Malabsorption syndromes

Japanese: 吸収不良症候群

Definition and classificationMalabsorption syndromes are primarily syndromes that present with a variety of pathological conditions and clinical symptoms due to impaired absorption of nutrients. The mechanism of nutrient absorption is divided into the phase of processing in the digestive lumen, the phase of absorption in the intestinal mucosa, and the phase of processing in the small intestinal absorptive epithelial cells and transport to the systemic circulation, and these syndromes can be classified based on disorders in each phase. From a pathophysiological perspective, maldigestion of nutrients can be considered a different mechanism from malabsorption, but digestive disorders and absorption disorders are closely related to each other, and clinically these syndromes are treated as a comprehensive combination of digestion and malabsorption.
PathophysiologyThe pathophysiology of malabsorption syndromes is classified into primary malabsorption caused by congenital defects or functional abnormalities in brush border membrane transporters in small intestinal absorptive epithelial cells, secondary malabsorption caused by acquired damage to absorptive epithelial cells, and intraluminal digestion/brush border membrane malabsorption.According to the Research Group for Specific Disease Digestive and Absorbent Disorders (then the Ministry of Health, Labor and Welfare), the most common underlying diseases are exocrine pancreatic disorders (35.1%), Crohn's disease (11.4%), post-small intestinal resection (10.9%: 4.7% of which are short bowel syndrome with less than 100cm of remaining small intestine), post-pancreatectomy (10.0%: 4.3% of which are total pancreatectomy), and post-gastrectomy (9.0%: 4.3% of which are total gastrectomy), and primary malabsorption is considered rare in Japan.
Ingested nutrients undergo digestion by pancreatic enzymes in the digestive tract, then membrane digestion by brush border membrane enzymes, followed by absorption by active transport by transport carriers or passive diffusion, metabolism within the absorbing cells, and then metabolization mainly in the liver via the portal vein and lymphatic vessels. Based on the pathology of this digestive and absorptive process, diseases are clinically classified into intraluminal digestive disorder type, intestinal mucosal digestive and absorptive disorder type, and transport pathway disorder type (Table 8-5-18).
1) Intraluminal digestive disorder type:
The majority of dietary fats are long-chain fats with 14 or more carbon atoms. Intraluminal digestion of fat begins with the formation of an emulsion due to chewing and intragastric churning, followed by partial hydrolysis by acid-stable lingual lipase and gastric lipase, and the fatty acids released during this process are involved in stimulating pancreatic lipase secretion. Long-chain fats are broken down into long-chain fatty acids and monoglycerides by the action of pancreatic lipase and then absorbed. For efficient digestion by pancreatic lipase, it is important to have an increase in intraluminal pH (optimum pH 6.5) due to the promotion of pancreatic bicarbonate secretion via secretin secretion caused by hydrogen ions flowing into the duodenum, micelle formation by bile salts, and the presence of pancreatic colipase. Therefore, in addition to pancreatic exocrine insufficiency, fat absorption disorders can also be caused by gastric churning disorders, decreased intraluminal pH in the small intestine in achlorhydria or Zollinger-Ellison syndrome, disorders of bile acid synthesis and bile secretion in hepatic and biliary diseases, reduced bile acid pools due to disorders of the bile acid enterohepatic circulation caused by ileal lesions or ileal resection, and deconjugation of bile acids due to bacterial overgrowth in blind loop syndrome.
Carbohydrates that humans can digest and absorb include polysaccharides such as starch, disaccharides such as sucrose and lactose, and monosaccharides such as glucose, and the monosaccharides that are actually absorbed through the absorptive epithelial cells of the small intestine are glucose, galactose, and fructose. Plant polysaccharides such as cellulose are not digested in the small intestine, but are fermented by intestinal bacteria in the large intestine. Ingested carbohydrates are broken down into α-restricted dextrin and disaccharides in the small intestinal lumen by amylase in saliva and pancreatic juice, and are further broken down into monosaccharides by brush border membrane disaccharidase, after which they are absorbed by transporters specific for each monosaccharide (see below). Therefore, intraluminal digestive disorders are primarily due to exocrine pancreatic insufficiency.
Most of the proteins ingested through food are partially digested by pepsin activated in the acidic environment of the stomach, and the released amino acids stimulate CCK secretion from the duodenal and small intestinal mucosa, promoting the secretion of pancreatic enzymes. Proteins are broken down into oligopeptides in the small intestinal lumen by trypsin, chymotrypsin, and elastase in the pancreatic juice. Oligopeptides are broken down into free amino acids or di- or tripeptides by peptidases on the surface of the brush border membrane, and are absorbed by specific transport carriers (see below). At this time, the conversion of pancreatic enzymes secreted as proenzymes into their active forms requires hydrolysis of peptide bonds by enteropeptidase (enterokinase), which is released from the microvilli of duodenal absorptive cells by bile salts.
