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The choice of a specific oral PPI and whether over-the-counter (rather than prescription) PPIs are prescribed are often determined by patient preference and payer coverage. A systematic review of 12 randomized trials examining the relative effectiveness of different PPI doses and dosing regimens found no consistent difference in symptom resolution and esophagitis healing rates [17].
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ing peptic ulcers", section on 'Oral versus intravenous dosing' and "Approach to acute upper gastrointestinal bleeding in adults", section on 'Acid suppression'.) Oral regimen Selecting a PPI — <span>The choice of a specific oral PPI and whether over-the-counter (rather than prescription) PPIs are prescribed are often determined by patient preference and payer coverage. A systematic review of 12 randomized trials examining the relative effectiveness of different PPI doses and dosing regimens found no consistent difference in symptom resolution and esophagitis healing rates [17]. In patients unable to swallow pills or capsules, options include an oral suspension of lansoprazole and a powder formulation of omeprazole-sodium bicarbonate for oral suspension. Dose a




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In patients unable to swallow pills or capsules, options include an oral suspension of lansoprazole and a powder formulation of omeprazole-sodium bicarbonate for oral suspension.
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of 12 randomized trials examining the relative effectiveness of different PPI doses and dosing regimens found no consistent difference in symptom resolution and esophagitis healing rates [17]. <span>In patients unable to swallow pills or capsules, options include an oral suspension of lansoprazole and a powder formulation of omeprazole-sodium bicarbonate for oral suspension. Dose and timing of administration — PPIs should be administered 30 to 60 minutes before breakfast for maximal inhibition of proton pumps. (See 'Pharmacology' above.) Dose reduction, par




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PPIs should be administered 30 to 60 minutes before breakfast for maximal inhibition of proton pumps. (See 'Pharmacology' above.)
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swallow pills or capsules, options include an oral suspension of lansoprazole and a powder formulation of omeprazole-sodium bicarbonate for oral suspension. Dose and timing of administration — <span>PPIs should be administered 30 to 60 minutes before breakfast for maximal inhibition of proton pumps. (See 'Pharmacology' above.) Dose reduction, particularly for maintenance of healing of erosive esophagitis may be possible in Asian populations. Polymorphisms in the CYP2C19 gene, which encodes the cytochrome P450




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Antisecretory drugs can be used with a PPI provided that there is a sufficient time interval between their administration. As an example, an H2RA can be taken before bedtime or during the night by individuals who report nocturnal breakthrough symptoms such as heartburn after taking a PPI in the morning or before dinner.
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e-2 receptor antagonists (H2RAs), analogues of prostaglandin E (eg, misoprostol), and somatostatin analogues (eg, octreotide), because of the marked reduction in acid inhibitory effects [1,19]. <span>Antisecretory drugs can be used with a PPI provided that there is a sufficient time interval between their administration. As an example, an H2RA can be taken before bedtime or during the night by individuals who report nocturnal breakthrough symptoms such as heartburn after taking a PPI in the morning or before dinner. Switching between PPIs — Switching PPIs is a reasonable strategy in patients with side-effects to an individual PPI and may be necessary due to cost differences. Although there is signi




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Switching PPIs is a reasonable strategy in patients with side-effects to an individual PPI and may be necessary due to cost differences. Although there is significant interindividual and intraindividual variability in intragastric pH control between PPIs, there are no consistent difference in relation to symptom resolution and esophagitis healing rates [17]. Switching PPIs in patients with well-controlled symptoms may also be associated with increased symptom severity and decreased patient satisfaction [20].
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taken before bedtime or during the night by individuals who report nocturnal breakthrough symptoms such as heartburn after taking a PPI in the morning or before dinner. Switching between PPIs — <span>Switching PPIs is a reasonable strategy in patients with side-effects to an individual PPI and may be necessary due to cost differences. Although there is significant interindividual and intraindividual variability in intragastric pH control between PPIs, there are no consistent difference in relation to symptom resolution and esophagitis healing rates [17]. Switching PPIs in patients with well-controlled symptoms may also be associated with increased symptom severity and decreased patient satisfaction [20]. (See "Approach to refractory gastroesophageal reflux disease in adults", section on 'Subsequent management'.) Discontinuing PPIs — PPIs should be prescribed at the lowest dose and for t




