duodenal ulcer

十二指腸潰瘍

WordNet

1. a circumscribed inflammatory and often suppurating lesion on the skin or an internal mucous surface resulting in necrosis of tissue (同)ulceration
2. in or relating to the duodenum; "duodenal ulcer"

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1. 潰瘍
2. 十二指腸の

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/09/03 13:30:53」(JST)

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Contributors

Peptic ulceration
Classification and external resources
Deep gastric ulcer
ICD-10	K25–K27
ICD-9	531–534
DiseasesDB	9819
MedlinePlus	000206
eMedicine	med/1776 ped/2341
MeSH	D010437

A peptic ulcer is a distinct breach in the mucosal lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer), a result of caustic effects of acid and pepsin in the lumen. Histologically, peptic ulcer is identified as necrosis of the mucosa which produces lesions equal to or greater than 0.5 cm (1/5"). It is the most common ulcer of an area of the gastrointestinal tract that is usually acidic and thus extremely painful. Helicobacter pylori is one of the most common causes of peptic ulcer. Ulcers can also be caused or worsened by drugs such as aspirin, ibuprofen, and other NSAIDs.

Four times as many peptic ulcers arise in the duodenum—the first part of the small intestine, just beyond the stomach—as in the stomach itself. About 4% of gastric ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign.

The appearance of an ulcer can be either the classic erosive, concave, crater-like ulcer (the image held by most patients) or convex, perhaps resembling a colonic polyp. As a generalization, the erosive concave type tend to be located in the stomach proper while the convex type tend to be found in the pylorus/duodenum.

These convex growths have an extensive variety of shapes and forms, but in all forms the ulcer projects above the level of the surrounding tissue. For extended periods these growths characteristically lack any surface breaks in the mucosic tissue and also initially lack any visual differentiation from the surrounding tissue even in larger sizes.

The surface integrity for this type ulcer enables growth over extended periods without the pain associated with crater ulcers. This site reference, contains a series of convex ulcer photos. The images display a range from normal appearing growths to quite abnormal appearances. But notably, until the advanced growth stages non-crater, convex ulcers lack any surface cratering or breaks in the mucosa.

While these convex growths resemble a tumour to some extent, they are actually abnormal growths of the gastric tissue, and involve the mucosa, submucosa, muscularis, and serosa layers, not a pathogenic organism. However, these growths, like crater style ulcers, may metamorph into pathogenic growths.

Classification

By region/area

• Duodenum (called duodenal ulcer)
• Esophagus (called esophageal ulcer)
• Stomach (called gastric ulcer)
• Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)

1. Esophagus
2. Stomach
3.Ulcers
4.Duodenum
5.Mucosa
6.Submucosa
7.Muscle

When peptic ulcers occur, they can be found in either the lining of the stomach, the lining of the duodenum, or in both. Peptic ulcers that occur in the stomach are named gastric ulcers whereas ulcers found in the duodenum are referred to as duodenal ulcers. Peptic ulcers can be minor (they only go through the first or the second layers of the stomach), or can be considered a medical emergency (they go through every layer of the stomach or duodenum lining causing major internal bleeding). A peptic ulcer is a defect that occurs in the first part of the small intestine or in the lining of the stomach. Small ulcers may not be noticeable, whereas large ulcers are considered medical emergencies. Abdominal pain is a common symptom seen with multiple types of ulcers. Common causes of ulcers can be: bacterial infections in the stomach or duodenum, a weakening of the stomach lining caused by a continuous use of an anti inflammatory, or the common belief that peptic ulcers are caused by stress. http://www.wisegeek.org/what-are-ulcers.htm .

Modified Johnson classification of peptic ulcers

• Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis along the locus minoris resistantiae. Not associated with acid hypersecretion.
• Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion.
• Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.
• Type IV: Proximal gastroesophageal ulcer
• Type V: Can occur throughout the stomach. Associated with chronic use of NSAIDs (such as aspirin).

Signs and symptoms

Symptoms of a peptic ulcer can be

• abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;
• bloating and abdominal fullness;
• waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease);
• nausea, and copious vomiting;
• loss of appetite and weight loss;
• hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
• melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);
• rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain, and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy.

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the patient's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear. Usually, children and the elderly do not develop any symptoms unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for every sufferer.

