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Nausea and vomiting of pregnancy: Clinical findings and evaluation

Nausea and vomiting of pregnancy: Clinical findings and evaluation
Literature review current through: Sep 2023.
This topic last updated: Apr 28, 2022.

INTRODUCTION — Nausea with or without vomiting is so common in early pregnancy that mild symptoms may be considered part of the normal physiology of pregnancy in the first trimester. However, these symptoms can significantly impact the quality of life of both the pregnant person and their family, especially when persistent and/or severe [1]. Although "morning sickness" is commonly used to describe nausea and vomiting of pregnancy, symptoms can occur at any time of the day or night.

Hyperemesis gravidarum is the term used to describe the severe end of the symptom spectrum (including weight loss exceeding 5 percent of pre-pregnancy body weight) [2]. Severe symptoms can negatively impact daily functioning, cause anxiety and depression, interfere with work performance, and lead some patients to consider termination of pregnancy or avoiding a future pregnancy [3-6].

The clinical manifestations and diagnostic evaluation of patients with nausea and vomiting of pregnancy will be reviewed here. Treatment and outcomes of this disorder are discussed separately. (See "Nausea and vomiting of pregnancy: Treatment and outcome".)

INCIDENCE — Some degree of nausea with or without vomiting occurs in up to 90 percent of pregnancies [7].

In a prospective study including almost 800 patients followed from conception, 57 percent reported nausea and 27 percent reported both nausea and vomiting by 8 weeks of gestation [8].

In a study that used the Pregnancy-Unique Quantification of Emesis (PUQE) score (table 1) to assess both the presence and severity of symptoms, 88 percent reported some level of symptoms: 29.4 percent had mild symptoms, 52.2 percent had moderate symptoms, and 6.4 percent had severe symptoms [9] (see 'Scoring systems' below). By contrast, a systematic review found that symptoms were severe in only 0.3 to 3.0 percent of pregnancies [7]. Ethnic differences and differences in the definition of the disease may account, in part, for the variability.

EPIDEMIOLOGY AND RISK FACTORS

Epidemiology — Nausea and vomiting of pregnancy appears to be more common in Western countries and urban areas and less common in Africa and Asia [10,11]. Younger, primigravid individuals are more likely to be affected than older, multiparous individuals [12], but data are inconsistent.

Risk factors — Nonpregnant people who experience nausea and vomiting related to estrogen-based medications, motion sickness, or migraines are more likely to experience pregnancy-related nausea and vomiting [13]. Supertasters are also at increased risk; by contrast, anosmic individuals appear to be at low risk for developing nausea and vomiting of pregnancy [14]. Other risk factors include multiple gestation [15,16], symptoms in a prior pregnancy, hydatidiform molar pregnancy [17], nonuse of multivitamins before six weeks of gestation or during the preconception period [18,19], and acid reflux or other gastrointestinal disorders [20].

Studies of risk factors for hyperemesis gravidarum have generally included only a small number of affected patients, and results have not been conclusive [12,21-23]. Risk factors appear to be similar to those for nausea and vomiting of pregnancy; however, genetic factors also appear to play a role [24]. In a population-based cohort study, the pregnant offspring of a parent who experienced hyperemesis gravidarum was at significantly higher risk of developing hyperemesis in their own pregnancy compared with the pregnant offspring of a parent who did not experience hyperemesis gravidarum (3 versus 1 percent), whereas the pregnant partners of offspring of a parent with hyperemesis were not at increased risk [25]. Other studies have reported a significantly higher risk of hyperemesis gravidarum in patients whose siblings or mothers had the disorder [24,26,27], in monozygotic twins compared with dizygotic twins [28], and in patients with certain genetically determined conditions [26,29,30].

Interestingly, studies consistently report a preponderance of female fetuses among pregnancies complicated by hyperemesis (odds of female fetus 1.27, 95% CI 1.21-1.34) [31], while alcohol use and cigarette smoking appear to be protective factors [23].

PATHOGENESIS — The pathogenesis of nausea and vomiting of pregnancy is unknown and likely multifactorial. The predominant theories are described below.