#HGE #IPP #Thérapeutique #Traitements #U2D #indications
We gradually taper PPI therapy in patients treated with PPIs for longer than six months. For patients on a standard or high-dose PPI (eg, omeprazole 40 mg daily or twice daily), we decrease the dose by 50 percent every week. For patients on twice daily dosing, the initial reduction can be accomplished by decreasing the dosing to once in the morning before breakfast until the patient is on the lowest dose of the medication. Once on the lowest dose for one week, the patient is instructed to discontinue the PPI. However, no specific method for discontinuing PPI therapy has been proven effective, and no approach is universally accepted. [21,22].
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agement'.) Discontinuing PPIs — PPIs should be prescribed at the lowest dose and for the shortest duration appropriate to the condition being treated. (See 'Indications for PPI therapy' above.) <span>We gradually taper PPI therapy in patients treated with PPIs for longer than six months. For patients on a standard or high-dose PPI (eg, omeprazole 40 mg daily or twice daily), we decrease the dose by 50 percent every week. For patients on twice daily dosing, the initial reduction can be accomplished by decreasing the dosing to once in the morning before breakfast until the patient is on the lowest dose of the medication. Once on the lowest dose for one week, the patient is instructed to discontinue the PPI. However, no specific method for discontinuing PPI therapy has been proven effective, and no approach is universally accepted. [21,22]. Studies have demonstrated rebound gastric acid hypersecretion following discontinuation of PPIs in patients with long-term use. The reasons are not entirely clear, but appear to be due




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Studies have demonstrated rebound gastric acid hypersecretion following discontinuation of PPIs in patients with long-term use. The reasons are not entirely clear, but appear to be due in part to the suppression of antral somatostatin expression, resulting in an increase in antral gastrin release and subsequent disruption of normal pH-related feedback inhibition of acid secretion that occurs after a meal [1].
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ne week, the patient is instructed to discontinue the PPI. However, no specific method for discontinuing PPI therapy has been proven effective, and no approach is universally accepted. [21,22]. <span>Studies have demonstrated rebound gastric acid hypersecretion following discontinuation of PPIs in patients with long-term use. The reasons are not entirely clear, but appear to be due in part to the suppression of antral somatostatin expression, resulting in an increase in antral gastrin release and subsequent disruption of normal pH-related feedback inhibition of acid secretion that occurs after a meal [1]. (See "Physiology of gastric acid secretion", section on 'Tolerance and acid rebound'.) ADVERSE EFFECTS — Long-term PPI use has been associated with several safety concerns. However, few




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ADVERSE EFFECTS — Long-term PPI use has been associated with several safety concerns. However, few of these concerns are supported by consistent data demonstrating a causal relationship.
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equent disruption of normal pH-related feedback inhibition of acid secretion that occurs after a meal [1]. (See "Physiology of gastric acid secretion", section on 'Tolerance and acid rebound'.) <span>ADVERSE EFFECTS — Long-term PPI use has been associated with several safety concerns. However, few of these concerns are supported by consistent data demonstrating a causal relationship. (See "Physiology of gastrin", section on 'Causes of hypergastrinemia'.) Gastrointestinal effects Clostridioides (formerly Clostridium) difficile and other enteric infections — PPI use h




