Como Eu Trato de IBP em pacientes submetidos à cirurgia bariátrica
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Como Eu Trato de IBP em pacientes submetidos à cirurgia bariátrica
Mestre em Cirurgia pela Escola Paulista de Medicina da Universidade Federal de São Paulo (EPM/UNIFESP);
membro titular da Sociedade Brasileira de Cirurgia Bariátrica e Metabólica (SBCBM). CRM: 45285-SP
Dados recentes dos EUA mostram que nas últimas duas décadas a incidência de obesidade adulta dobrou e a infantil triplicou. Em função da incidência elevada e dos riscos associados para a saúde, o aumento nessas circunstâncias constitui uma epidemia que representa sério e crescente problema de saúde pública, sendo hoje a obesidade a primeira causa de mortalidade prevenível.
Com a obesidade os fatores de risco para a doença cardiovascular (DCV) aumentam, incluindo hipertensão arterial (HA), hiperlipidemia e diabetes. As doenças mais comuns associadas à obesidade são apnéia de sono, asma brônquica, esteatose hepática, doença articular de quadril, joelhos e tornozelos, incontinência urinária de esforço e síndrome dos ovários policísticos (SOP), além do risco aumentado de câncer de esôfago, útero, próstata, fígado e rim. Uma variedade de outras desordens físicas e psiquiátricas é igualmente predominante entre os severamente obesos, que mostram risco elevado para depressão e ansiedade. A obesidade severa tem taxas mais elevadas de morbidade e mortalidade e conseqüente qualidade de vida diminuída.
Ademais da importância e da gravidade no desenvolvimento das patologias associadas à obesidade, o excesso de peso é fator de risco determinante para o refluxo gastroesofágico (RGE) patológico ou a hérnia hiatal. Uma proporção elevada de pacientes severamente obesos tem sintomas e resultados endoscópicos de RGE patológico(1, 6) cuja predominância na população obesa decorre da baixa pressão do esfíncter inferior do esôfago nesses pacientes(18, 21). Sabe-se também que a obesidade aumenta o risco de adenocarcinoma do esôfago independente de outros fatores, particularmente entre homens portadores de RGE(15).
Lamentavelmente, a terapêutica médica e as mudanças dietéticas e do estilo de vida provaram ser ineficazes no tratamento dos obesos mórbidos e de suas doenças associadas. Entretanto, os estudos têm relatado bons resultados com a cirurgia no paciente severamente obeso. O tratamento cirúrgico da obesidade permite perda de peso sustentada e reduções significativas das doenças associadas ao peso adicional(6). Existem diferentes tipos de cirurgia para obesidade severa; as mais utilizadas atualmente são a banda gástrica ajustável, a gastroplastia redutora à Fobi-Capella, a derivação biliopancreática à Scopinaro e o switch duodenal(5). Recentemente acrescentaram-se a essas técnicas cirúrgicas os benefícios da videocirurgia. Menos invasiva e proporcionando vantagens na recuperação pós-operatória, a cirurgia endoscópica tem sido freqüentemente utilizada no tratamento da obesidade mórbida.
Entre as técnicas cirúrgicas utilizadas, a banda gástrica ajustável tem sido preconizada por ser um procedimento de menores complexidade e risco cirúrgico. Colocada no corpo gástrico alto, logo abaixo da transição esôfago gástrica, a banda, quando insuflada, promoverá dificuldade de esvaziamento do novo reservatório gástrico constituído, o que causará maior saciedade(3). Entretanto estudos demonstram que alguns pacientes acabam desenvolvendo alterações de motilidade com conseqüente dilatação esofágica, além de RGE significativo. Preconiza-se nesses casos a manutenção de um bloqueador da bomba de prótons com a finalidade de diminuir a secreção ácida e o refluxo(2, 4, 7, 9, 14).
A derivação gastrojejunal em Y de Roux, também chamada de gastroplastia redutora à Fobi-Capella, envolve componentes restritivos e mal absortivos, tendo-se transformado na cirurgia bariátrica mais executada nos EUA. Acredita-se que a gastroplastia redutora seja um procedimento eficaz na prevenção do RGE por imaginar-se que o pequeno reservatório gástrico não produza ácido e por não haver refluxo gastroduodenal(8, 10-12, 16).
A confecção de um novo reservatório gástrico unido a um segmento jejunal em tese diminuiria a secreção ácida que poderia refluir ao esôfago. Entretanto alguns desses pacientes desenvolvem estenose da anastomose gastro-jejunal, o que acontece em até 12% dos casos, tipicamente no primeiro mês após a cirurgia. Normalmente a anastomose é projetada para ter o diâmetro de 1 cm. Com a estenose o paciente pode apresentar sintomas de dor retroesternal, azia e vômitos pós-prandiais, necessitando eventualmente de dilatação endoscópica por uma ou mais vezes. A obstrução da anastomose pode igualmente conduzir ao RGE e à esofagite severa.