Hormonal changes – No single hormonal profile accurately predicts the development of nausea and vomiting of pregnancy or hyperemesis gravidarum. Elevated serum concentrations of estrogen and progesterone have been implicated in the pathogenesis of these disorders. Pregnancy-related hormones relax smooth muscle and thus slow gastrointestinal transit time and may alter and/or delay gastric emptying. Although several lines of evidence support a role for hormones in the severity of nausea and vomiting of pregnancy, especially estrogen, the fact that sex hormone levels peak in the third trimester, long after symptoms of nausea and vomiting or hyperemesis have typically resolved, is inconsistent with this theory [32,33].

By comparison, serum concentrations of human chorionic gonadotropin (hCG) peak during the first trimester, the time when hyperemesis gravidarum is typically seen. The observations that serum hCG concentration is higher in patients with hyperemesis than in other pregnant patients with nausea and vomiting and symptoms are worse in patients with multiple gestations and hydatidiform moles (conditions associated with high hCG levels) also support a possible etiologic role for this hormone [34,35]. However, high hCG levels are not consistently associated with nausea and vomiting [36]. The presence of specific hCG isoforms or hCG receptor mutations may explain differences in symptomatology among patients with similar hCG levels [34,37].

The role of several other hormones in the pathogenesis of hyperemesis has been studied, but no consistent relationship has been found [11].

Abnormal gastrointestinal motility – Gastric motility may be abnormal (delayed or dysrhythmic) in patients with hyperemesis [11]. Studies addressing motility disturbances have reported conflicting results, suggesting that these abnormalities are not highly predictive of the disease. (See "Pathogenesis of delayed gastric emptying".)

The lower esophageal sphincter is relaxed in pregnancy, leading to an increase in gastroesophageal reflux, and gastric acidity may be increased. Gastroesophageal reflux results in heartburn and, in some individuals, nausea [38]. However, if this were the mechanism for hyperemesis, symptoms should worsen as pregnancy advances, rather than improve. Nevertheless, patients who experience persistent symptoms of nausea and vomiting in pregnancy should be evaluated for concomitant gastroesophageal reflux disease.

Helicobacter pylori – Most individuals with H. pylori do not develop severe nausea and vomiting of pregnancy, but the infection may play a role in the pathogenesis of the disease in some patients. In a systematic review and meta-analysis of epidemiological studies, a significant association was found between H. pylori infection and hyperemesis gravidarum/nausea and vomiting of pregnancy compared with asymptomatic controls (odds ratio 3.21, 95% CI 2.01-5.10) [39]. Summary sensitivity for diagnosis of hyperemesis gravidarum was 73 percent (95% CI 62.0-81.4) and specificity was 55 percent (95% CI 47.4-61.5). However, there was significant heterogeneity among studies and most studies did not distinguish between active infection and past infection or strain of H. pylori. (See "Nausea and vomiting of pregnancy: Treatment and outcome", section on 'Consider testing for H. pylori infection'.)

Genetic factors – A genetic component to nausea and vomiting of pregnancy and hyperemesis has been suggested based on studies that show an increased risk for development of hyperemesis among female relatives of patients previously affected by severe nausea and/or vomiting or hyperemesis gravidarum [26,27]. The incidence of hyperemesis gravidarum appears to be similar in patients who have the same partner throughout pregnancy and those who change partners, suggesting that paternal genes expressed by the fetus play at most a minor role and that maternal genes largely influence whether or not the individual will be affected [40].

A genome-wide research study that found an association between the genes GDF15 and IGFBP7 and hyperemesis gravidarum may be the most promising area of investigation regarding the pathogenesis of nausea and vomiting of pregnancy [41-43]. GDF15 is highly expressed in placental trophoblast cells and its protein appears to promote placentation and regulate physiological body weight and appetite via activation of neurons in the hypothalamus and area postrema (vomiting center) of the brainstem. In cancer patients, excessive production of GDF15 is the key driver of anorexia, while a mouse model of cancer cachexia showed that inhibition of GDF15 restored appetite and weight gain. IGFBP7 also plays a role in placentation, appetite, and cachexia. The dual role of GDF15 and IGFBP7 in placentation and appetite may explain why upregulation is associated with both a higher frequency of nausea and vomiting of pregnancy and a lower frequency of miscarriage. In the future, drugs targeting the production or action of GDF15 and IGFBP7 may be useful for treating nausea and vomiting of pregnancy.