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PPI use has been associated with an increased risk of C. difficile infection, even in the absence of antibiotic use [23-33]. Associations with other enteric infections, including salmonellosis and campylobacteriosis, have also been reported [34-39]. However, the pathophysiologic mechanism involved in the increased risk of infection is unclear.
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sal relationship. (See "Physiology of gastrin", section on 'Causes of hypergastrinemia'.) Gastrointestinal effects Clostridioides (formerly Clostridium) difficile and other enteric infections — <span>PPI use has been associated with an increased risk of C. difficile infection, even in the absence of antibiotic use [23-33]. Associations with other enteric infections, including salmonellosis and campylobacteriosis, have also been reported [34-39]. However, the pathophysiologic mechanism involved in the increased risk of infection is unclear. A 2017 meta-analysis of 50 observational studies found that PPI use was significantly associated with an increased risk of C. difficile infection (relative risk [RR] 1.3; 95% CI 1.1-14)




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A 2017 meta-analysis of 50 observational studies found that PPI use was significantly associated with an increased risk of C. difficile infection (relative risk [RR] 1.3; 95% CI 1.1-14). The risk of C. difficile infection appears to be greater with PPIs as compared to H2 receptor antagonists [30,31].
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eric infections, including salmonellosis and campylobacteriosis, have also been reported [34-39]. However, the pathophysiologic mechanism involved in the increased risk of infection is unclear. <span>A 2017 meta-analysis of 50 observational studies found that PPI use was significantly associated with an increased risk of C. difficile infection (relative risk [RR] 1.3; 95% CI 1.1-14). The risk of C. difficile infection appears to be greater with PPIs as compared to H2 receptor antagonists [30,31]. PPI use has also been associated with an increased risk of recurrent C. difficile infection [31]. In a 2017 meta-analysis of 16 observational studies that included 7703 patients with C.




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Microscopic colitis — PPI use has been associated with microscopic colitis, including lymphocytic and collagenous colitis. In a case-control study that included 95 cases of microscopic colitis, exposure to PPIs was significantly higher in patients with microscopic colitis as compared with controls (38 versus 13 percent, OR 4.5, 95% CI 2.0-9.5) [41]. Similar results have been reported in other case-control studies, however, it is unclear if this association varies by PPI and if there is a dose-response relationship in either dose or duration of use [42,43].
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(OR, 1.4; 95% CI, 1.1-1.8). (See "Clostridioides (formerly Clostridium) difficile infection in adults: Epidemiology, microbiology, and pathophysiology", section on 'Gastric acid suppression'.) <span>Microscopic colitis — PPI use has been associated with microscopic colitis, including lymphocytic and collagenous colitis. In a case-control study that included 95 cases of microscopic colitis, exposure to PPIs was significantly higher in patients with microscopic colitis as compared with controls (38 versus 13 percent, OR 4.5, 95% CI 2.0-9.5) [41]. Similar results have been reported in other case-control studies, however, it is unclear if this association varies by PPI and if there is a dose-response relationship in either dose or duration of use [42,43]. (See "Microscopic (lymphocytic and collagenous) colitis: Clinical manifestations, diagnosis, and management", section on 'Medications'.) Hypergastrinemia — Induction of hypergastrinemia




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Hypergastrinemia — Induction of hypergastrinemia has been associated with gastric carcinoid tumors in rats. However, these observations are not generalizable to species with gastrin physiology more analogous to humans [44]. While patients treated with omeprazole for up to 11 years have shown some enterochromaffin-like cell hyperplasia, no dysplasia or neoplastic changes have been observed [45]. An increased risk of colon cancer due to hypergastrinemia has also not been established [46]
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relationship in either dose or duration of use [42,43]. (See "Microscopic (lymphocytic and collagenous) colitis: Clinical manifestations, diagnosis, and management", section on 'Medications'.) <span>Hypergastrinemia — Induction of hypergastrinemia has been associated with gastric carcinoid tumors in rats. However, these observations are not generalizable to species with gastrin physiology more analogous to humans [44]. While patients treated with omeprazole for up to 11 years have shown some enterochromaffin-like cell hyperplasia, no dysplasia or neoplastic changes have been observed [45]. An increased risk of colon cancer due to hypergastrinemia has also not been established [46]. (See "Physiology of gastrin".) Atrophic gastritis — Patients on long-term PPI therapy have a propensity to develop chronic atrophic gastritis. However, the risk of atrophic gastritis i