Em alguns pacientes há ulceração marginal à estenose do estoma, diagnosticada pela endoscopia. Sua incidência varia entre 1% e 16%(13, 19). Os fatores associados ao seu desenvolvimento incluem o tamanho do novo reservatório gástrico e sua secreção ácida residual, sua orientação, presença de linhas de suturas ou grampos e isquemia da mucosa. Os antiinflamatórios não-esteroidais (AINEs) e o Helicobacter pylori (HP) podem igualmente contribuir, estando nesses casos indicados tratamento com inibidores da bomba de prótons (IBP) e erradicação do HP quando presente. O efetivo controle da secreção ácida exerce papel fundamental na cicatrização das lesões, bem como na sua profilaxia(20, 22).
No grupo de cirurgias com maior componente mal absortivo temos a derivação biliopancreática à Scopinaro, que mantém um reservatório gástrico maior e um grande desvio intestinal. A câmara gástrica maior predispõe a uma incidência de úlcera de boca anastomótica em 5% a 12% dos casos, estando indicado o uso de IBPs(17). No swicht duodenal realiza-se uma gastrectomia verti- cal, preservando-se o antro gástrico e o piloro. A confecção desse tubo gástrico de forma mais estreita pode ocasionar dificuldade de esvaziamento na região do corpo gástrico e conseqüente RGE. Nesses casos deve-se indicar o uso de IBPs e procinéticos.
Sabe-se que a redução dos fatores de proteção da mucosa representa importante papel na gênese de úlceras e erosões gástricas, principalmente em pacientes submetidos a cirurgias no trato digestivo. Portanto deve-se reforçar a preocupação de proteger a mucosa gastrointestinal nos pacientes submetidos à cirurgia bariátrica. O rabeprazol sódico é considerado um potente, rápido e consistente IBP(23-26). Skoczylas et al.(27) comprovaram o aumento da produção de muco gástrico associado ao rabeprazol. Em ensaio clínico bastante interessante, se estudou o efeito do rabeprazol na secreção de mucina gástrica, do muco e da sua viscosidade em 21 voluntários assintomáticos num estudo duplo-cego. Essa secreção aumentou significativamente durante a administração de rabeprazol quando em comparação com os normais (p < 0,05). Os autores concluíram que a propriedade farmacológica original do rabeprazol aumenta significativamente a produção de muco e de mucina gástrica em períodos de hiperacidez. Este efeito pode trazer benefícios clínicos adicionais ao proteger a mucosa gástrica no intervalo alimentar, principalmente em pacientes submetidos a cirurgia bariátrica.
Leitura sugerida
1. Csendes A, Burdiles P, Rojas J, Burgos A, Henríquez A. Pathological gastroesophageal reflux in patients with severe, morbid and hyper obesity. Rev Med Chil 2001; 129(9): 1038-43.
2. Suter M, Dorta G, Giusti V, Calmes J. Gastric banding interferes with esophageal motility and gastroesophageal reflux. Arch Surg 2005; 140: 639-43.
3. Iovino P, Angrisani L, Tremolaterra F, Nirchio E, Ciannella M, Borrelli V, etal. Abnormal esophageal acid exposure is common in morbidly obese patients and improves after a successful lap-band system implantation. Surg Endosc 2002; 16(11): 1631-5. Epub 2002.
4. Weiss HG, Nehoda H, Labeck B, Peer-Kühberger R, Klingler P, Gadenstätter M, et al. Treatment of morbid obesity with laparoscopic adjustable gastric banding affects esophageal motility. Am J Surg 2000; 180: 479-82.
5. Consensus Development Conference Panel. Gastrointestinal surgery for severe obesity: consensus development conference statement. Ann Intern Med 1991; 115: 956-61.
6. Suter M, Dorta G, Giusti V, Calmes JM. Gastro-esophageal reflux and esophageal motility disorders in morbidly obese patients. Obes Surg 2004; 14: 959-66.
7. Husemann B. Esophageal motility disorders after SAGB [abstract]. Obes Surg 2002; 12: 466.
8. Korenkov M, Köhler L, Yücel N, et al. Esophageal motility and reflux symptoms after bariatric surgery. Obes Surg 2002; 12: 72-6.
9. Wiesner W, Hauser M, Schöb O, Weber M, Hauser RS. Pseudo-achalasia following laparoscopically placed adjustable gastric banding. Obes Surg 2001; 11: 513-8.
