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Melena

MedGen UID:
7523
Concept ID:
C0025222
Pathologic Function
Synonym: Melenas
SNOMED CT: Altered blood passed per rectum (2901004); Altered blood in stool (2901004); Black, tarry stool (2901004); Melena (2901004); Tarry stools (2901004)
 
HPO: HP:0002249

Definition

The passage of blackish, tarry feces associated with gastrointestinal hemorrhage. Melena occurs if the blood remains in the colon long enough for it to be broken down by colonic bacteria. One degradation product, hematin, imbues the stool with a blackish color. Thus, melena generally occurs with bleeding from the upper gastrointestinal tract (e.g., stomach ulcers or duodenal ulcers), since the blood usually remains in the gut for a longer period of time than with lower gastrointestinal bleeding. [from HPO]

Conditions with this feature

Hereditary factor IX deficiency disease
MedGen UID:
945
Concept ID:
C0008533
Disease or Syndrome
Hemophilia B is characterized by deficiency in factor IX clotting activity that results in prolonged oozing after injuries, tooth extractions, or surgery, and delayed or recurrent bleeding prior to complete wound healing. The age of diagnosis and frequency of bleeding episodes are related to the level of factor IX clotting activity. In individuals with severe hemophilia B, spontaneous joint or deep-muscle bleeding is the most frequent sign. Individuals with severe hemophilia B are usually diagnosed during the first two years of life; without prophylactic treatment, they may average up to two to five spontaneous bleeding episodes each month. Individuals with moderate hemophilia B seldom have spontaneous bleeding; however, they do have prolonged or delayed oozing after relatively minor trauma and are usually diagnosed before age five to six years; the frequency of bleeding episodes varies from once a month to once a year. Individuals with mild hemophilia B do not have spontaneous bleeding episodes; however, without pre- and postoperative treatment, abnormal bleeding occurs with surgery or tooth extractions; the frequency of bleeding may vary from once a year to once every ten years. Individuals with mild hemophilia B are often not diagnosed until later in life. In any individual with hemophilia B, bleeding episodes may be more frequent in childhood and adolescence than in adulthood. Approximately 30% of heterozygous females have factor IX clotting activity lower than 40% and are at risk for bleeding (even if the affected family member has mild hemophilia B), although symptoms are usually mild. After major trauma or invasive procedures, prolonged or excessive bleeding usually occurs, regardless of severity.
Hereditary factor VIII deficiency disease
MedGen UID:
5501
Concept ID:
C0019069
Disease or Syndrome
Hemophilia A is characterized by deficiency in factor VIII clotting activity that results in prolonged oozing after injuries, tooth extractions, or surgery, and delayed or recurrent bleeding prior to complete wound healing. The age of diagnosis and frequency of bleeding episodes are related to the level of factor VIII clotting activity. Individuals with severe hemophilia A are usually diagnosed during the first two years of life following oral or soft tissue bleeding either with procedures or due to a known family history of hemophilia. Without prophylactic treatment, individuals may average up to two to five spontaneous bleeding episodes each month including spontaneous joint bleeds or deep-muscle hematomas, and prolonged bleeding or excessive pain and swelling from minor injuries, surgery, and tooth extractions. Individuals with moderate hemophilia A seldom have spontaneous bleeding, although it varies between individuals; however, they do have prolonged or delayed bleeding after relatively minor trauma and are usually diagnosed before age five to six years; the frequency of bleeding episodes varies, usually from once a month to once a year. Individuals with mild hemophilia A do not have spontaneous bleeding episodes; however, without pre- and postoperative treatment, abnormal bleeding occurs with surgery or tooth extractions; the frequency of bleeding episodes varies widely, typically from once a year to once every ten years. Individuals with mild hemophilia A are often not diagnosed until later in life. Approximately 30% of heterozygous females have factor VIII clotting activity below 40% and are at risk for bleeding (even if males in the family are only mildly affected). After major trauma or invasive procedures, prolonged or excessive bleeding usually occurs, regardless of severity. In addition, 25% of heterozygous females with normal factor VIII clotting activity report an increased bleeding tendency.
Wiskott-Aldrich syndrome
MedGen UID:
21921
Concept ID:
C0043194
Disease or Syndrome