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Atrophic gastritis — Patients on long-term PPI therapy have a propensity to develop chronic atrophic gastritis. However, the risk of atrophic gastritis is small, and in the rare patient who develops atrophic gastritis, the clinical consequences are uncertain [45,47,48].
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rplasia, no dysplasia or neoplastic changes have been observed [45]. An increased risk of colon cancer due to hypergastrinemia has also not been established [46]. (See "Physiology of gastrin".) <span>Atrophic gastritis — Patients on long-term PPI therapy have a propensity to develop chronic atrophic gastritis. However, the risk of atrophic gastritis is small, and in the rare patient who develops atrophic gastritis, the clinical consequences are uncertain [45,47,48]. (See "Risk factors for gastric cancer".) Intestinal colonization of multi-drug resistant organisms — PPIs may increase the risk of intestinal colonization with multi-drug resistant orga




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Intestinal colonization of multi-drug resistant organisms — PPIs may increase the risk of intestinal colonization with multi-drug resistant organisms. In a meta-analysis of 12 observational studies that included 22,305 patients, after adjusting for potential confounders, acid suppression increased the odds of intestinal carriage of multi-drug resistant organisms of the Enterobacterales order (producing extended-spectrum beta-lactamases, carbapenemases, or plasmid-mediated AmpC beta-lactamases) and of vancomycin-resistant enterococci (OR 1.74; 95%CI, 1.4-2.2) [49]. Possible mechanisms include an increase in bacteria that survive transit from the stomach to the intestine due to reduction in gastric acid by PPIs and direct alteration of the composition of intestinal microbiota, leading to a decrease in mean species diversity.
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r, the risk of atrophic gastritis is small, and in the rare patient who develops atrophic gastritis, the clinical consequences are uncertain [45,47,48]. (See "Risk factors for gastric cancer".) <span>Intestinal colonization of multi-drug resistant organisms — PPIs may increase the risk of intestinal colonization with multi-drug resistant organisms. In a meta-analysis of 12 observational studies that included 22,305 patients, after adjusting for potential confounders, acid suppression increased the odds of intestinal carriage of multi-drug resistant organisms of the Enterobacterales order (producing extended-spectrum beta-lactamases, carbapenemases, or plasmid-mediated AmpC beta-lactamases) and of vancomycin-resistant enterococci (OR 1.74; 95%CI, 1.4-2.2) [49]. Possible mechanisms include an increase in bacteria that survive transit from the stomach to the intestine due to reduction in gastric acid by PPIs and direct alteration of the composition of intestinal microbiota, leading to a decrease in mean species diversity. Malabsorption of minerals and vitamins Magnesium malabsorption — PPIs can cause hypomagnesemia due to reduced intestinal absorption [50]. A meta-analysis of nine observational studies t




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Magnesium malabsorption — PPIs can cause hypomagnesemia due to reduced intestinal absorption [50]. A meta-analysis of nine observational studies that included a total of 109,798 patients found that those who took a PPI had a significantly higher risk (RR 1.43, 95% CI, 1.08-1.88) of developing hypomagnesemia as compared with those who did not [51]. Clinical manifestations of hypomagnesemia include neuromuscular excitability (eg, tremor, tetany, convulsions), weakness, and apathy.
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e to reduction in gastric acid by PPIs and direct alteration of the composition of intestinal microbiota, leading to a decrease in mean species diversity. Malabsorption of minerals and vitamins <span>Magnesium malabsorption — PPIs can cause hypomagnesemia due to reduced intestinal absorption [50]. A meta-analysis of nine observational studies that included a total of 109,798 patients found that those who took a PPI had a significantly higher risk (RR 1.43, 95% CI, 1.08-1.88) of developing hypomagnesemia as compared with those who did not [51]. Clinical manifestations of hypomagnesemia include neuromuscular excitability (eg, tremor, tetany, convulsions), weakness, and apathy. Severe PPI-induced hypomagnesemia has been associated with QT interval prolongation and torsades de pointes [52,53]. The risk of hypomagnesemia appears to be mainly in patients who have




