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Achlorhydria | |
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Hydrogen chloride (major component of gastric acid)
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Classification and external resources | |
ICD-10 | K31.8 |
ICD-9 | 536.0 |
DiseasesDB | 29513 |
eMedicine | med/18 |
MeSH | D000126 |
Achlorhydria /eɪklɔərˈhaɪdriə/ or hypochlorhydria refers to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively.[1] It is associated with various other medical problems.
Irrespective of the cause, achlorhydria can result as known complications of bacterial overgrowth and intestinal metaplasia and symptoms are often consistent with those diseases:
Since acidic pH facilitates the absorption of iron, achlorhydric patients often develop iron deficiency anemia.
Bacterial overgrowth and B12 deficiency (pernicious anemia) can cause micronutrient deficiencies that result in various clinical neurological manifestations, including visual changes, paresthesias, ataxia, limb weakness, gait disturbance, memory defects, hallucinations, and personality and mood changes, should also be obtained.
Risk of particular infections, such as Vibrio vulnificus (commonly from seafood) is increased. Even without bacterial overgrowth, low stomach acid (high pH) can lead to nutritional deficiencies through decreased absorption of basic electrolytes (magnesium, zinc, etc.) and vitamins (including vitamin C, vitamin K, and the B complex of vitamins). Such deficiencies may be involved in the development of a wide range of pathologies, from fairly benign neuromuscular issues to life-threatening diseases.
For practical purposes, gastric pH at endoscopy should be done in someone with suspected achlorhydria. Older testing methods using fluid aspiration through a nasogastric tube can be done, but these procedures can cause significant discomfort and are less efficient ways to obtain a diagnosis.
A complete 24-hour profile of gastric acid secretion is best obtained during an esophageal pH monitoring study.
Achlorhydria may also be documented by measurements of extremely low levels of pepsinogen A (PgA) (< 17 mcg/L) in blood serum. The diagnosis may be supported by high serum gastrin levels (>500-1000 pg/mL).[3]
The "Heidelberg test" is an alternative way to measure stomach acid and diagnose hypochlorhydria/achlorhydria.
A check can exclude deficiencies in iron, calcium, prothrombin time, vitamin B-12, vitamin D, and thiamine. Complete blood count with indices and peripheral smears can be examined to exclude anemia. Elevation of serum folate is suggestive of small bowel bacterial overgrowth. Bacterial folate can be absorbed into the circulation.
Once achlorhydria is confirmed, a hydrogen breath test can check for bacterial overgrowth.
Treatment focuses on addressing the underlying cause of symptoms.
Treatment of gastritis that leads to pernicious anemia consists of parenteral vitamin B-12 injection. Associated immune-mediated conditions (e.g., insulin dependent diabetes mellitus, autoimmune thyroiditis) should also be treated. However, treatment of these disorders has no known effect in the treatment of achlorhydria.
Achlorhydria associated with Helicobacter pylori infection may respond to H pylori eradication therapy, although resumption of gastric acid secretion may only be partial and it may not always reverse the condition completely.[4]
Antimicrobial agents, including metronidazole, amoxicillin/clavulanate potassium, ciprofloxacin, and rifaximin, can be used to treat bacterial overgrowth.
Achlorhydria resulting from long-term PPI use may be treated by dose reduction or withdrawal of the PPI.
Little is known on the prognosis of achlorhydria, although there have been reports of an increased risk of gastric cancer.[5]
A 2007 review article noted that non-Helicobacter bacterial species can be cultured from achlorhydric (pH > 4.0) stomachs, whereas normal stomach pH only permits the growth of Helicobacter species. Bacterial overgrowth may cause false positive H. Pylori test results due to the change in pH from urease activity.[6]
Small bowel bacterial overgrowth is a chronic condition. Retreatment may be necessary once every 1–6 months.[7] Prudent use of antibacterials now calls for an antibacterial stewardship policy to manage antibiotic resistance.[8]
Experiments have shown that non-Helicobacter bacteria can induce atrophic gastritis in achlorhydric mice, which in turn can cause gastric carcinoma.[9]
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リンク元 | 「プロトンポンプ阻害薬」「低酸症」「低塩酸症」 |
プロトンポンプ H+/K+ ATPase ・・・これはNa+/K+ ATPaseと60%相同性を持つ 2,4のαサブユニットと同数のβサブユニットを含む。 αサブユニット10回膜貫通, 120-150kDa, glycoprotein αは管腔側、原形質膜まで。細胞内輸送に必要。 βサブユニットは管腔側に突き出ており、反対側は膜内に埋もれている。 休止期には小胞体内内腔へのH+,K+,Cl-の移動、分泌期には小胞は管腔の細胞膜と癒合してK+, Cl-を管腔側に排出する一方でH+を排出でしてK+を取り込む。 PPIは弱塩基性 PPIはH+と反応してPPIaとなりS-S-活性体となり、H+,K+-ATPaseのSH基と結合して不可逆的に阻害する。 比較 PPI:胃潰瘍の治癒率↑ H2R阻害薬:十二指腸潰瘍の治癒率↑ PPI問題 胃潰瘍8 十二指腸6 逆流性食道炎8 副作用 血中ガストリン↑→ECL cell↑→リバウンドが激しい week end therapy: 週末3日だけ投与後休薬 ピレンゼピン(Mi R blocker), PG(プロスタグランジン) → ガストリン↑を軽減 ラベプラゾール:ガストリン濃度を上げず酸分泌↓ →リバウンドが少ない。 PPI抵抗性潰瘍:PPIによる酸分泌抑制不十分 ①個人差によるPPIの用量不足 ②胃内でのPPIの不活性化→ 胃内容の排泄遅延。PPIが不活化、アルカリに晒される。
-hypochlorhydria
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