2) Intestinal mucosal digestive and absorptive disorder:
Intraluminal digested fat hydrolysis products form micelles or ribosomes with bile salts, facilitating passage through the microvilli lipid membrane of absorptive epithelial cells. In this case, bile salts are not absorbed, but reach the terminal ileum and are reabsorbed and enter the bile acid pool via enterohepatic circulation. Fatty acid absorption was thought to be by passive diffusion, but the recent cloning of human fatty acid transport protein (hsFATP4) revealed the existence of an active transport process for long-chain fatty acids. Absorbed fatty acids are resynthesized into triglycerides in absorptive epithelial cells, and then associate with cholesterol esters, phospholipids, and apoproteins to form chylomicrons, which are then transported to the systemic circulation via the intestinal lymphatics. In this case, fatty acid-binding proteins (FABPs) are involved in the intracellular transport of intracellular metabolic fatty acids. In addition, beta-lipoprotein deficiency is thought to be a factor in the intestinal absorption intracellular lipid metabolism disorder. In contrast, medium-chain fatty acids with carbon chains of 6 to 12 are efficiently absorbed from the gastric mucosa and intestinal epithelium and transported to the portal vein.
On the other hand, it has been revealed that digestive enzymes and transporters are present in the intestinal absorptive epithelial brush border membrane for the digestion and absorption of carbohydrates and amino acids through the intestinal mucosa, and disorders of digestion and absorption through the intestinal mucosa caused by these disorders are called brush border membrane disease (Table 8-5-19).
Carbohydrates that are broken down into α-restricted dextrin and disaccharides during intraluminal digestion are broken down into monosaccharides by disaccharidases present in the brush border membrane, and are then absorbed by transporters specific to each monosaccharide. SGLT1 (Na/glucose cotransporter) and GLUT5 (fructose transporter) are expressed in the brush border membrane of small intestinal absorptive epithelial cells, and GLUT2 is expressed in the basement membrane. Congenital glucose and galactose malabsorption is characterized by watery diarrhea due to sugar malabsorption that begins early in life, but it has been revealed to be an autosomal recessive genetic disease caused by a congenital deficiency of SGLT1 function.
Free amino acids that are broken down into free amino acids during intraluminal digestion are absorbed by transporters specific for acidic, neutral, and basic amino acids. Meanwhile, oligopeptides that reach the small intestine are broken down into amino acids by peptidases on the brush border membrane, but the peptide transporter PepT1 absorbs di- and tripeptides by co-transporting them with hydrogen ions. Brush border membrane peptidases are broadly divided into aminopeptidases that act on the N-terminus of peptides and carboxypeptidases that act on the C-terminus (aminopeptidase A, N, W, dipeptidyl aminopeptidase IV, dipeptidyl carboxypeptidase, carboxypeptidase P, M, endopeptidase 24,11, glutathione dipeptidase, dipeptidase). At least eight types of brush border membrane amino acid transporters are known to be expressed. These include the ASC system transporters (SNAT, ASCT1), the K ⁺ Na ⁺ glutamate transporter (EAAC1), the neutral and basic amino acid transporters (rBAT/D2/NBAT, 4F2hc), the arginine transporter (mCAT), and the peptide transporter (PepT1). In Hartnup disease, the neutral amino acid transporter is defective, in blue diaper syndrome, the transport of tryptophan alone is impaired, and in cystinuria, the cotransporter of four amino acids, cystine, lysine, arginine, and ornithine, is defective. However, there are still many unknowns regarding the involvement of these brush border membrane enzymes and transporters in the etiology and pathology of malabsorption syndromes.
It is known that an acquired decrease in the effective absorption area occurs due to various underlying diseases. Extensive small intestinal resection is a typical example. In patients with short bowel syndrome, where the remaining small intestine is 50 cm or less, it is difficult to absorb sufficient nutrients to maintain life, and they have no choice but to rely on total parenteral nutrition. In addition, malabsorption syndromes seen in Crohn's disease, which is accompanied by extensive small intestinal lesions, and celiac sprue, which causes diffuse intestinal villous atrophy, also fall into the broad category of malabsorption syndromes caused by intestinal mucosal digestive and absorptive disorders.
3) Transport pathway obstruction type:
Fat is resynthesized in intestinal absorptive cells, bound to lipoproteins, and transported to the lacteal cavity, where it flows from the intestinal lymphatics to the thoracic duct lymphatics, enters the general circulation, and is transported throughout the body. Therefore, obstruction of lymphatic vessels due to Crohn's disease, Whipple's disease, or lymphoma, or lymphatic dysplasia, causes impaired fat digestion and absorption. Furthermore, carbohydrates and proteins are transported via the portal vein to the liver where they are metabolized, but disorders of the vascular system, such as liver disease, cause intestinal congestion, which affects absorption.
Clinical symptoms and diagnosis The diagnostic criteria for this disease, according to the Ministry of Health and Welfare's Research Group on Specific Diseases for Digestive and Absorbent Disorders (1985 Achievements), are as follows: 1) frequent symptoms include diarrhea, fatty stools, weight loss, emaciation, anemia, lethargy, abdominal distension, edema, and gastrointestinal bleeding (including occult blood in the feces); 2) frequent reductions in nutritional indicators such as serum protein (6 g/dL or less), albumin, total cholesterol (120 mg/dL or less), and serum iron; and 3) abnormalities in digestive and absorptive tests. This disease is strongly suspected when there is a large amount of stool (steatorrhea) that is pale-colored, oily, shiny, and foul-smelling, and there is weight loss relative to the amount of food consumed. To confirm this disease, it is useful to test for fecal fat, as fat is the most susceptible to digestive and absorptive disorders. Fat absorption disorder is diagnosed when 10 or more lipid droplets are found in one field of a Sudan III stained fecal smear under a 100x microscope in a patient with a normal diet of approximately 50 g fat/day, or when daily fecal fat is 6 g or more by the van de Kamer method in a patient with a normal diet (up to 100-125 g fat/day). If abnormalities in fecal fat are found, it is clear that there is a digestive and absorptive disorder, and a d-xylose absorption test is performed to distinguish whether this is due to intraluminal digestive disorder or intestinal mucosal digestive and absorptive disorder. If it is the former, pancreatic and biliary function is evaluated using a pancreatic exocrine function test (PFD: BT-PABA method). If it is the latter, the underlying disease is identified using a combination of gastrointestinal X-rays, abdominal ultrasound, CT, endoscopic examination, and biopsy. If ileal lesions are suspected, a vitamin _B12 absorption test and a bile acid loading test are useful. Celiac sprue is a typical small intestinal disease that causes digestive and absorptive disorders of the intestinal mucosa. Gluten is involved in the pathology, and the disease is accompanied by crypt hyperplasia, resulting in the loss of normal villus morphology and the appearance of "flat mucosa." This condition is rare in Japan. Recently, attention has been focused on diarrhea and malabsorption in immunodeficiency, especially AIDS, and many of these cases are caused by opportunistic infections.
On the other hand, it is also important to keep in mind the existence of selective nutrient absorption disorders, such as pernicious anemia, although these are rare.
TreatmentThe principle of treatment for this disease is to first improve the malnutrition, then identify the underlying disease or pathology causing the digestive and absorptive disorder and provide fundamental treatment. To objectively evaluate the nutritional state, it is important to perform a nutritional assessment using physical measurements, body composition, blood and urine biochemical tests, immune function, metabolism, and muscle strength as indicators, and measurement of short half-life proteins is a useful indicator of improvement of malnutrition. If the digestive and absorptive disorder is mild, a high-energy, high-protein, high-vitamin diet should be administered, with 30 to 40 g of fat per day in the diet. If the patient has intraluminal digestive disorder, digestive enzyme preparations should be administered as replacement therapy, with 3 to 5 times the usual dose or high-potency digestive enzyme preparations. If oral intake is difficult due to digestive symptoms or the condition, enteral nutrition using elemental or semi-digested nutrients or total parenteral nutrition should be considered. In this case, it is necessary to always pay attention to setting the amount of calories administered appropriate for maintaining physical activity and supplementing trace elements, etc. [Fujiyama Yoshihide]
■ References <br /> Tadao Baba: Malabsorption syndrome. Latest Internal Medicine Series, Special Volume 3 (separate volume), Internal Medicine Clinical Reference Book, Diseases Volume II, pp150-156, Nakayama Shoten, Tokyo, 1998.
Mason JB: Mechanisms of nutrient absorption and malabsorption. In: UpToDate (La Mont JT ed), UpToDate, Wellesley, 2012.
Ishikawa, Makoto, Takahashi, Tsuneo: Epidemiological survey report. Ministry of Health, Labour and Welfare, Specific Disease Digestive and Absorption Disorders Research Group, 1982 Achievement Collection, pp15-26, 1983.
Tomoyuki Tsujikawa, Masahiro Uda, et al.: Morphology and function of the small intestine. Gastroenterology, 35: 483-489, 2002.