Complications

• Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
• Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example is Valentino's syndrome, named after the silent-film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum.
• Perforation and penetration are when the ulcer continues into adjacent organs such as the liver and pancreas.
• Gastric outlet obstruction is the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to peptic ulcers. Patient often presents with severe vomiting without bile.
• Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.

Cause

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be increased, or as in most cases, decreased, resulting in hypo- or achlorhydria. Gastrin stimulates the production of gastric acid by parietal cells. In H. pylori colonization responses to increased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation. Studies in the varying occurrence of ulcers in third world countries despite high H. pylori colonization rates suggest dietary factors play a role in the pathogenesis of the disease.

Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort-phenomenon independent of the progress in treatment of the disease. The cohort-phenomenon is probably explained by improved standards of living which has lowered the incidence of H. pylori infections.

Although some studies have found correlations between smoking and ulcer formation, others have been more specific in exploring the risks involved and have found that smoking by itself may not be much of a risk factor unless associated with H. pylori infection. Some suggested risk factors such as diet, and spice consumption, were hypothesized as ulcerogens (helping cause ulcers) until late in the 20th century, but have been shown to be of relatively minor importance in the development of peptic ulcers. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, have not been found to affect ulcers to any significant extent. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk, and even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk factor.

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers.

Diagnosis

Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.

The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate.

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the patient has recently been taking certain drugs, such as antibiotics or proton pump inhibitors.

The diagnosis of Helicobacter pylori can be made by:

• Urea breath test (noninvasive and does not require EGD);
• Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform H. pylori cultures;
• Direct detection of urease activity in a biopsy specimen by rapid urease test;
• Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
• Stool antigen test;
• Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon atom to detect H. pylori. To perform this exam the patient will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the patient will be asked to blow into a bag that is sealed. If the patient is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the greater (large) curvature of the stomach; most are also a consequence of chronic H. pylori infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

Macroscopic appearance

A benign gastric ulcer (from the antrum) of a gastrectomy specimen.

Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.

Microscopic appearance

A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and lamina propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.

Differential diagnosis

• Gastritis
• Stomach cancer
• Gastroesophageal reflux disease
• Pancreatitis
• Hepatic congestion
• Cholecystitis
• Biliary colic
• Inferior myocardial infarction
• Referred pain (pleurisy, pericarditis)
• Superior mesenteric artery syndrome

Treatment

Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken.

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers, which are a side-effect of the NSAIDs.

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.

Ranitidine and famotidine, which are both H2 antagonists, provide relief of peptic ulcers, heartburn, indigestion and excess stomach acid and prevention of these symptoms associated with excessive consumption of food and drink. Ranitidine and famotidine are available over the counter at pharmacies, both as brand-name drugs and as generics, and work by decreasing the amount of acid the stomach produces allowing healing of ulcers.

Sucralfate (Carafate) has also been a successful treatment of peptic ulcers.

Epidemiology

Disability-adjusted life year for peptic ulcer disease per 100,000 inhabitants in 2004.

  no data

  less than 20

  20–40

  40–60

  60–80

  80–100

  100–120

  120–140

  140–160

  160–180

  180–200

  200–220

  more than 220

The lifetime risk for developing a peptic ulcer is approximately 10%. Globally, as of 2010, approximately 250,000 people died of peptic ulcer disease down from 320,000 in 1990.

In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc.). Prevalence is higher in third world countries where it is estimated at about 70% of the population, whereas developed countries show a maximum of 40% ratio. Overall, H. pylori infections show a worldwide decrease, more so in developed countries. Transmission is by food, contaminated groundwater, and through human saliva (such as from kissing or sharing food utensils).

A minority of cases of H. pylori infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort, abdominal pain or gastritis.

Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of the 20th century, when epidemiological trends started to point to an impressive fall in its incidence. The reason that the rates of peptic ulcer disease decreased is thought to be the development of new effective medication and acid suppressants and the discovery of the cause of the condition, H. pylori.

In the United States about 4 million people have active peptic ulcers and about 350,000 new cases are diagnosed each year. Four times as many duodenal ulcers as gastric ulcers are diagnosed. Approximately 3,000 deaths per year in the United States are due to duodenal ulcer and 3,000 to gastric ulcer.

History

See also: Timeline of peptic ulcer disease and Helicobacter pylori

John Lykoudis, a general practitioner in Greece, treated patients for peptic ulcer disease with antibiotics, beginning in 1958, long before it was commonly recognized that bacteria were a dominant cause for the disease.

