Gastrointestinal Complications of Diabetes Mellitus Bahasa Indonesia

8/21/2019 Gastrointestinal Complications of Diabetes Mellitus Bahasa Indonesia

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Komplikasi Diabetes mellitus dapatmenyerang setiap organ tubuh manusiadan tingkat keparahan komplikasi

tergantung pada berapa lama dankeparahan Diabetes seseorang danpenyait penyerta.

Komplikasi pada sistem pencernaan dapat

berupa: esophageal dysmotility, gastro-esophageal refux disease (GED!,gastroparesis, enteropathy, non alcoholic"atty li#er disease ($%&'D! and glycogenichepatopathy.


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engobatan komplikasi saluranpencernaan akibat D) dimulai dulu

dengan mengendalikan kadar glukosadarah agar terkontrol baik.

*urnal ini membahas tentangperkembangan terbaru komplikasidiaabetes pada saluran pencernaan,diagnosis , e#aluasi, danpengobatannya


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re#alensi penyakit D) kini semakinbertambah banyak di dunia hinggamencapai + uta orang, hal ini teradiakibat peningkatan populasi di dunia, arus

urbanisasi, obesitas, dan gaya hidup yangtidak sehat.

leh karena itu perlu untuk mendeteksi

dini komplikasi akibat D) danmengobatinya sedini mungkin.


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/he thoracic esophagus and lo0eresophageal sphincter ('E1! terdiri dariserabut otot halus dan dipersara2 olehplexus myentericus dan sara" otonomini dapat rusak akibat penderitaDiabetic neuropati yang lama.

%kibat otonom neuropati danremodeling dari otot esophagusmengakibatkan gangguan peristaltik,dan melemahkan sphinter 'E1.


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re#alensi dari esophageal dismotilityadalah +3.

/idak ada perbedaan dari D) tipe 4dan tipe 5

Geala klasiknya berupa dis"agia danheart burn.


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re#alensi dari GED adalah 643 danErosi" Eso"agitis adalah 3 padadiabetes neuropati dan hanya ++,+ 3 to

pada diabetes tanpa neuropati. 7al ini menunukkna neuropati

berhubungan dengan EE dan

merupakan "aktor resiko teradinyakomplikasi.


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enegakan diagnosis harusmenggunakan manometry dan

pengukuran p7 pada oeso"agus. engobatan dari refuks menggunakan

obat ( metoclopramide8prokinetik,proton pump inhibitor!.asien uga

dianurkan untuk banyak minum airputih untuk mencegah esophagitis.


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Gastroparesis merupakan bertambahlamanya 0aktu pengosongan lambung

merupakan salah satu komplikasitersering akibat D).

Delayed gastric emptying ditemukanpada 593-3 pasien diabetes tipe 4

and +;3 o" patients diabetes tipe 5. 'ebih sering ditemukan pada 0anita

dan penderita obesitas.


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Geala geala gastroparesis adalahnausea, #omiting, early satiety,

postprandial "ullness, bloating andupper abdominal pain.

1ekitar +3 pasien mengalamipenurunan berat badan, 4< 3

mengalami kenaikan berat badan


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%namnesis yang baik, emeriksaan 2sik yangakurat kemudian dengan menyingkirkankemungkinan lain dengan( complete blood count,thyroid stimulating hormone test, metabolic panel

and optional amylase and pregnancy test!membantu menegakkan diagnosis gastroparesis. gastric emptying scintigraphymerupakan gold

standard test untuk menegakkan gastroparesis Gastroparesis pengobatan: modi2kasi diet,obat

obatan untuk memperkuat peristaltik, mengurangigeala mual muntah, non-medication inter#entions,psychological therapies dan perlu pertimbanganbedah ika sudah stadium gastric "ailure.


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General approaches to management o"gastroparesis include ensuring goodhydration, correcting electrolyte imbalances,management o" glycemic control andsymptom reduction 0ithpharmacotherapeutic agents.

Dietary modi2cations include increasingli=uid-based meals (as the rate o" emptying

li=uid "rom the stomach is usually the samein diabetic gastroparesis!, reducing "at andnon-digestible 2bre intake, a#oiding largemeals 0ith high calorie contents andensuring small "re=uent meals spreadthroughout the day.


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rokinetics are medications thataugment gastrointestinal motility. >n

general these increase gastric motilityand enhance stomach emptying


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)osapride is a selecti#e -7/6 agonistthat accelerates gastric emptying.

>ntra#enous use o" the ghrelin agonis. 1urgical treatment "or patients 0ith

re"ractory gastroparetic symptoms 0hoha#e "ailed to impro#e 0ith othermeasures


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Diabetes-related enteropathy may present 0ithdiarrhea, constipation or "ecal incontinence.