Table 8-5-18
Classification of malabsorption syndromes based on their pathology (partially modified from Baba, 1998)

Table 8-5-18

Table 8-5-19
Brush border membrane disease (partially modified from Baba, 1998)

Table 8-5-19

Source : Internal Medicine, 10th Edition About Internal Medicine, 10th Edition Information

Japanese:

定義・分類
　吸収不良症候群は一義的には栄養素の吸収障害により種々の病態・臨床症状を呈する症候群をいう．栄養素の吸収機構は消化管管腔での処理相，腸管粘膜での吸収相，そして小腸吸収上皮細胞での処理と全身循環への移送相に分けられ，各相での障害から本症候群を分類することができる．病態生理的には，栄養素の消化不良（maldigestion）は，吸収不良（malabsorption）とは異なる機序としてとらえることができるが，消化障害と吸収障害は互いに密接に関連するものであり，臨床的に本症候群は消化・吸収不良を包括して取り扱う．
病態生理
　吸収不良症候群の病態生理は，小腸吸収上皮細胞の刷子縁膜輸送担体の先天的な欠損や機能的異常による原発性吸収不良と，後天的な要因による吸収上皮細胞傷害による続発性吸収不良，そして管腔内消化・刷子縁膜消化不良に分類される．厚生省（当時）特定疾患消化吸収障害調査研究班によれば，原疾患の頻度は膵外分泌障害（35.1％），Crohn病（11.4％），小腸切除後（10.9％：うち残存小腸100cm未満の短腸症候群4.7％），膵切除後（10.0％：うち膵全摘4.3％），胃切除後（9.0％：うち胃全摘4.3％）が多くを占め，原発性吸収不良はわが国ではまれとされる．
　摂取された栄養素は，消化管内での膵酵素による消化，ついで，刷子縁膜酵素による膜消化と，それに続く輸送担体による能動輸送あるいは受動拡散による吸収，そして吸収細胞内での代謝を受け，門脈やリンパ管を経て主として肝で代謝される過程を経る．この消化吸収過程の病態から管腔内消化障害型，腸粘膜消化吸収障害型と輸送経路障害型に臨床的には病型分類される（表8-5-18）．
1）管腔内消化障害型：
食事中脂肪の大部分は炭素鎖が14以上の長鎖脂肪である．脂肪の管腔内消化は咀嚼と胃内攪拌によるエマルジョン形成に始まり，acid-stableなlingual lipaseとgastric lipaseによる部分水解を受け，ここで遊離された脂肪酸が膵リパーゼ分泌刺激に関与する．長鎖脂肪は膵リパーゼの作用により長鎖脂肪酸とモノグリセリドに分解されて吸収される．この際，膵リパーゼによる効率的な消化には，十二指腸内に流入した水素イオンによるセクレチン分泌を介した膵重炭酸分泌促進による管腔内pHの上昇（至適pH6.5），胆汁酸塩によるミセル形成，膵コリパーゼの存在が重要である．したがって，膵外分泌機能不全以外にも，胃での攪拌障害，無酸あるいはZollinger-Ellison症候群での小腸管腔内pHの低下，また肝胆道疾患での胆汁酸合成や胆汁分泌障害，回腸病変や回腸切除による胆汁酸腸肝循環障害による胆汁酸プールの減少，盲係蹄症候群での細菌異常増殖による胆汁酸の脱抱合などによっても脂肪吸収障害が生じる．