Other – Several other theories to explain nausea and vomiting of pregnancy and hyperemesis gravidarum have been suggested, including specific nutrient deficiencies (eg, zinc, vitamin B6), alterations in lipid levels, changes in the autonomic nervous system, and immunologic dysregulation [11,21]. In addition, psychologists have pointed out that nausea can be a somatic symptom of depression, although depression can also be a reaction to severe or prolonged nausea [44]. None of these theories are consistently associated with, or highly predictive of, the disease.

CLINICAL PRESENTATION — Symptoms typically start at 5 to 6 weeks of gestation, peak at approximately 9 weeks, and usually subside by 16 to 20 weeks. However, symptoms may continue until the third trimester in 15 to 20 percent of patients and until delivery in 5 percent [13,45-47]. Sixty percent of patients are asymptomatic six weeks after onset of nausea [45]. If vomiting begins in the latter half of pregnancy and/or persists beyond a few days postpartum [48], other etiologies should be investigated.

Although the lay term for mild pregnancy-related nausea and vomiting is "morning sickness," the symptoms may occur at any time of day, may only occur in the evening, and often (80 percent) persist throughout the day [49].

DIAGNOSIS — Nausea and vomiting of pregnancy and hyperemesis gravidarum are clinical diagnoses without definitive diagnostic criteria. It is generally a diagnosis of exclusion (see 'Differential diagnosis' below) based on its first occurrence in early pregnancy with gradual resolution over weeks.

Nausea and vomiting of pregnancy – The diagnosis of nausea and vomiting of pregnancy is based on the presence of nausea and/or vomiting that appears to be related to pregnancy rather than another etiology. Patients with the common mild form of nausea and vomiting of pregnancy maintain normal vital signs and have normal physical and laboratory examinations and pregnancy course.

Hyperemesis gravidarum – Hyperemesis gravidarum is considered the severe end of the spectrum of nausea and vomiting of pregnancy, although there is no clear demarcation between common pregnancy-related "morning sickness" and this less frequent, more pathologic disorder.

Common criteria for diagnosis of hyperemesis are persistent vomiting accompanied by weight loss exceeding 5 percent of prepregnancy body weight and ketonuria unrelated to other causes [50].

Alternatively, the diagnosis can be made in patients with pregnancy-related vomiting that occurs more than three times per day with weight loss greater than 3 kg (6.2 lbs) or 5 percent of body weight and ketonuria [51].

Also alternatively, an international consensus proposed four simplified criteria for hyperemesis gravidarum, whereby [52]:

-Symptoms start in early pregnancy, before a gestational age of 16 weeks

-Nausea and/or vomiting is severe

-The patient is unable to eat and/or drink normally

-Daily activities are strongly limited

In contrast to patients with mild disease, those with hyperemesis may present with orthostatic hypotension, laboratory abnormalities (eg, electrolyte, thyroid, and liver abnormalities), and physical signs of hypovolemia. They often require hospitalization for stabilization and initiation of pharmacotherapy. In addition, many patients with hyperemesis gravidarum can also present with hypersalivation, a condition called ptyalism, which can further complicate the management of hyperemesis gravidarum [53].

Scoring systems — The Motherisk-PUQE Scoring Index (table 1) and the Rhodes Index are tools that can be used to assess the severity of nausea and vomiting of pregnancy. The Motherisk-PUQE Scoring Index was designed specifically for pregnant people to assess symptoms in the 12 hours prior to clinical evaluation and has been used predominantly in research studies [54-56]. The modified PUQE score (table 2) was designed to assess symptoms over the course of the entire first trimester of pregnancy [55].

The indices use a system that assigns points for the number of hours that the individual feels nauseated, the number of times they vomit, and the number of times they have dry heaves in a typical day. A high score indicates that the patient should be evaluated for hypovolemia and their serum electrolyte levels should be checked.