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Severe PPI-induced hypomagnesemia has been associated with QT interval prolongation and torsades de pointes [ 52,53]. The risk of hypomagnesemia appears to be mainly in patients who have been on PPIs long-term (generally longer than one year) but cases have been reported within one year of starting PPI therapy [52,54].
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ing hypomagnesemia as compared with those who did not [51]. Clinical manifestations of hypomagnesemia include neuromuscular excitability (eg, tremor, tetany, convulsions), weakness, and apathy. <span>Severe PPI-induced hypomagnesemia has been associated with QT interval prolongation and torsades de pointes [52,53]. The risk of hypomagnesemia appears to be mainly in patients who have been on PPIs long-term (generally longer than one year) but cases have been reported within one year of starting PPI therapy [52,54]. This potential risk has led to recommendations to monitor serum magnesium levels in specific patients at high risk for hypomagnesemia. Monitoring for hypomagnesemia in patients on PPIs




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Calcium and fracture risk — Although hypochlorhydria could theoretically reduce calcium absorption, the effect appears to be relevant only for the absorption of water insoluble calcium (eg, calcium carbonate) and can be overcome by ingestion of a slightly acidic meal [55]. The absorption of water soluble calcium salts or calcium in dairy products are not impacted by PPI-induced hypochlorhydria. When calcium supplementation is necessary in patients taking PPIs, we use calcium supplements that do not require acid for absorption, such as calcium citrate.
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PPIs is discussed in detail separately. (See 'Laboratory testing' above and "Hypomagnesemia: Clinical manifestations of magnesium depletion", section on 'Overview of clinical manifestations'.) <span>Calcium and fracture risk — Although hypochlorhydria could theoretically reduce calcium absorption, the effect appears to be relevant only for the absorption of water insoluble calcium (eg, calcium carbonate) and can be overcome by ingestion of a slightly acidic meal [55]. The absorption of water soluble calcium salts or calcium in dairy products are not impacted by PPI-induced hypochlorhydria. When calcium supplementation is necessary in patients taking PPIs, we use calcium supplements that do not require acid for absorption, such as calcium citrate. (See 'Laboratory testing' above and "Drugs that affect bone metabolism", section on 'Proton pump inhibitors'.) PPI-induced hypochlorhydria can augment osteoclastic activity, thereby dec




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Vitamin B12 malabsorption — Long-term therapy with PPIs has been associated with vitamin B12 malabsorption [60,61]. However, absorption of oral B12 supplements is not affected.
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s [59]. The association between PPIs and bone metabolism and risk of fracture are discussed in detail separately. (See "Drugs that affect bone metabolism", section on 'Proton pump inhibitors'.) <span>Vitamin B12 malabsorption — Long-term therapy with PPIs has been associated with vitamin B12 malabsorption [60,61]. However, absorption of oral B12 supplements is not affected. (See 'Laboratory testing' above and "Treatment of vitamin B12 and folate deficiencies", section on 'Treatment of vitamin B12 deficiency'.) Iron malabsorption — Gastric acid plays a role