Helicobacter pylori was rediscovered in 1982 by two Australian scientists, Robin Warren and Barry J. Marshall as a causative factor for ulcers. In their original paper, Warren and Marshall contended that most gastric ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food as had been assumed before.

The H. pylori hypothesis was poorly received, so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organisms extracted from a patient and five days later developed gastritis. His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria at the urging of his wife, since halitosis is one of the symptoms of infection. This experiment was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal.

In 1997, the Centers for Disease Control and Prevention, with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. This campaign reinforced the news that ulcers are a curable infection, and that health can be greatly improved and money saved by disseminating information about H. pylori.

In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr. Marshall and his long-time collaborator Dr. Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease." Professor Marshall continues research related to H. pylori and runs a molecular biology lab at UWA in Perth, Western Australia.

Some believed that mastic gum, a tree resin extract, actively eliminates the H. pylori bacteria. However, multiple subsequent studies have found no effect of using mastic gum on reducing H. pylori levels.

Notes

References

External links

• Gastric Ulcer
• Approach to acute upper gastrointestinal bleeding in adults (Wolters Kluwer UpToDate)

Radiology and Endoscopy from MedPix

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. 消化性潰瘍：マネージメント peptic ulcer disease management
• 2. 消化性潰瘍：臨床症状および診断 peptic ulcer disease clinical manifestations and diagnosis
• 3. 難治性または再発性の消化性潰瘍に対するアプローチ approach to refractory or recurrent peptic ulcer disease
• 4. 消化性潰瘍の合併症の概要 overview of the complications of peptic ulcer disease
• 5. 出血性消化性潰瘍の治療の概要 overview of the treatment of bleeding peptic ulcers

English Journal

• Ilaprazole for the treatment of duodenal ulcer: a randomized, double-blind and controlled phase III trial.

• Wang L, Zhou L, Hu H, Lin S, Xia J.SourceDepartment of Health Statistics (L.W, JL.X), The Fourth Military Medical University , Xi'an, Shaanxi , China.
• Current medical research and opinion.Curr Med Res Opin.2012 Jan 3. [Epub ahead of print]
• Abstract Objective: The new proton pump inhibitor (PPI), ilaprazole performed better at the dose of 10 mg/d relative to 5 or 20 mg/d in a previous phase II trial. A larger phase III trial was carried out to confirm the efficacy and safety of ilaprazole (10 mg/d) compared with omeprazole (
• PMID 22070512

• Placebo responses and placebo effects in functional bowel disorders.

• Enck P, Horing B, Weimer K, Klosterhalfen S.SourceDepartment of Psychosomatic Medicine, University Hospital Tübingen, Tübingen, Germany.
• European journal of gastroenterology & hepatology.Eur J Gastroenterol Hepatol.2012 Jan;24(1):1-8.
• The nature and determinants of the placebo response are widely unknown, as are the underlying psychological and biological mechanisms. Placebo response rates in functional bowel disorders (functional dyspepsia, irritable bowel syndrome) trials are similar to those in nonintestinal pain conditions an
• PMID 21915059

• The Intact dupA Cluster Is a More Reliable Helicobacter pylori Virulence Marker than dupA Alone.

• Jung SW, Sugimoto M, Shiota S, Graham DY, Yamaoka Y.SourceAddress correspondence to Yoshio Yamaoka, yyamaoka@bcm.tmc.edu.
• Infection and immunity.Infect Immun.2012 Jan;80(1):381-7. Epub 2011 Oct 28.
• The duodenal ulcer promoting (dupA) gene, located in the plasticity region of Helicobacter pylori, is associated with duodenal ulcer development. dupA was predicted to form a type IV secretory system (T4SS) with vir genes around dupA (dupA cluster). We investigated the prevalence of dupA and dupA cl
• PMID 22038914

Japanese Journal

• ピロリ菌除菌製剤 (特集 酸関連疾患 : 最新の診断・治療動向) -- (酸関連疾患治療薬の有用性)

• 沖本 忠義,兒玉 雅明,村上 和成
• 日本臨床 73(7), 1169-1174, 2015-07
• NAID 40020512210

• 胃潰瘍・十二指腸潰瘍 (特集 酸関連疾患 : 最新の診断・治療動向) -- (酸関連疾患の病因・病態・検査・診断・治療)

