Gastritis - No

Japanese: 胃炎 - いえん

Histologically, it is an inflammation of the stomach wall, particularly the gastric mucosa, and advances in gastric endoscopy and gastric biopsies have made it possible to make a fairly well-founded diagnosis. In general, it is broadly divided into acute and chronic gastritis based on the clinical course and histological findings. Acute gastritis is an acute inflammation of the gastric mucosa, and the cause is often clear, whereas chronic gastritis is essentially an atrophy of the gastric mucosa, particularly the gastric glands, and there are still many unknowns about its etiology. In general, there is often no recognized causal relationship between the two, and in clinical practice they are considered to be independent diseases.

[Hisayuki Masuda and Hiromichi Arakawa]

Acute gastritis

Gastritis generally develops suddenly, has a short course, and often has a clear cause. It is usually divided into four types: acute exogenous gastritis, corrosive gastritis, acute infectious (or contagious) gastritis, and acute suppurative (or cellulitis) gastritis.

(1) Acute extrinsic gastritis This is a common type of gastritis, also known as acute gastric catarrh. It can be caused by poor diet, excessive alcohol, coffee, chemical irritation from spices, salicylic acid preparations, digitalis, iodine, antibiotics, and other drugs, overcooled or overheated foods, overeating or drinking indigestible food, or spoiled foods. In some people, it can also be caused by an allergic reaction to milk, eggs, crab, or fish. Symptoms begin a few hours after a poor diet or other cause has taken effect, with nausea, belching, and a feeling of pressure in the stomach, which gradually worsens as pain progresses, leading to vomiting. Patients may experience loss of appetite, a white coating on the tongue, and bad breath. If enteritis occurs at the same time, diarrhea may occur. The course is short, lasting from one day to one week. Treatment begins with the rapid elimination of the harmful substance that caused the disease and resting the stomach and the whole body. If it appears that the harmful substance still remains in the stomach, the back of the throat is stimulated to induce vomiting or gastric lavage is performed, and if intestinal symptoms are also present, a laxative is used. The patient is fasted for 1-2 days, starting with small amounts of weak bancha tea, and as the symptoms improve, the diet is changed to gruel, then porridge, and then regular food. Even if the symptoms disappear, lesions in the gastric mucosa will continue for several days, so it is best to keep the patient on a diet for as long as possible. Antispasmodics and antiemetics are given for pain, nausea, and vomiting, respectively. If dehydration is severe, fluid replenishment is necessary.

(2) Corrosive gastritis This occurs when a corrosive agent is accidentally ingested or consumed with the intent of suicide. These include strong acids such as sulfuric acid, hydrochloric acid, and carbolic acid, strong alkalis such as sodium hydroxide, potassium hydroxide, and ammonium carbonate, heavy metals such as mercury, silver nitrate, and arsenic compounds, formalin, and phosphorus. If the corrosive agent is diluted, acute exogenous gastritis occurs. Symptoms include corrosion of the lips and oral mucosa, and corrosive changes in the pharynx, esophagus, and stomach. Nausea and vomiting are severe, and the vomit contains blood, each of which has a unique odor. It is accompanied by severe pain in the stomach, dry mouth, and drooling. In severe cases, the patient goes into shock. The prognosis depends on the type, concentration, and amount of the corrosive agent, but in mild cases the patient can recover completely, but in severe cases the patient may die without recovering from shock. Sometimes severe complications such as glottal edema, gastric bleeding, and gastric perforation occur. In addition, after the severe inflammation has subsided, aftereffects such as esophageal stenosis and pyloric stenosis may remain. Treatment involves emergency treatment for shock, as well as gastric lavage as soon as possible using a caustic antagonist. Diet should be the same as for severely bleeding gastric ulcers.

(3) Acute infectious gastritis This is seen in infectious diseases such as typhoid, scarlet fever, pneumonia, influenza, diphtheria, and botulism (sausage poisoning). This is caused by bacterial toxins damaging the gastric mucosa, and gastritis also occurs in uremia for the same reason. Endoscopic examination reveals redness, edema, erosion, and bleeding in the gastric mucosa. The most common subjective symptom is loss of appetite, and patients often complain of a feeling of fullness in the stomach without abdominal pain. Nausea, vomiting, and hematemesis may also be seen. The course is generally good, and improves as the acute infection is cured, but it has a tendency to become chronic, so early treatment is necessary. Treatment of the underlying disease is important, and prevention is also possible. Gastric acid secretion often decreases, so a comprehensive digestive enzyme preparation is effective. A dietary therapy is carried out in which various vitamins are given in small amounts and frequently.