%d#anced glycation end products causedamage to cellular D$% and tissues in diabetes.

Damage to the myenteric ner#e plexus due toautonomic neuropathy and 2brosis o" theintestinal muscular layers result in stasis o" theintestinal contents. educed bo0el motilityresults in constipation that may sometimes

lead to o#erfo0 incontinence. 1mall intestinal bacterial o#ergro0th (1>?!,0hich can result in diarrhea, is usually aconse=uence o" intestinal stasis.


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@onstipation alternating 0ith diarrhea,painless, may be associated 0ith "ecalincontinence and occurs during the day butmore o"ten at night.

1e#ere constipation leading to megacolon orcolonic intestinal pseudo-obstruction occursrarely. 1tercoral ulcer, per"oration ando#erfo0 diarrhea are encounteredin"re=uently.

&ecal incontinence, particularly nocturnal, dueto internal and external sphincter dys"unctionsecondary to autonomic neuropathy is atroublesome symptom caused by acutehyperglycemia.


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atients should undergo endoscopicexamination, ultrasound or computedtomography to exclude other diagnosis.

$on-in#asi#e diagnostic tests "or smallintestine bacterial o#ergro0th are largelybased on excretion o" hydrogen in exhaledbreath.

% radio opa=ue marker test is use"ul "or

excluding possible slo0 transit constipation. /ests "or "ecal incontinence include

endoanal ultrasound and anorectalmanometry.


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%nti-diarrheal : i"aximin, amoxicillin-cla#ulanic acid, doxycycline,ciprofoxacin, metronidaBole, neomycinand norfoxacin.

'operamide "or "ecal incontinence. @onstipation may be treated 0ith prompt

hydration, regular exercise and increased

intake o" dietary 2bre. 'actulose andosmotic laxati#es "or se#ere cases.


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@hronic constipation treated 0ithprucalopride, a selecti#e -7/6

receptor agonist that enhances colonictransit and lubiprostone, 0hichstimulates colonic 0ater andelectrolyte secretion through acti#ation

o" type 5 chloride channels inenterocytes.


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$%&'D re=uires that there is e#idence o"hepatic steatosis, either by imaging orby histology, and that there are no

causes "or secondary hepatic "ataccumulation such as signi2cant alcoholconsumption, use o" steatogenicmedication or hereditary disorders.


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$%&'D is considered to be the hepaticmani"estation o" metabolic syndrome0hich encompasses the clinical tetrad o"hyperinsulinemia 0ith insulin resistance,#isceral obesity, dyslipidemia andhypertension.

7istologically, $%&'D is "urthersubdi#ided into nonalcoholic "atty li#er($%&'! and nonalcoholic steatohepatitis($%17!.


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)aority patients are asymptomatic,

1ome may present 0ith nonspeci2c

symptoms such as malaise and rightupper =uadrant pain.

@linical disease in $%&'D ranges "rommild ele#ation o" li#er enBymes tose#ere li#er disease 0ith 2brosis andnodular degeneration.


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ecent study identi2ed thatapproximately +;3 o" $%&'D cases

0ith isolated steatosis 0ill progress to$%17 and, o" these, approximately5;3 0ill de#elop cirrhosis.

%bout 6;3 o" these cirrhotic patientsde#elop decompensated li#er diseaseincluding hepatocellular carcinoma0hich higher the mortality rate.


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/he diagnosis o" $%&'D re=uires thatthere is hepatic steatosis by imaging orhistology, there is no signi2cant alcohol

o#erconsumption, there are nocompeting etiologies "or hepaticsteatosis, and there are no co-existingcauses "or chronic li#er disease.


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/he "ollo0ing conditions should beexcluded: history o" alcohol intake C 5;g8d, nutritional causes (e.g., total

parenteral nutrition and rapid 0eight loss!,metabolic disorders (glycogen storagedisorders!, chronic hepatitis @ (particularlygenotype +!, other causes o" chronic li#erdiseases (autoimmune li#er disease,

ilsons disease and hemochromatosis!and endocrine disorders such aspolycystic o#ary syndrome,hypopituitarism and hypothyroidism.


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Drug-induced steatosis can be causedby a number o" agents including

glucocorticoids, synthetic estrogens,amiodarone, methotrexate and highlyacti#e antiretro#iral drugs.

$%&' is considered benign 0hereas$%17 can progress to cirrhosis, li#er"ailure, and li#er cancer.


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'i#er biopsy is recommended in patients 0ith$%&'D 0ho ha#e the metabolic syndrome.

@irculating le#els o" cytokeratin-4< "ragments "oridenti"ying steatohepatitis in patients 0ith $%&'D.