Some clinicians find these tools helpful in assessing the severity of the patient's symptoms. The PUQE score and the modified PUQE score [55] have been validated for guiding management of nausea and vomiting of pregnancy in the clinical setting [57,58], but these scores do not appear to be predictive of the course of disease (ie, weight change one week after hospital admission, duration of hospital stay, and readmission) [59].

EVALUATION

Initial evaluation — The standard initial evaluation of pregnant patients with persistent nausea and vomiting includes:

Weight

Orthostatic blood pressure measurements and heart rate

Laboratory tests (See 'Laboratory tests' below.)

Confirmation of fetal viability (ie, presence of fetal cardiac activity)

Obstetric ultrasound examination for fetal number or presence of a molar pregnancy (if not previously performed) (See 'Imaging' below.)

Laboratory tests — Laboratory evaluation is indicated in patients with persistent nausea and vomiting to determine the severity of disease, assess the patient's volume/metabolic status, identify or exclude other diagnoses that could account for the symptoms, and guide replacement therapy.

The standard initial basic evaluation of all pregnant patients with persistent nausea and vomiting includes:

Serum electrolytes

Urine ketones and specific gravity

Based on patient-specific factors, such as severity of disease and associated signs and symptoms, we order a comprehensive metabolic panel and selectively order one or more of the following additional blood tests:

Blood urea nitrogen

Creatinine

Complete blood count

Liver chemistries

Amylase/lipase

Phosphorus, magnesium, and calcium levels

Thyroid function tests

Stool antigen testing for H. pylori can be performed during pregnancy to avoid exposure to tagged carbon required for a standard breath test. Blood antibody testing indicates presence only of antibodies and cannot distinguish between present or past infection. (See "Indications and diagnostic tests for Helicobacter pylori infection in adults", section on 'Stool antigen assay'.)

Imaging

If not previously performed, an obstetric ultrasound examination is performed to confirm fetal cardiac activity and look for multiple gestation or gestational trophoblastic disease, which can be associated with nausea and vomiting of pregnancy.

Ultrasound examination of the liver is indicated if liver disease is suspected, and additional imaging is needed if appendicitis is suspected. (See 'Differential diagnosis' below.)

Other — Additional laboratory testing or imaging should be considered for patients who are refractory to standard therapy or in whom another cause of symptoms is suspected. (See "Nausea and vomiting of pregnancy: Treatment and outcome", section on 'Consider testing for H. pylori infection'.)

Spectrum of findings and interpretation — Laboratory abnormalities that can be caused by nausea and vomiting of pregnancy include:

Electrolyte and acid-base derangements, such as hypokalemia and hypochloremic metabolic alkalosis (from vomiting gastric secretions). Ketosis can occur if caloric intake is minimal.

An increase in hematocrit, indicating hemoconcentration due to plasma volume depletion. The degree of hemoconcentration may be masked by the physiologic decline in hematocrit that normally occurs in pregnancy, although this is maximal in the second trimester. Lymphocyte count tends to be higher in patients with hyperemesis [39].

Other signs of hypovolemia include an elevated blood urea nitrogen and urine specific gravity. The serum creatinine concentration will increase only if the degree of hypovolemia is sufficiently severe to lower the glomerular filtration rate.

Abnormal liver chemistries values occur in approximately 50 percent of patients who are hospitalized with hyperemesis [60]. The most striking abnormality is an increase in serum aminotransferases. Alanine aminotransferase (ALT) is typically elevated to a greater degree than aspartate aminotransferase (AST). However, values for both are typically only mildly elevated (ie, in the low hundreds or two to three times the upper limit of normal) and rarely as high as 1000 units/L. Hyperbilirubinemia may occur but rarely exceeds 4 mg/dL [61].

The degree of abnormality in liver chemistries correlates with the severity of vomiting; the highest elevations are seen in patients with the most severe or protracted vomiting. Abnormal liver chemistries resolve promptly upon resolution of vomiting.

Given the characteristic clinical manifestations of hyperemesis, a liver biopsy to exclude other causes for the laboratory abnormalities is unnecessary. When a liver biopsy has been performed, it was either normal or showed nonspecific findings. Inflammation was absent, but necrosis with cell drop out, steatosis centrilobular vacuolization, and rare bile plugs have been seen [61-63]. These changes help to explain the mechanism for the liver test abnormalities.