(4) Acute suppurative gastritis This is a rare disease caused by infection with pyogenic bacteria, which leads to cellulitis or localized abscesses in the stomach wall, especially under the gastric mucosa. It is often caused by streptococci, but can also be caused by staphylococci and Escherichia coli. It often occurs secondary to sepsis, but in rare cases it can occur due to gastric ulcers, gastric cancer, infection from a foreign body in the stomach, or the spread of suppurative inflammation to surrounding organs. Symptoms include chills and shivers, severe stomach pain, vomiting, and high fever, which develop suddenly and resemble sepsis, followed by peritonitis, circulatory disorders, and severe white blood cell increase. Diagnosis is extremely difficult, and since the symptoms are sudden and the patient's overall condition deteriorates, surgery is often performed as an acute abdominal disease. Treatment involves gastrectomy and the administration of antibiotics effective against the causative bacteria.

[Hisayuki Masuda and Hiromichi Arakawa]

Chronic gastritis

It is one of the most common diseases. With the advancement and spread of endoscopy and direct biopsy, the diagnosis of chronic gastritis, which was previously made by exclusion diagnosis using X-ray examination, is now actively performed. There is primary gastritis and associated gastritis that is accompanied or coexists with gastric cancer, benign gastric tumors, gastric or duodenal ulcers, etc. However, X-ray, endoscopic, and histological examinations cannot distinguish between the two, and essentially no difference can be found. Associated gastritis tends to be hidden behind the main lesion and not considered a problem in clinical practice. Currently, direct biopsy is the best way to diagnose it, but there are still problems with performing gastric biopsies on all patients, so endoscopic examination is performed as the second best option. However, it is true that there is a discrepancy between the diagnoses of endoscopic examination and biopsy, and this point must be taken into consideration.

Endoscopic findings can be divided into three types: superficial gastritis, in which the mucosa becomes edematous and has patchy redness; atrophic gastritis, in which the mucosa becomes thin and blood vessels become visible; and hypertrophic gastritis, in which the mucosa becomes thickened and hard in an uneven manner.Histological findings from gastric biopsy can be divided into two types: superficial gastritis, in which there is cellular infiltration on the surface of the gastric mucosa but no atrophy of the gastric glands, and atrophic gastritis, in which there is atrophy or loss of gastric glands.

The cause is largely unknown, but there is no proof that it progresses from acute gastritis. It generally begins as superficial gastritis, and during this period it can be cured with proper treatment, but as it progresses to atrophic gastritis, it becomes irreversible, and as it progresses further, it is thought that atrophy becomes more severe. The causes include both internal and external factors. The main exogenous factors are dietary errors, such as eating too quickly, not chewing properly, irregular meal times, and long-term habits of eating overcooled or overheated food and drink, as well as foods that irritate the gastric mucosa, fatty roasted foods, indigestible foods, foods with strong sour or sweet tastes, and regular use of spices, coffee, alcohol, and tobacco. Other causes include drugs such as salicylic acid preparations, digitalis, antibiotics, anticancer drugs, and arsenic, bacterial infections such as staphylococcus aureus, and X-ray exposure. Endogenous factors that are considered to be important include genetics, aging, infectious diseases such as acute pneumonia, sinusitis, tonsillitis, and periodontitis, endogenous poisoning such as uremia, circulatory disorders such as arteriosclerosis and cirrhosis of the liver, diseases of the organs surrounding the stomach such as the liver, bile duct, and pancreas, and reflux of duodenal juice into the stomach.

There are no specific symptoms, and they often occur regardless of histological changes in the gastric mucosa. Common symptoms include abdominal pain, stomach bloating or discomfort, nausea, vomiting, loss of appetite, weight loss, heartburn, and belching, but there are also many asymptomatic cases. It is characterized by repeated acute exacerbations, and at such times patients often visit a doctor complaining of subjective symptoms. Symptoms are aggravated by poor dietary habits, lack of sleep, overwork, and mental stress. Gastric acid secretion decreases depending on the degree of atrophic changes, and in severe cases, achlorhydria occurs.

In cases where there are no symptoms, no special treatment is usually performed, but it is necessary to prevent the progression of atrophy and remove the causes of acute exacerbation. It is also important to remove substances harmful to the gastric mucosa and to ensure mental and physical rest. Eat bland meals 5 to 6 times a day and chew thoroughly, but do not become too concerned about dietary therapy. If necessary, adjust dentures and avoid using drugs that damage the gastric mucosa. Eliminate stress and strive to live a regular life. Drug therapy is performed according to symptoms. Antacids are effective for heartburn and are also effective for achlorhydria. Anticholinergics and local anesthetics are effective for abdominal pain, and sedatives and tranquilizers are administered for nervous patients or those with a strong tendency toward psychosomatic disorders, and general digestive enzyme preparations are administered for achlorhydria, and iron preparations and vitamin _B12 are administered for anemia.