　ヒトが消化吸収できる糖質はでんぷんなどの多糖類やスクロース・ラクトースなどの二糖類，さらにグルコースなどの単糖類であり，実際に小腸吸収上皮細胞から吸収されるのはグルコース，ガラクトース，フルクトースの単糖類である．セルロースなどの植物性多糖類は小腸では消化されず，大腸で腸内細菌により発酵を受ける．摂取された糖質は唾液や膵液中のアミラーゼにより小腸管腔内でα制限デキストリンや二糖類まで分解され，さらに刷子縁膜二糖類分解酵素によって単糖類に分解された後，それぞれの単糖類に特異的な輸送担体によって吸収される（後述）．したがって，管腔内消化障害は主として膵外分泌機能不全による．
　食事により摂取された蛋白質の大部分は，胃の酸性環境下で活性化されたペプシンで部分消化され，遊離されたアミノ酸は十二指腸・小腸粘膜からのCCK分泌を刺激し膵酵素分泌を促す．蛋白質は膵液中のトリプシン，キモトリプシン，エラスターゼにより小腸管腔内でオリゴペプチドに分解される．オリゴペプチドは刷子縁膜表面のペプチダーゼにより遊離アミノ酸あるいはジ・トリペプチドまで分解され，それぞれ特異的な輸送担体により吸収される（後述）．この際，プロエンザイムとして分泌された膵酵素の活性型への変換には胆汁酸塩によって十二指腸吸収細胞の微絨毛から遊離されるエンテロペプチダーゼ（エンテロキナーゼ）によるペプチド結合の水解を必要とする．
2）腸粘膜消化吸収障害型：
管腔内消化された脂肪水解産物は胆汁酸塩とミセルあるいはリボソームを形成し，吸収上皮細胞微絨毛脂質膜の通過を容易にする．この際，胆汁酸塩は吸収されず終末回腸部に至り再吸収され腸肝循環により胆汁酸プールに入る．脂肪酸の吸収は受動拡散によると考えられていたが，最近になってhuman fatty acid transport protein（hsFATP4）がクローニングされたことにより，長鎖脂肪酸の能動輸送過程の存在が明らかにされた．吸収された脂肪酸は吸収上皮細胞内でトリグリセリドに再合成されコレステロールエステル，リン脂質とアポ蛋白と会合してカイロミクロンを形成して腸管リンパ管を介して全身循環に移送される．この際，細胞内代謝脂肪酸の細胞内輸送に脂肪酸結合蛋白（FABP）が関与する．また，βリポ蛋白欠損症は腸吸収細胞内脂肪代謝障害の要因となると考えられる．これに対して，炭素鎖が6～12の中鎖脂肪酸は胃粘膜や腸上皮から効率よく吸収され門脈に移送される．
　一方，糖質，アミノ酸の腸粘膜消化吸収には腸吸収上皮刷子縁膜に消化酵素，輸送担体の存在することが明らかにされ，その障害による腸粘膜消化吸収障害は刷子縁膜病（brush border membrane disease）と称されている（表8-5-19）．
　管腔内消化にてα制限デキストリンや二糖類に分解された糖質は，刷子縁膜に存在する二糖類分解酵素によって単糖類まで分解された後，それぞれの単糖類に特異的な輸送担体によって吸収される．小腸吸収上皮細胞の刷子縁膜にはSGLT1（Na/グルコース共輸送担体），GLUT5（フルクトース輸送担体）が，同基底膜にはGLUT2が発現している．先天性グルコース・ガラクトース吸収不良は生後早期より始まる糖の吸収不良による水様下痢を主症状とするが，SGLT1機能が先天的に欠損した常染色体劣性遺伝性疾患であることが明らかにされている．