The WAS-related disorders, which include Wiskott-Aldrich syndrome, X-linked thrombocytopenia (XLT), and X-linked congenital neutropenia (XLN), are a spectrum of disorders of hematopoietic cells, with predominant defects of platelets and lymphocytes caused by pathogenic variants in WAS. WAS-related disorders usually present in infancy. Affected males have thrombocytopenia with intermittent mucosal bleeding, bloody diarrhea, and intermittent or chronic petechiae and purpura; eczema; and recurrent bacterial and viral infections, particularly of the ear. At least 40% of those who survive the early complications develop one or more autoimmune conditions including hemolytic anemia, immune thrombocytopenic purpura, immune-mediated neutropenia, rheumatoid arthritis, vasculitis, and immune-mediated damage to the kidneys and liver. Individuals with a WAS-related disorder, particularly those who have been exposed to Epstein-Barr virus (EBV), are at increased risk of developing lymphomas, which often occur in unusual, extranodal locations including the brain, lung, or gastrointestinal tract. Males with XLT have thrombocytopenia with small platelets; other complications of Wiskott-Aldrich syndrome, including eczema and immune dysfunction, are usually mild or absent. Males with XLN have congenital neutropenia, myeloid dysplasia, and lymphoid cell abnormalities.
Tyrosinemia type I
MedGen UID:
75688
Concept ID:
C0268490
Disease or Syndrome
Untreated tyrosinemia type I usually presents either in young infants with severe liver involvement or later in the first year with liver dysfunction and renal tubular dysfunction associated with growth failure and rickets. Untreated children may have repeated, often unrecognized, neurologic crises lasting one to seven days that can include change in mental status, abdominal pain, peripheral neuropathy, and/or respiratory failure requiring mechanical ventilation. Death in the untreated child usually occurs before age ten years, typically from liver failure, neurologic crisis, or hepatocellular carcinoma. Combined treatment with nitisinone and a low-tyrosine diet has resulted in a greater than 90% survival rate, normal growth, improved liver function, prevention of cirrhosis, correction of renal tubular acidosis, and improvement in secondary rickets.
Hereditary mucoepithelial dysplasia
MedGen UID:
220887
Concept ID:
C1274795
Congenital Abnormality
Hereditary mucoepithelial dysplasia (HMD) is a rare autosomal dominant genodermatosis characterized by onset in infancy of a panepithelial defect involving the oral, nasal, conjunctival, vaginal, cervical, perineal, urethral, and bladder mucosa. Patients develop cataracts, blindness, nonscarring alopecia, perineal psoriasiform lesions, and follicular keratoses (Witkop et al., 1982). Although 1 family was reported to have progressive severe interstitial lung disease (Witkop et al., 1979), this feature has not been reported in other families and is not considered a criterion for diagnosis. However, the clinical triad of nonscarring alopecia, well-demarcated fiery red mucosa, and psoriasiform perineal involvement has been consistently observed (review by Boralevi et al., 2005).
Telangiectasia, hereditary hemorrhagic, type 2
MedGen UID:
324960
Concept ID:
C1838163
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Telangiectasia, hereditary hemorrhagic, type 1
MedGen UID:
1643786
Concept ID:
C4551861
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Gastric adenocarcinoma and proximal polyposis of the stomach
MedGen UID:
1657285
Concept ID:
C4749917
Neoplastic Process
APC-associated polyposis conditions include (classic or attenuated) familial adenomatous polyposis (FAP) and gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS). FAP is a colorectal cancer (CRC) predisposition syndrome that can manifest in either classic or attenuated form. Classic FAP is characterized by hundreds to thousands of adenomatous colonic polyps, beginning on average at age 16 years (range 7-36 years). For those with the classic form of FAP, 95% of individuals have polyps by age 35 years; CRC is inevitable without colectomy. The mean age of CRC diagnosis in untreated individuals is 39 years (range 34-43 years). The attenuated form is characterized by multiple colonic polyps (average of 30), more proximally located polyps, and a diagnosis of CRC at a later age than in classic FAP. For those with an attenuated form, there is a 70% lifetime risk of CRC and the mean age of diagnosis is 50-55 years. Extracolonic manifestations are variably present and include polyps of the stomach and duodenum, osteomas, dental abnormalities, congenital hypertrophy of the retinal pigment epithelium (CHRPE), benign cutaneous lesions, desmoid tumors, adrenal masses, and other associated cancers. GAPPS is characterized by proximal gastric polyposis, increased risk of gastric adenocarcinoma, and no duodenal or colonic involvement in most individuals reported.