[Hisayuki Masuda and Hiromichi Arakawa]

Special types of chronic gastritis

(1) Erosive gastritis Chronic multiple erosions are seen on the tops of small protuberances that line the course of the gastric mucosal folds, and because they resemble the suckers on the legs of an octopus, they are called "octopus wart" erosive gastritis. Symptoms include upper abdominal hunger pain, stomach discomfort, heartburn, belching, and repeated vomiting of blood, but most symptoms are mild, and like duodenal ulcers, many cases show increased gastric acid secretion. Diagnosis is largely based on endoscopic examination, which is essential to determine whether there is bleeding from the erosions and the stage of the disease, such as the acute or healing stage. Gastric and duodenal ulcers may occur together. The prognosis is generally good, but there is a tendency for recurrence depending on the season. Treatment is similar to that for gastric and duodenal ulcers, but no treatment is required if there are no symptoms.

(2) Giant hypertrophic gastritis Described by Pierre Menétrier (1859-1935) in 1888, this disease is also known as Menétrier's disease. The gastric mucosa is abnormally thickened, with giant, tortuous, somewhat hard folds, and is accompanied by hypoproteinemia. It has been proven in recent years that the cause is the leakage of a large amount of albumin into the gastric juice, and this disease has been attracting attention as one of the protein-losing gastroenteropathy diseases. Symptoms include stomach pain or discomfort, nausea and vomiting, loss of appetite, diarrhea, gastrointestinal bleeding, edema, and weight loss, but there are also cases where there are no symptoms. Antacids are effective for treating stomach symptoms. For hypoproteinemia, infusion of plasma or amino acid preparations and a high-protein diet are given, but in severe cases, total gastrectomy is considered.

In addition to the above, there are other types of so-called special gastritis, such as gastric tuberculosis and gastric syphilis, but both are rare.

[Hisayuki Masuda and Hiromichi Arakawa]

Source: Shogakukan Encyclopedia Nipponica About Encyclopedia Nipponica Information | Legend

Japanese:

組織学的に胃壁ことに胃粘膜の炎症で、胃内視鏡検査や胃生検の進歩により、かなり根拠をもって診断がつけられるようになった。一般に、臨床経過や組織学的所見から急性胃炎と慢性胃炎に大別される。急性胃炎は胃粘膜の急性炎症で、原因の明らかなことが多いが、慢性胃炎は本質的には胃粘膜とくに胃腺(いせん)の萎縮(いしゅく)であるが、その成因についてはなお不明の点が多い。一般に、この両者の間には因果関係は認められないことが多く、診療上それぞれ独立した疾患と考えられる。

［増田久之・荒川弘道］

急性胃炎

一般に急激に発病し、経過は短く、明らかな原因を指摘できることが多い胃炎で、普通、急性外因性胃炎、腐食性胃炎、急性感染性（または伝染性）胃炎、急性化膿(かのう)性（または蜂巣炎(ほうそうえん)性）胃炎の四つに分けている。

(1)急性外因性胃炎　普通にみられる胃炎で、急性胃カタルともいわれる。食事の不摂生、過度のアルコール、コーヒー、香辛料やサリチル酸製剤、ジギタリス、ヨード剤、抗生物質などの薬剤の化学的刺激、過冷または過熱の食品、不消化物の暴飲暴食、腐敗した食品などで発病するほか、特定の人では牛乳、卵、カニ、魚肉などを食べるとアレルギー反応で発病する。症状は、食事の不摂生などの原因が作用したあと数時間たってから、悪心(おしん)、げっぷ、胃部圧迫感などで始まり、しだいに疼痛(とうつう)が増大して嘔吐(おうと)をみる。食欲不振や舌に白苔(はくたい)と口臭を認める。腸炎を併発すると下痢がみられる。経過は短く1日から1週間である。治療はまず、病因となった有害物の速やかな排除と、胃および全身の安静で、有害物がまだ胃内に残っていると思われるときは、のどの奥を刺激して嘔吐させるか、または胃洗浄を行い、腸の症状を伴っているときは下剤を用いる。1～2日絶食させ、薄い番茶の少量から始めて、症状が軽快するにつれて、重湯(おもゆ)からしだいに粥(かゆ)、常食に移行する。自覚症状が消失しても胃粘膜の病変は数日間続くので、できるだけ長く食事療法をさせるほうがよい。疼痛や悪心、嘔吐に対してはそれぞれ鎮痙(ちんけい)剤や制吐剤を与える。脱水症状の激しいときは、水分の補給が必要である。