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Iron malabsorption — Gastric acid plays a role in the absorption of nonheme iron, and the use of PPIs has been associated with decreased iron absorption [62-66]. However, in most cases the decreased absorption does not appear to be of clinical significance. One exception may be in patients who require oral iron supplementation [65,67]. Such patients may need a higher dose or longer duration of supplementation [65]
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r, absorption of oral B12 supplements is not affected. (See 'Laboratory testing' above and "Treatment of vitamin B12 and folate deficiencies", section on 'Treatment of vitamin B12 deficiency'.) <span>Iron malabsorption — Gastric acid plays a role in the absorption of nonheme iron, and the use of PPIs has been associated with decreased iron absorption [62-66]. However, in most cases the decreased absorption does not appear to be of clinical significance. One exception may be in patients who require oral iron supplementation [65,67]. Such patients may need a higher dose or longer duration of supplementation [65]. (See "Treatment of iron deficiency anemia in adults", section on 'Dosing and administration (oral iron)'.) Kidney disease — PPIs can cause acute interstitial nephritis (AIN) [68-71]. S




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Kidney disease — PPIs can cause acute interstitial nephritis (AIN) [68-71]. Similar to other cases of drug-induced AIN, AIN due to PPI use is not dose-dependent, and recurrence or exacerbation can occur with a second exposure to the same or a related drug.
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,67]. Such patients may need a higher dose or longer duration of supplementation [65]. (See "Treatment of iron deficiency anemia in adults", section on 'Dosing and administration (oral iron)'.) <span>Kidney disease — PPIs can cause acute interstitial nephritis (AIN) [68-71]. Similar to other cases of drug-induced AIN, AIN due to PPI use is not dose-dependent, and recurrence or exacerbation can occur with a second exposure to the same or a related drug. (See "Clinical manifestations and diagnosis of acute interstitial nephritis", section on 'Drugs'.) PPI use has also been associated with an increased risk of incident chronic kidney dis




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Drug-induced lupus — In postmarketing safety surveillance, new onset of cutaneous lupus erythematosus and systemic lupus erythematosus (SLE), and exacerbation of existing disease have been reported in patients on PPIs [77-79]. Most cases of CLE-associated with PPI use are subacute and occur within weeks to years after continuous PPI therapy. PPI-associated SLE usually occurs days to years after initiating PPI treatment and typically presents with a rash. Most patients improve within 4 to 12 weeks of discontinuation of PPI therapy.
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ethodological limitations (residual confounding) [72,73,76]. Further studies are needed to help better define an etiologic relationship between PPI use and the development and worsening of CKD. <span>Drug-induced lupus — In postmarketing safety surveillance, new onset of cutaneous lupus erythematosus and systemic lupus erythematosus (SLE), and exacerbation of existing disease have been reported in patients on PPIs [77-79]. Most cases of CLE-associated with PPI use are subacute and occur within weeks to years after continuous PPI therapy. PPI-associated SLE usually occurs days to years after initiating PPI treatment and typically presents with a rash. Most patients improve within 4 to 12 weeks of discontinuation of PPI therapy. (See "Drug-induced lupus", section on 'Causative drugs'.) Other associations of unclear significance COVID-19 — It is unclear if PPI use is associated with an increased risk of COVID-19




Flashcard 6298315394316

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O quinto desafio posto pelo Big Data pelas empresas é o de definir a abordagem que será feita dessa massa de dados que está circulando
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Afi na l, p a ra q ue um da d o se c o nver t a em infor ma ção útil e util izáv el é pr ec iso o olh o do analisador, é pr eciso c olo ca r uma pe rgunta a esse da do q u e permita ori entar a anális e de da d os pa r a o o bjet ivo de uma empresa. N ão é t o da a in formação qu e est á ci rcula ndo q u e é relevant e ou ú til pa ra os o bje t ivos espe cí f i cos de uma em presa.

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Flashcard 6298316442892

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Big Data é:
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v o l u m e + v a r i e d a d e + a gi l i d a d e + e f e t i v i d a d e , t u d o a g r e g a n d o + v a l o r + a t u a l i d a d e .