Serum amylase and lipase are elevated in 10 to 15 percent of patients and may increase as much as fivefold (as opposed to a 5- to 10-fold increase in acute pancreatitis) [45]. In one study, all patients with increased serum amylase values had normal pancreatic amylase values, implying that the elevated amylase levels are most likely of salivary rather than pancreatic origin [64]. Although the origin of the increased serum lipase is unknown in the setting of hyperemesis, serum lipase in general appears to be primarily of pancreatic origin, but other organs (such as stomach, duodenum, small bowel, colon, liver) may produce lipase [65].

Gestational transient or physiologic hyperthyroidism, can be seen in 3 to 11 percent of patients in early pregnancy [66]. This is likely due to high serum concentrations of human chorionic gonadotropin, which has TSH receptor stimulating activity [34]. In fact, many patients with hyperemesis gravidarum have abnormally high serum T4 levels and low TSH levels. (See "Overview of thyroid disease and pregnancy".)

Other terms used to describe this condition include transient thyrotoxicosis of hyperemesis, gestational thyrotoxicosis, gestational transient thyrotoxicosis, and transient nonimmune hyperthyroidism of early pregnancy [34,67-69].

The transient hyperthyroidism of hyperemesis is a temporary condition that resolves spontaneously without treatment. Complete resolution of biochemical hyperthyroidism usually occurs by 18 weeks of gestation as the symptoms of hyperemesis gravidarum improve [67,70]. Obstetric outcomes are not affected by this transient hyperthyroid condition. Expectant management of patients with hyperemesis gravidarum and gestational transient hyperthyroidism typically leads to a decrease in serum-free T4 levels in parallel with a decrease in hCG levels after the first trimester [71]. Thus, thyroid function tests do not have to be measured routinely in patients with hyperemesis gravidarum unless they have overt signs or symptoms of hyperthyroidism [72].

Features that distinguish gestational transient hyperthyroidism from other causes of hyperthyroidism (most likely Graves' disease in a pregnant patient) are the vomiting, absence of goiter and ophthalmopathy, and absence of the common symptoms and signs of hyperthyroidism (heat intolerance, muscle weakness, tremor). Both serum free T4 concentrations and serum T3 concentrations are usually unequivocally elevated in pregnant patients with true hyperthyroidism.

Treatment of hyperthyroidism should not be undertaken without clear evidence of a primary thyroid disorder (eg, goiter, elevated free thyroid hormone or elevated TSH receptor antibody levels). (See "Hyperthyroidism during pregnancy: Treatment".)

Hypomagnesemia and hypocalcemia. Marked dietary deprivation can lead to progressive magnesium depletion. Magnesium depletion can cause hypocalcemia by producing parathyroid hormone (PTH) resistance, which occurs when serum magnesium concentrations fall below 0.8 mEq/L (1 mg/dL or 0.4 mmol/L) or by decreasing PTH secretion, which occurs in patients with more severe hypomagnesemia. (See "Etiology of hypocalcemia in adults", section on 'Disorders of magnesium metabolism'.)

DIFFERENTIAL DIAGNOSIS

Nausea and vomiting that first develops after 10 weeks of gestation is not likely due to nausea and vomiting of pregnancy, which typically begins earlier in gestation. Associated signs and symptoms, such as bilious emesis, abdominal pain, fever, headache, abnormal neurologic findings, diarrhea, constipation, leukocytosis, goiter, cyclicity, or hypertension, also suggest another diagnosis is likely; many conditions unrelated to pregnancy can cause persistent nausea and vomiting (table 3). Rarely, chronic use of marijuana has been associated with daily vomiting, abdominal pain, and frequent bathing/showering in hot water to relieve symptoms (cannabinoid hyperemesis syndrome). The differential diagnosis of these conditions, including indications for endoscopy, is reviewed separately. (See "Approach to the adult with nausea and vomiting", section on 'Approach to management' and "Cyclic vomiting syndrome", section on 'Chronic cannabis use'.)

Preeclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), and acute fatty liver of pregnancy are also causes of pregnancy-related nausea and vomiting, but onset is in the latter half of pregnancy (usually the third trimester), hypertension is usually present, and thrombocytopenia is common. (See "Preeclampsia: Clinical features and diagnosis" and "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)" and "Acute fatty liver of pregnancy".)

Hyperparathyroidism in pregnancy is uncommon, but should be considered, as hypercalcemia may contribute to vomiting [73,74]. (See "Primary hyperparathyroidism: Clinical manifestations" and "Primary hyperparathyroidism: Diagnosis, differential diagnosis, and evaluation".)

In patients with long-standing, poorly controlled diabetes, gastroparesis may cause nausea and vomiting, early satiety, postprandial fullness, abdominal pain, or bloating. (See "Gastroparesis: Etiology, clinical manifestations, and diagnosis" and "Treatment of gastroparesis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Nausea and vomiting of pregnancy".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Morning sickness (The Basics)" and "Patient education: Hyperemesis gravidarum (The Basics)" and "Patient education: Pregnancy symptoms (The Basics)")

Beyond the Basics topic (see "Patient education: Nausea and vomiting of pregnancy (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical presentation –Some degree of nausea with or without vomiting occurs in up to 90 percent of pregnancies, typically with onset at 5 to 6 weeks of gestation, peaking at 9 weeks, and usually getting better by 16 to 18 weeks of gestation. Hyperemesis gravidarum represents the severe form of nausea and vomiting of pregnancy, and accounts for <5 percent all cases.

Symptoms may occur at any time of day, may only occur in the evening, and often (80 percent) persist throughout the day. Symptoms may continue until the third trimester in 15 to 20 percent of patients and until delivery in 5 percent. Sixty percent of patients are asymptomatic six weeks after onset of nausea. (See 'Clinical presentation' above and 'Diagnosis' above and 'Incidence' above.)

Risk factors – Nonpregnant people who experience nausea and vomiting after estrogen exposure, from motion sickness, with migraine, or with exposure to certain tastes (supertasters) are more likely to have pregnancy-related nausea and vomiting. Other risk factors include multiple gestation , symptoms in a prior pregnancy, hydatidiform molar pregnancy , nonuse of multivitamins before six weeks of gestation or during the preconception period, and acid reflux or other gastrointestinal disorders. There can also be a genetic component to nausea and vomiting of pregnancy. (See 'Epidemiology and risk factors' above.)

Diagnosis – Patients with the common mild form of nausea and vomiting of pregnancy maintain normal vital signs and have normal physical and laboratory examinations and pregnancy course.

The diagnosis of hyperemesis gravidarum is made clinically in a patient with onset of persistent vomiting accompanied by weight loss exceeding 5 percent of prepregnancy body weight and ketonuria in the first trimester, unrelated to other causes. The diagnosis can also be made in patients with pregnancy-related vomiting that occurs more than three times per day with weight loss greater than 3 kg (6.2 lbs) or 5 percent of body weight and ketonuria (See 'Diagnosis' above.)

The PUQE score (table 1) and the modified PUQE score (table 2) have been validated for guiding management of nausea and vomiting of pregnancy in the clinical setting. (See 'Scoring systems' above.)

When to consider an alternative diagnosis – If vomiting begins in the latter half of pregnancy and/or persists beyond a few days postpartum, other underlying conditions should be considered and investigated (ie, gastroenteritis, pancreatitis, preeclampsia, metastatic malignancy). Many conditions unrelated to pregnancy can cause persistent nausea and vomiting (table 3). (See 'Differential diagnosis' above.)

Evaluation – The standard initial evaluation of pregnant patients with persistent vomiting includes measurement of weight, orthostatic blood pressure measurements and heart rate, laboratory tests (urine ketones and specific gravity, serum electrolytes), confirmation of fetal viability, and an ultrasound examination, if not previously performed, to look for gestational trophoblastic disease or multiple gestation. Stool antigen testing for H. pylori can be performed during pregnancy to avoid exposure to tagged carbon required for a standard breath test. (See 'Evaluation' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Susan Ramin, MD, and Jerrie S Refuerzo, MD, who contributed to an earlier version of this topic review.

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Topic 6792 Version 67.0

References

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