(2)腐食性胃炎　腐食性薬剤の誤飲または自殺の目的で飲用した場合におこる。硫酸、塩酸、石炭酸などの強酸や、水酸化ナトリウム、水酸化カリウム、炭酸アンモニウムなどの強アルカリ、昇汞(しょうこう)、硝酸銀、ヒ素化合物などの重金属、ホルマリン、リンなどである。腐食剤が薄ければ急性外因性胃炎がおこる。症状は口唇、口腔(こうくう)粘膜に腐食を認め、咽頭(いんとう)、食道および胃に腐食性変化が現れる。悪心、嘔吐が激しく、吐物に血液が混じり、それぞれ特有の臭気を放つ。胃部の激痛、口渇とよだれを伴う。重症ではショックに陥る。予後は腐食剤の種類、濃度、量によるが、軽症では完全に治りうるが、重症ではショックが回復しないまま死亡することがある。ときに声門浮腫(ふしゅ)、胃出血、胃穿孔(せんこう)などの重篤な合併症をおこす。また重篤な炎症の治ったのちに、食道狭窄(きょうさく)や幽門狭窄などの後遺症を残すこともある。治療は、ショックに対する救急処置と並行して、腐食剤に拮抗(きっこう)する薬剤でできるだけ早期に胃洗浄をする。食事は厳重な出血性胃潰瘍(かいよう)の場合と同様にする。

(3)急性感染性胃炎　腸チフス、しょうこう熱、肺炎、インフルエンザ、ジフテリア、ボツリヌス中毒（ソーセージ中毒）などの感染症の際にみられる。これは細菌毒素が胃粘膜を障害しておこるもので、尿毒症の際にも同様の理由で胃炎がおこる。内視鏡検査で胃粘膜に発赤、浮腫、びらんと出血を認める。自覚症状では食欲不振がもっとも多く、腹痛はなく胃部膨満感を訴えることが多い。悪心、嘔吐、吐血をみることもある。経過は一般に良好で、急性感染症の治癒とともに軽快するが、慢性化する傾向があるので、早期治療が必要である。治療は原疾患の治療がたいせつで、これにより予防も可能である。胃酸分泌の低下することが多いので、総合消化酵素剤は有効である。各種ビタミンを与え、少量ずつ回数を多くした食事療法を行う。

(4)急性化膿性胃炎　化膿菌の感染によって胃壁ことに胃粘膜下に蜂巣炎、あるいは限局性の膿瘍をおこすもので、まれな疾患である。連鎖球菌でおこることが多く、ブドウ球菌、大腸菌なども原因となる。敗血症から二次的におこることが多いが、まれに胃潰瘍、胃癌(いがん)、胃内異物からの感染、周囲臓器の化膿性炎症の波及でおこることもある。症状は、悪寒戦慄(せんりつ)、胃部激痛、嘔吐、高熱などの敗血症様症状で急激に発病し、ついで腹膜炎症状をきたし、循環障害、高度の白血球増加を認める。診断はきわめて困難で、症状が急激で全身状態が不良となるので、急性腹症として手術されることが多い。治療は胃切除術とともに、原因菌に有効な抗生物質の投与を行う。

［増田久之・荒川弘道］

慢性胃炎

もっともありふれた疾患の一つである。内視鏡検査と直視下生検法の進歩、普及により、これまでX線検査による除外診断でなされていた慢性胃炎の診断が、積極的に行われるようになった。原発性胃炎と、胃癌、胃の良性腫瘍、胃・十二指腸潰瘍などに随伴または共存する随伴性胃炎とがある。しかしX線、内視鏡および組織学的検査でも両者の区別をつけることはできず、本質的に差は認められない。随伴性胃炎は主病変の陰に隠れて、診療上問題にされない傾向がある。現在では直視下生検によって診断することが最良であるが、すべての患者に胃生検をするのには、なお問題があるので、次善の策として内視鏡検査が行われる。しかし、内視鏡検査と生検の診断との間には不一致があるのは事実で、この点考慮しなければならない。

　内視鏡所見から、粘膜が浮腫状となり斑(はん)状の発赤がみられる表層性胃炎、粘膜が薄くなって血管がみえる萎縮性胃炎、粘膜が凹凸に肥厚して硬くなった肥厚性胃炎の3型に分けられ、また胃生検による組織所見から、胃粘膜表層に細胞浸潤があり、胃腺の萎縮のない表層性胃炎と、胃腺の萎縮、消失のある萎縮性胃炎の2型に分けられる。

