150 lbs); however, she then regained 61 lbs gradually over the years. Her comorbidities included MS, type 2 diabetes, and hyperlipidemia. MS had been diagnosed 25 years earlier. She required intravenous steroids once years ago and described occasional right arm numbness but did not take an ongoing medication for MS. She noted fatigue, generalized weakness and bilateral lower extremity paresthesias. She had not seen her bariatric surgeon in years.
Laboratory evaluation revealed:
hemoglobin A1c 8.5% comprehensive metabolic panel notable for fasting
glucose of 206 complete blood count notable for mean corpuscular
volume 75 bariatric laboratory tests notable for iron saturation
12%, vitamin B12 93, vitamin D 17
The patient was educated about a low-carbohydrate diet and an exercise regimen and was prescribed metformin, which was titrated up to 1000 mg twice daily by 500 mg per week.
https://t.me/medicina_free
She was also prescribed intramuscular vitamin B12, vitamin D 50,000 mg, iron supplements, and a multivitamin.
Over the next 6 months, she lost 30 lbs. Her iron and vitamin levels normalized, and her hemoglobin A1c decreased to
5.7%. Her energy improved and weakness and paresthesias resolved. At this point, she had reached a weight plateau and her hunger was increasing. She was given lorcaserin and was able to lose another 45 lbs over the next few months. She is now maintaining her weight with a low-carbohydrate diet, daily exercise routine, metformin, and lorcaserin.
This case illustrates several important points.
Patients with obesity and MS can present with symptoms common to both diseases, including fatigue and weakness. Treating a patient’s obesity can improve these symptoms.
Patients who have undergone bariatric surgery and present with neurologic symptoms should be evaluated for vitamin deficiencies (especially iron, thiamine, and vitamin B12). Patients who have undergone bariatric surgery require life-long follow-up, including yearly laboratory tests to evaluate for these deficiencies.
The patient had difficulty maintaining her weight loss after surgery and reached a weight plateau a few months after initial presentation because of metabolic adaptation (described in the chapter).
Weight-centric diabetes management includes prioritizing medications that can help with weight loss (metformin, GLP-1 agonists, SGLT2 inhibitors) instead of medications that can lead to weight gain. See Table
11.1.
Metformin is FDA approved for the treatment of type 2 diabetes but is commonly used off-label for other conditions, including type 2 diabetes prevention in patients with prediabetes or impaired fasting glucose, treatment of polycystic ovarian syndrome, and obesity/overweight.
https://t.me/medicina_free
Successful weight loss requires a comprehensive approach including diet, exercise, and behavioral modifications.
Antiobesity medications can be used after surgery to help patients lose more weight, maintain weight loss, or lose regained weight.
References
Hales CM, Carroll MD, Fryar CD, Ogden CL. Prevalence of obesity among adults
and youth: United States, 2015–2016. NCHS Data Brief. 2017;(288). Hyattsville, MD: National Center for Health Statistics.
Ogden CL, Flegal KM. Changes in terminology for childhood overweight and
obesity. Natl Health Stat Rep. 2010;(25):1-5.
Finkelstein EA, Trogdon JG, Cohen JW, Dietz W. Annual medical spending
attributable to obesity: payer-and service-specific estimates. Health Aff (Millwood). 2009;28(5):w822-w831.
Lovren F, Teoh H, Verma S. Obesity and atherosclerosis: mechanistic insights. Can
J Cardiol. 2015;31(2):177-183.
Magkos F, Fraterrigo G, Yoshino J. Effects of moderate and subsequent progressive
weight loss on metabolic function and adipose tissue biology in humans with obesity. Cell Metab. 2016;23(4):591-601. pii:S1550-4131(16):30053-5.
Wing RR, Lang W, Wadden TA, et al. Benefits of modest weight loss in improving
cardiovascular risk factors in overweight and obese individuals with type 2 diabetes. Diabetes Care. 2011;34(7):1481-1486.
Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of
hormonal adaptations to weight loss. N Engl J Med. 2011;365(17):1597-1604.
Greenway FL. Physiological adaptations to weight loss and factors favouring
weight regain. Int J Obes (Lond). 2015;39(8):1188-1196.
Fothergill E, Guo J, Howard L, et al. Persistent metabolic adaptation 6 years after
“The Biggest Loser” competition. Obesity (Silver Spring). 2016;24(8):1612-
1619.
Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond).
2010;34:S47-S55.
Gianfrancesco MA, Barcellos LF. Obesity and multiple sclerosis susceptibility: a
review. J Neurol Neuromed. 2016;1(7):1-5.
Rasul T, Frederiksen J. Link between overweight/obese in children and youngsters
and occurrence of multiple sclerosis. J Neurol. 2018;265(12):2755-2763. [Epub ahead of print]
MS Prevalence. National Multiple Sclerosis Society. Available at
https://www.nationalmssociety.org/About-the-Society/MS-Prevalence. Accessed
October 12, 2018.
Huitema MJD, Schenk GJ. Insights into the mechanisms that may clarify obesity as
a risk factor for multiple sclerosis. Curr Neurol Neurosci Rep. 2018;18(4):18.
https://t.me/medicina_free