　管腔内消化にて遊離アミノ酸にまで分解された遊離アミノ酸は，酸性・中性・塩基性アミノ酸それぞれに特異的な輸送担体により吸収される．一方，小腸に達したオリゴペプチドは刷子縁膜上のペプチダーゼによりアミノ酸まで分解されるが，ペプチド輸送担体PepT1は水素イオンとの共輸送によりジ・トリペプチドを吸収する．刷子縁膜ペプチダーゼはペプチドのN末端に作用するアミノペプチダーゼとC末端に作用するカルボキシペプチダーゼに大別される（アミノペプチダーゼA，N，W，ジペプチジルアミノペプチダーゼⅣ，ジペプチジルカルボキシペプチダーゼ，カルボキシペプチダーゼP，M，エンドペプチダーゼ24,11，グルタチオンジペプチダーゼ，ジペプチダーゼ）．刷子縁膜アミノ酸輸送担体は少なくとも8種類の発現が知られている．すなわち，ASC系輸送担体（SNAT，ASCT1），K^＋Na^＋グルタミン酸輸送担体（EAAC1），中性・塩基性アミノ酸輸送担体（rBAT/D2/NBAT，4F2hc），アルギニン酸輸送担体（mCAT），ペプチド輸送担体（PepT1）などであり，Hartnup病では中性アミノ酸輸送系が欠損し，blue diaper症候群はトリプトファンのみの輸送障害，シスチン尿症はシスチン・リジン・アルギニン・オルニチンの4種のアミノ酸の共輸送系の欠損とされる．しかしながら，これら刷子縁膜酵素，輸送担体の吸収不良症候群の病因・病態への関与についてはいまだ不明な点が残されている．
　後天的な吸収実効面積の減少はさまざまな原疾患により生じることが知られている．広範な小腸切除はその代表的なものであり，残存小腸が50 cm以下の短腸症候群では生命維持のための十分な栄養素の吸収は困難であり，完全静脈栄養に頼らざるをえない．また，広範な小腸病変を伴うCrohn病やびまん性に腸絨毛萎縮をきたすセリアックスプルーでみられる吸収不良症候群も広義の腸粘膜消化吸収障害型吸収不良症候群の範疇に入る．
3）輸送経路障害型：
脂肪は腸吸収細胞内で再合成され，リポ蛋白と結合した形で乳び腔に移送され，腸リンパ管から胸管リンパ管に流れ，大循環に入り全身に運ばれる．したがって，Crohn病，Whipple病あるいはリンパ腫によるリンパ管の閉塞，リンパ管形成不全で脂肪の消化吸収障害を生じる．また，糖質や蛋白質は門脈から肝に運ばれ代謝されるが，肝障害などの血管系の障害は腸管うっ血をもたらして吸収に影響を及ぼすことになる．
臨床症状・診断
　本症の診断基準は厚生省特定疾患消化吸収障害調査研究班（昭和60年度業績集）によって，①下痢，脂肪便，体重減少，るいそう，貧血，無力倦怠感，腹部膨満，浮腫，消化管出血（便潜血を含む）などの症状がみられることが多く，②血清蛋白（6 g/dL以下），アルブミン，総コレステロール（120 mg/dL以下）および血清鉄などの栄養指標の低下を示すことが多く，③消化吸収試験で異常を認める場合とされている．淡い色調の油でつやのある悪臭を伴う多量の排便（脂肪便）があり，摂食量に比して体重減少を認める場合には本症を強く疑う．本症の確診には，脂肪が最も消化吸収障害を受けやすいことから糞便中脂肪を検査することが有用である．