　成因は不明の点が多いが、急性胃炎からの移行については確証はない。一般に表層性胃炎として始まり、この期間には適正な治療によって治りうるが、進行して萎縮性胃炎になると非可逆性となり、さらに進行して萎縮がより高度になると考えられる。その原因として内・外因性要素があげられる。外因性要素のおもなものは食事の過誤で、早食い、そしゃく不十分、食事時間の不規則、過冷または過熱飲食物摂取の習慣が長く続いた場合、また胃粘膜を刺激する食品、脂肪のあぶり焼きしたもの、不消化物、酸味または甘味の強いもの、香辛料、コーヒー、アルコール、たばこの常用などである。サリチル酸製剤、ジギタリス、抗生物質、抗癌剤、ヒ素などの薬剤やブドウ球菌などの細菌感染、X線照射が原因となることもある。内因性要素としては、遺伝、加齢、急性肺炎、副鼻腔炎、扁桃(へんとう)炎、歯周炎などの感染症、尿毒症などの内因性中毒、動脈硬化、肝硬変などの循環障害、肝・胆道・膵(すい)など胃周囲臓器の疾患、また十二指腸液の胃内逆流も重視されている。

　症状は特有のものはなく、胃粘膜の組織学的変化と無関係に出没することが多い。一般に腹痛、胃部膨満感または不快感、悪心、嘔吐、食欲不振、体重減少、胸やけ、げっぷなどがよくみられるが、無症状のものが少なからずみられる。急性増悪を繰り返すのが特徴で、そのときに自覚症状を訴えて医師を訪れることが多い。食事の不摂生や睡眠不足、過労、精神的ストレスなどが症状を悪化させる。萎縮性変化の程度に応じて胃酸分泌の低下がみられ、高度の場合には無酸症となる。

　治療は、症状のない場合にはとくに治療を行わないのが普通であるが、萎縮の進行を阻止し、急性増悪の原因を除去することは必要であり、胃粘膜に対する有害物を除き、心身の安静を図ることがたいせつである。刺激の少ない食事を1日5～6回に分けてとり、十分なそしゃくを心がけるが、食事療法にあまり神経質になりすぎないようにする。必要なら義歯を整え、胃粘膜に障害を与える薬剤の使用を避ける。ストレスを去り、規則正しい生活に努める。薬物療法は症状に応じて行う。胸やけには制酸剤がよく、無酸症でも効果がある。腹痛には抗コリン剤、局所麻酔剤が有効、神経質な場合や心身症傾向の強い場合は鎮静剤、精神安定剤、無酸症には総合消化酵素剤、貧血のある場合は鉄剤、ビタミンB₁₂を投与する。

［増田久之・荒川弘道］

慢性胃炎の特殊型

(1)びらん性胃炎　慢性多発性びらんで、胃粘膜ひだの走行に沿って並ぶ小隆起の頂上にびらんがみられ、一見タコの足の吸盤に似ていることから「タコいぼ型」びらん性胃炎といわれる。症状は、上腹部の空腹痛、胃部不快感、胸やけ、げっぷ、繰り返す吐血などであるが、症状の軽いものが多く、十二指腸潰瘍と同じく、胃酸分泌亢進(こうしん)を示すものが多い。診断は内視鏡検査によるところが大きく、びらんからの出血の有無、急性期や治癒期などの病期の判定に不可欠である。胃・十二指腸潰瘍を合併することがある。予後は一般に良好であるが、四季による再発傾向がある。治療は胃・十二指腸潰瘍の治療に準ずるが、無症状の場合はとくに治療の必要はない。

(2)巨大肥厚性胃炎　1888年メネトリエPierre Menétrier（1859―1935）によって記載され、メネトリエ病ともいわれている。胃粘膜が異常に肥厚し、蛇行したやや硬い感じの巨大なひだがみられ、低タンパク血症を伴う。その原因として多量のアルブミンが胃液中に漏出することが近年証明され、タンパク漏失性胃腸症の一つとして注目されている。症状は、胃部痛または不快感、悪心および嘔吐、食欲不振、下痢、消化管出血、浮腫、体重減少などであるが、無症状の場合もある。治療は、胃の症状には制酸剤が有効である。低タンパク血症には血漿(けっしょう)製剤やアミノ酸製剤の輸液、高タンパク食を与えるが、高度の場合は胃全摘を考慮する。

　なお、以上のほか、特殊性胃炎といわれるものに胃結核と胃梅毒があるが、いずれもまれである。

［増田久之・荒川弘道］

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