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Flashcard 6298317491468

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utilizam-se características ou atributos que alguns pesquisadores adotam como sendo os cinco Vs. Porém, a base necessária para o reconhecimento de Big Data é formada por três propriedades:
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) N o â m b i t o d a c i ê n c i a d e d a d o s n a d e f i n i ç ã o d e B i g D a t a

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Flashcard 6298319850764

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É aí que entra o conceito de Big Data Analytics
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o e s t u d o e i n t e r p r e t a ç ã o d e g r a n d e s q u a n t i d a d e s d e d a d o s a r m a z e n a d o s c o m a f i n a l i d a d e d e e x t r a i r p a d r õ e s d e c o m p o r t a m e n t o .

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Flashcard 6298320899340

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são bastante utilizados em órgãos fazendários – como a Receita Federal – para evitar sonegação de tributos. Ué, professor... isso não seria Business Intelligence? Não, vamos ver a diferença..
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e s s a f o r m a , o B i g D a t a A n a l y t i c s p o d e r á a u x i l i a r e m p r e s a s p r i v a d a s o u a d m i n i s t r a d o r e s d e ó r g ã o s p ú b l i c o s a e n t e n d e r s e u s u s u á r i o s , e n co n t r a r o p o r t u n i d a d e s n ã o p e r c e b i d a s a n t e r i o r m e n t e , f o r n e c e r u m s e r v i ço m e l h o r e m i t i g a r p o s s í v e i s f r a u d e s

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Flashcard 6298321947916

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Nós já sabemos que a imensa par te dos dados di sp o níve is no mundo hoje for am criad os ap enas nos últimos dois anos .
Answer
Estes dados são caracterizados por sua velocidade, volume, variedade, veracidade e valor – conforme vimos anteriormente. Mais de 2.5 trilhões de bytes são gerados todos os dias por meio de nossos smartphones, tablets, sensores, redes sociais e cartões de crédito, mas o que pode ser feito com todos esses dados é que é a pergunta relevante.

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Flashcard 6298322996492

Question
combinação de sistemas de softwares matemáticos de alta tecnologia que juntos são capazes de tratar dados estruturados e não-estruturados, analisá-los e extrair um significado de alto valor para organizações
Answer
u t i l i z a - s e

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Flashcard 6298879266060

Question
Propriedade #2
Answer
um banco de dados é uma col eção logicamente coerente de dados inte r - relacionados c om al gum significado inerente. Galera, se voc ê t iver uma variedade aleatória de dados, você n ão tem um banco de da dos;

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Flashcard 6298968132876

Question
Propriedade #3
Answer
[default - edit me]

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Flashcard 6298969181452

Question
um aplicativo que manipula dados int er -rel aci onados.
Answer
Banco de dados é:

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Flashcard 6298970230028

Question
Dados são fatos conhecidos que poderiam ser registrados e que possuiriam significado implícito
Answer
Nós podemos afirmar que – hoje em dia – os ba ncos de dados desem penham um p apel crítico em quase todas as áreas em que os comput adores são usados , i ncluindo n egóc ios, comércio eletrônic o, engenharia, medicin a, gen é tica, direito e até... concurso! De toda forma, est amos avançando demais sem antes expl icar um detalhe import ante da n ossa defin iç ão. Nós vimos q ue um banc o de dados é uma coleção de dados r e laciona dos, mas o que são dados?

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Flashcard 6298973637900

Question
Dados
Answer
são fatos brutos, em sua forma primária – e, muitas vezes, os dados podem não fazer sentido sozinhos;

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Flashcard 6298974948620

Question
Por exemplo: o número 75 isoladamente faz alg um s entido ? N ão, isso é apenas um dado. No e n tanto, se eu dissesse: “ Prezados alunos, vocês sabem q uantos quilos e u peso? 75! ″ ? Agora faz sen tido! Isso não é apenas um dado, isso agora é uma informação [Obs: uma informação errada p orque eu dei uma engo rdada e não vou revelar meu peso real].
Answer
Podemos concluir que um banco de dados é uma estrutura de dados organizada que permite a extração de informações.