/ransient elastography (/E!, 0hich measures li#erstiFness non-in#asi#ely, sho0ed high sensiti#ityand speci2city "or identi"ying 2brosis in $%&'D .

/here is some e#idence that the Enhanced 'i#er&ibrosis test 0hich uses the 2brosis markers

hyaluronic acid, amino-terminal propeptide-o"-type->>>-collagen and tissue-inhibitor o" matrix-metalloproteinase-4, compares "a#ourably 0ith theuse o" /E.


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/he management o" patients 0ith $%&'Dconsists o" treating li#er disease and theassociated metabolic co-morbiditiessuch as obesity, hyperlipidemia, insulinresistance and /5D).

'i"estyle modi2cation and 0eight

reduction li"estyle modi2cation canreduce aminotrans"erase le#els andimpro#e hepatic steatosis


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>nsulin sensitiBing agents : thethiaBolidinediones (pioglitaBone!.

>ncretin mimetics : exenatide andliraglutide.

?ariatric surgery


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Glycogenic hepatopathy is de2ned aspathological o#erloading o" hepatocytes 0ithglycogen leading to hepatic enlargementand8or derangement o" li#er enBymes and isusually seen in patients 0ith longstandingpoorly-controlled type 4 diabetes mellitus(/4D)!.

>nsulin acti#ates the enByme glycogensynthase phosphatase 0hich

dephosphorylates and acti#ates glycogensynthase, another enByme that is re=uired "orthe con#ersion o" glucose-4-phosphate toglycogen. /his results in increased glycogenstorage in the li#er and blocks glycogenolysis.


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/he histological picture is characteriBedby pale appearance o" the hepatocytes

0ith compression o" the sinusoids,glycogenated nuclei and giantmitochondria. 1teatosis may bepresent, usually mild, or absent.

Glycogen accumulation, the hallmarko" this condition is demonstrated by%1-diastase staining.


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/he disease is under-recogniBed and usually presents0ith abdominal pain, nausea, #omiting andabnormalities in li#er "unction tests.

>t cannot be distinguished "rom $%&'D clinically or by

ultrasound and con2rmation re=uires a li#er biopsy. /he disorder should be suspected 0hen li#er

dys"unction occurs in patients 0ith /4D), especially0hen #iral, autoimmune and metabolic li#er diseasesare excluded by laboratory in#estigations.

/he hallmark o" this condition is its re#ersibility 0ithimpro#ed glycemic control.

Hnlike hepatic steatosis, glycogen o#erload is notkno0n to progress to 2brosis distinct "rom "atty li#erdisease.


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rompt impro#ement 0ith optimaldiabetes control by insulin treatment0ithin 6 0k is usually seen in thesepatients


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/he term Ihepatogenous diabetesJ (7D! is used todescribe diabetes de#eloping in patients 0ithcirrhosis.

$umerous "actors, including reduced insulin

clearance, peripheral hyperinsulinemia and do0n-regulation o" insulin receptors, lead tode#elopment o" diabetes in cirrhosis.

7D is clinically diFerent "rom /5D) in that it is less"re=uently associated 0ith microangiopathy and

patients suFer "rom complications o" cirrhosis more"re=uently. 7o0e#er, 7D is not yet recogniBed by the %merican

Diabetes %ssociation and the orld 7ealthrganiBation.


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4. th Edition o" the Diabetes %tlas released on orld Diabetes Day.?russels, ?elgium: >nternational Diabetes &ederation, 5;44.(%ccessed on th %pril 5;4+.! %#ailable "rom: http:88000.id".org8diabetesatlas8ne0s82"th-edition-release.

5. &rokaer *?, %ndersen 1D, Eskaer $, &unch-*ensen , Dre0es %),Gregersen 7. >mpaired contractility and remodeling o" the uppergastrointestinal tract in diabetes mellitus type-4. orld *Gastroenterol. 5;;94+:6


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. ang R, itchumoni @1, @handrarana K, 1hah $. >ncreasedpre#alence o" symptoms o" gastroesophageal refux diseases in type 5diabetics 0ith neuropathy. orld * Gastroenterol. 5;;. 7igh pre#alence o" gastroesophageal refux symptomsin type 5 diabetics 0ith hypoadiponectinemia and metabolic syndrome.$utr )etab ('ond! 5;45L:6. M)@ "ree articleN Mub)edN

L. ilson *%, Sela )&. $e0 esophageal "unction testing (impedance,

?ra#o p7 monitoring, and high-resolution manometry!: clinicalrele#ance. @urr Gastroenterol ep. 5;;

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Gastrointestinal Complications of Diabetes Mellitus Bahasa Indonesia

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