脂肪50 g/日前後の常食摂取下で糞便塗抹SudanⅢ染色で100倍率鏡顕下に1視野10個以上の脂肪滴を認める場合，あるいは常食摂取（脂肪100～125 g/日まで）で一日糞便中脂肪がvan de Kamer法で6 g以上の場合に脂肪吸収障害とする．糞便中脂肪の異常を認めると，消化吸収障害が存在することが明らかであり，d-キシロース吸収試験を行い管腔内消化障害によるものか，腸粘膜消化吸収障害によるものかを鑑別する．前者であれば膵外分泌機能試験（PFD：BT-PABA法）などで膵・胆機能を評価する．後者であれば，消化管X線検査，腹部超音波検査，CT，内視鏡検査，生検などを組み合わせて原疾患を確定する．回腸病変が疑われる場合にはビタミンB₁₂吸収試験，胆汁酸負荷試験が有用である．腸粘膜消化吸収障害をきたす小腸疾患の代表的疾患としてセリアックスプルー（celiac sprue）があり，グルテンが病態に関与しcryptの過形成を伴い正常の絨毛形態が失われ“flat mucosa”を呈するがわが国ではまれである．最近になって免疫不全とくにAIDSにおける下痢や吸収不良が注目されるようになっており，その多くは日和見感染による．
　一方で，悪性貧血に代表されるような，頻度は多くないものの選択的な栄養素の吸収障害の存在も念頭におく必要がある．
治療
　本症の治療の原則は，まず低栄養状態の改善を行い，さらに消化吸収障害を生じている原疾患・病態を確定して根本的治療を行うことにある．栄養状態を客観的に評価するためには，身体計測，身体構成，血液・尿生化学的検査，免疫能，代謝・筋力を指標とした栄養アセスメントを行うことが重要であり，低栄養状態の改善の指標としては短半減期蛋白の測定が有用である．　消化吸収障害が軽度な場合には，高エネルギー，高蛋白，高ビタミン食とし，食事中の脂肪を1日30～40 gとする．管腔内消化障害型であれば消化酵素製剤を補充療法として常用量の3～5倍あるいは高力価消化酵素製剤を投与する．消化器症状や病態により経口摂取が困難な場合には成分栄養剤・半消化体栄養剤による経腸栄養さらには完全静脈栄養を考慮する．この場合，身体活動維持に適切な投与カロリー量の設定と微量元素などの補充を常に留意する必要がある．［藤山佳秀］
■文献
馬場忠雄：吸収不良症候群．最新内科学大系　特別巻3（別冊）内科臨床リファレンスブック疾患編Ⅱ，pp150-156，中山書店，東京，1998.
Mason JB: Mechanisms of nutrient absorption and malabsorption. In: UpToDate (La Mont JT ed), UpToDate, Wellesley, 2012.
石川　誠，高橋恒男：疫学調査報告．厚生省特定疾患消化吸収障害調査研究班昭和57年度業績集，pp15-26, 1983.
辻川知之，宇田勝弘，他：小腸の形態と機能．消化器科，35: 483-489, 2002.

表8-5-18
吸収不良症候群の病態からみた病型分類（馬場，1998 より一部改変）">

表8-5-18

表8-5-19
刷子縁膜病（馬場，1998 より一部改変）">

表8-5-19

出典　内科学第10版内科学第10版について　情報

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