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Flashcard 6298975997196

Question
Outra característica importante de um banco de dados é que ele pode ser gerado e mantido manualmente, ou pode ser computadorizado
Answer
[default - edit me]

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Flashcard 6298977045772

Question
Galera, nós podemos afirmar que um banco de dados pode ter qualquer tamanho e complexidade.
Answer
[default - edit me]

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número 75 isoladamente faz algum sentido? N
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Flashcard 6298979667212

Question
número 75 isoladamente faz algum sentido? [...]
Answer
N

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número 75 isoladamente faz algum sentido? N

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Flashcard 6298981240076

Question
número 75 isoladamente faz [...] sentido? N
Answer
algum

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número 75 isoladamente faz algum sentido? N

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Flashcard 6298982288652

Question
número [...] isoladamente faz algum sentido? N
Answer
75

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Os Relatórios Contábeis de Propósito Geral das Entidades do Setor Público (RCPGs) devem ser elaborados com base no regime de competência.
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Flashcard 6299248889100

Question
Os Relatórios Contábeis de Propósito Geral das Entidades do Setor Público (RCPGs) devem ser elaborados com base no [...]
Answer
regime de competência.


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Os Relatórios Contábeis de Propósito Geral das Entidades do Setor Público (RCPGs) devem ser elaborados com base no regime de competência.

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Flashcard 6299250461964

Question
Os Relatórios Contábeis de Propósito Geral das Entidades do [...] devem ser elaborados com base no regime de competência.
Answer
Setor Público (RCPGs)

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Os Relatórios Contábeis de Propósito Geral das Entidades do Setor Público (RCPGs) devem ser elaborados com base no regime de competência.

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Flashcard 6299255442700

Question
Ativo – recurso controlado no presente pela entidade como resultado de evento passado. o Recurso – item com potencial de serviços ou com a capacidade de g[...]s econômicos. Potencial de serviços – capacidade de prestar serviços que contribuam para alcançar os objetivos da entidade. Benefícios econômicos – entradas de caixa ou reduções das saídas de caixa. o O potencial de serviços ou a capacidade de gerar benefícios econômicos podem surgir diretamente do próprio recurso ou dos direitos de sua utilização. o Para ser um ativo, a entidade deve possuir seu controle. Alguns indicadores de controle: Propriedade legal; Acesso ao recurso ou capacidade de negar o restringir o acesso; Meios que assegurem que o recurso seja utilizado para alcançar os seus objetivos; Direito legítimo ao potencial de serviços ou à capacidade para gerar os benefícios econômicos advindos do recurso. o A propriedade legal não é uma característica essencial do ativo, mas sim um indicador de controle, pois um item pode ser um ativo mesmo que a entidade não detenha a sua propriedade legal. Passivo – obrigação presente, derivada de evento passado, cuja extinção deva resultar na saída de recursos da entidade. o Um passivo deve envolver uma saída de recursos da entidade para ser liquidado ou extinto. A obrigação que pode ser liquidada ou extinta sem a saída de recursos da entidade não é um passivo. o A obrigação deve estar relacionada a um terceiro para poder gerar um passivo. A identificação de terceiros é uma indicação da existência de obrigação que dá origem a um passivo.
Answer
erar benefício

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Ativo – recurso controlado no presente pela entidade como resultado de evento passado. o Recurso – item com potencial de serviços ou com a capacidade de gerar benefícios econômicos. Potencial de serviços – capacidade de prestar serviços que contribuam para alcançar os objetivos da entidade. Benefícios econômicos – entradas de caixa ou reduções das saíd

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Flashcard 6299268025612

Question
Preço líquido de venda
Answer
montante que a entidade pode obter com a venda do ativo após deduzir os gastos para a venda. É diferente do valor de mercado, uma vez que não exige mercado aberto, ativo e organizado ou estimativa de preço em tal mercado e que inclua os gastos para a venda da entidade. Reflete as restrições na venda e é específico à entidade.

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