10. Clements RH, Gonzalez QH, Foster A, et al. Gastrointestinal symptoms are more intense in morbidly obese patients and are improved with laparoscopic Roux-en-Y gastric bypass. Obes Surg 2003; 13: 610-4.
11. Frezza EE, Ikramuddin S, Gourash W, et al. Symptomatic improvement in gastroesophageal reflux disease (GERD) following laparoscopic Roux-en-Y gastric bypass. Surg Endosc 2002; 16: 1027-31.
12. Smith SC, Edwards CB, Goodman GN. Symptomatic and clinical improvement in morbidly obese patients with gastroesophageal reflux disease following Roux-en-Y gastric bypass. Obes Surg 1997; 7: 479-84.
13. Pope GD, Goodney PP, Burchard KW, Proia RR, Olafsson A, Lacy BE, et al. Peptic ulcer/stricture after gastric bypass: a comparison of technique and acid suppression variables. Obesity Surgery 2002; 12(1): 30-3.
14. Miner Jr P, Katz PO, Chen Y, Sostek M. Gastric acid control with esomeprazole, lansoprazole, omeprazole, pantoprazole and rabeprazole: a five-way crossover study. Am J Gatroenterol 2003; 98: 2616-20.
15. Whiteman DC, Sadeghi S, Pandeya N, Smithers BM, Gotley DC, Bain CJ, et al.; Australian Cancer Study. Combined effects of obesity, acid reflux and smoking on the risk of adenocarcinomas of the oesophagus. Gut 2008; 57(2): 173-80. Epub 2007.
16. Houghton SG, Romero Y, Sarr MG. Effect of Roux-en-Y gastric bypass in obese patients with Barrett?s esophagus: attempts to eliminate duodenogastric reflux. Surg Obes Relat Dis 2008; 4(1): 1-4; discussion 4-5. Epub 2007.
17. Merrouche M, Sabaté JM, Jouet P, Harnois F, Scaringi S, Coffin B, et al. Gastro-esophageal reflux and esophageal motility disorders in morbidly obese patients before and after bariatric surgery. Obes Surg 2007; 17(7): 894-900.
18. Herbella FA, Sweet MP, Tedesco P, Nipomnick I, Patti MG. Gastroesophageal reflux disease and obesity. Pathophysiology and implications for treatment. J Gastrointest Surg 2007; 11(3): 286-90.
19. Sapala JA, Wood MH, Sapala MA, Flake TM Jr. Marginal ulcer after gastric bypass: a prospective 3-year study of 173 patients. Obes Surg 1998; 8(5): 505-16.
20. Rasmussen JJ, Fuller W, Ali MR. Marginal ulceration after laparoscopic gastric bypass: an analysis of predisposing factors in 260 patients. Surg Endosc 2007; 21(7): 1090-4. Epub 2007.
21. Wu JC, Mui LM, Cheung CM, Chan Y, Sung JJ. Obesity is associated with increased transient lower esophageal sphincter relaxation. Gastroenterology 2007; 132(3): 883-9. Epub 2006.
22. Siilin H, Wanders A, Gustavsson S, Sundbom M. The proximal gastric pouch invariably contains acid-producing parietal cells in Roux-en-Y gastric bypass. Obesity Surgery 2005; 15(6): 771-7.
23. Robinson M, Fitzgerald S, Hegedus R, Murthy A, Jokubaitis L; FAST Trial Investigators. Onset of symptom relief with rabeprazole: a community- based, open-label assessment of patients with erosive oesophagitis. Aliment Pharmacol Ther 2002; 16(3): 445-54.
24. Pantoflickova D, Dorta G, Jornod P, Ravic M, Blum AL. Identification of the characteristics influencing the degree of antisecretory activity of PPIs. Gastroenterology 2000; 118(4, Suppl. 2, part 2 Of 2): 1290.
25. De Korwin JD, Ducrotte P, Vallot T. Les nouveaux inhibiteurs de la pompe à protons, un progres dans la prise en charge des maladies acide-peptiques? New-generation proton pump inhibitors, a progress in the treatment of acidrelated diseases?]. La Presse Medicale 2004; 33(11): 746-54.
26. Robinson M, Horn J. Clinical pharmacology of proton pump inhibitors: what the practising physician needs to know. Drugs 2003: 63(24): 2739-54.
27. Skoczylas T, Sarosiek I, Sostarich S, McElhinney C, Durham S, Sarosiek J. Significant enhancement of gastric mucin content after rabeprazole administration: its potential clinical significance in acid-related disorder. Dig Dis Sci 2003; 48(2): 322-8.
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