• 松井 繁長,樫田 博史,朝隈 豊 [他]
• 日本臨床 73(7), 1116-1122, 2015-07
• NAID 40020512010

• 個別化医療へ向けたバイオバンクジャパンの取り組み

• 松田 浩一
• 血液内科 70(4), 521-526, 2015-04
• NAID 40020439684

Related Pictures

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★リンクテーブル★

リンク元	「十二指腸潰瘍」「DU」
拡張検索	「hemorrhagic duodenal ulcer」
関連記事	「duodenal」

「十二指腸潰瘍」

　　[★]

英

duodenal ulcer, DU

ラ

ulcus duodeni

関

胃潰瘍、胃十二指腸潰瘍、消化性潰瘍

まとめ

• 十二指腸粘膜にびらん・潰瘍を来した病態であり、攻撃因子(ストレス、薬剤、ゾリンジャー・エリソン症候群、甲状腺機能亢進症)が防御因子(慢性肺気腫、喫煙、肝硬変、関節リウマチ、低栄養、腎不全、糖尿病、ステロイド、NSAID、ビスホスホネート)を上回ったことにより生じると考えられている。20-40歳に多く、十二指腸球部前壁に好発する。空腹時・夜間に心窩部痛を覚え、摂食により軽快、その他胸焼け・悪心嘔吐が認められることがある。吐血よりむしろ下血が認められることがある。治癒後瘢痕性の幽門狭窄による通過障害を来すことがある。再発は胃潰瘍よりも頻繁である。胃酸の分泌過多が原因と考えられているが、血中ガストリンは正常なことが多い。検査上、血清中ペプシノゲンIの上昇が認められる。

病因

参考1

• 症候性の潰瘍

• 感染

• ピロリ菌
• 単純ヘルペスウイルス
• サイトメガロウイルス
• Helicobacter heilmanni
• その他：結核菌、淋菌

• 薬物

• NSAID
• アスピリン
• 高用量のアセトアミノフェン
• ビスホスホネート(+NSAID)
• クロピドグレル(+NSAID or 高リスク患者)
• コルチコステロイド(+NSAID)
• シロリムス
• スピロノラクトン
• mycophenolate mofetil
• potassium chloride
• 抗悪性腫瘍薬(

• 内分泌

• ガストリノーマ
• 全身性肥満細胞症
• 骨髄増殖疾患における好酸球症
• 前庭部G細胞機能亢進

• 手術後

• 前庭部切除
• 胃バイパス術後

• crack cocaine使用を含めた血行不全
• (器質的な)十二指腸閉塞(輪状膵など)
• 放射線療法
• 浸潤性疾患

• サルコイドーシス
• クローン病

• 特発性の潰瘍

• 特発性過分泌十二指腸潰瘍(ピロリ菌陰性)
• 非NSAID家族性消化性潰瘍, ピロリ菌陰性
• 非NSAID消化性潰瘍, ピロリ菌陰性

• 合併症としての潰瘍

• ICUストレス潰瘍
• 肝硬変
• 臓器移植
• 腎不全
• COPD

病態

• ガストリンの分泌を十分に抑制できない。
• 壁細胞が過形成している　←ガストリンの作用
• 胃酸の基礎分泌量が上昇している
• ペプシンの分泌が増加している。
• 空腹時の血中ガストリン濃度は変わっていない

• 十二指腸潰瘍では胃潰瘍より胃酸の過剰分泌が明らかである。

• 好発部位：球部小弯側前壁
• 穿孔・穿通：潰瘍が筋層以下に進展すれば生じうるが、胃潰瘍より多い。→穿通性潰瘍　→穿孔性潰瘍

合併症

• 穿孔・穿通：穿孔性潰瘍、穿通性潰瘍

• 好発部位：球部前壁潰瘍
• 症状：突然現れる上腹部痛。前屈位・側臥位となる。上腹部腹壁緊張亢進、筋性防御、板状硬をみとめ、Blumberg徴候陽性となる。

• 出血
• 狭窄

検査

• 十二指腸球部は壁が薄いために、潰瘍により容易に変形をきたす。タッシェ(憩室様突出)をともなうクローバー城辺型が認められる。

国試

• 101D041

参考

• 1. [charged] Epidemiology and etiology of peptic ulcer disease - uptodate [1]

「DU」

　　[★] 十二指腸潰瘍 duodenal ulcer

「hemorrhagic duodenal ulcer」

　　[★]

出血性十二指腸潰瘍

「duodenal」

　　[★]

• adj.

• 十二指腸の

関

duodenum