Professional guidelines

PubMed

Novak I, Bass LM
Gastrointest Endosc Clin N Am 2023 Apr;33(2):401-421. doi: 10.1016/j.giec.2022.11.003. PMID: 36948753
Wilkins T, Wheeler B, Carpenter M
Am Fam Physician 2020 Mar 1;101(5):294-300. PMID: 32109037
Kamboj AK, Hoversten P, Leggett CL
Mayo Clin Proc 2019 Apr;94(4):697-703. doi: 10.1016/j.mayocp.2019.01.022. PMID: 30947833

Recent clinical studies

Etiology

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Clin Geriatr Med 2021 Feb;37(1):155-172. doi: 10.1016/j.cger.2020.09.001. PMID: 33213769
Kamboj AK, Hoversten P, Leggett CL
Mayo Clin Proc 2019 Apr;94(4):697-703. doi: 10.1016/j.mayocp.2019.01.022. PMID: 30947833
Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, Graupera I, Poca M, Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santaló M, Muñiz E, Guarner C
N Engl J Med 2013 Jan 3;368(1):11-21. doi: 10.1056/NEJMoa1211801. PMID: 23281973
Srygley FD, Gerardo CJ, Tran T, Fisher DA
JAMA 2012 Mar 14;307(10):1072-9. doi: 10.1001/jama.2012.253. PMID: 22416103
Kumar R, Mills AM
Emerg Med Clin North Am 2011 May;29(2):239-52, viii. doi: 10.1016/j.emc.2011.01.003. PMID: 21515178

Diagnosis

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Acta Gastroenterol Belg 2023 Apr-Jun;86(2):382. doi: 10.51821/86.2.11669. PMID: 37428177
Yang X, Xu L, Liang C, Yang L
Ann Emerg Med 2023 Jul;82(1):e13-e14. doi: 10.1016/j.annemergmed.2023.01.031. PMID: 37349077
Costable NJ, Greenwald DA
Clin Geriatr Med 2021 Feb;37(1):155-172. doi: 10.1016/j.cger.2020.09.001. PMID: 33213769
Kamboj AK, Hoversten P, Leggett CL
Mayo Clin Proc 2019 Apr;94(4):697-703. doi: 10.1016/j.mayocp.2019.01.022. PMID: 30947833
Forrest JA, Finlayson ND, Shearman DJ
Lancet 1974 Aug 17;2(7877):394-7. doi: 10.1016/s0140-6736(74)91770-x. PMID: 4136718

Therapy

Novak I, Bass LM
Gastrointest Endosc Clin N Am 2023 Apr;33(2):401-421. doi: 10.1016/j.giec.2022.11.003. PMID: 36948753
Costable NJ, Greenwald DA
Clin Geriatr Med 2021 Feb;37(1):155-172. doi: 10.1016/j.cger.2020.09.001. PMID: 33213769
Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, Graupera I, Poca M, Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santaló M, Muñiz E, Guarner C
N Engl J Med 2013 Jan 3;368(1):11-21. doi: 10.1056/NEJMoa1211801. PMID: 23281973
Srygley FD, Gerardo CJ, Tran T, Fisher DA
JAMA 2012 Mar 14;307(10):1072-9. doi: 10.1001/jama.2012.253. PMID: 22416103
Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW
Arthritis Rheum 2010 Apr;62(4):1060-8. doi: 10.1002/art.27327. PMID: 20131255

Prognosis

Piccirillo M, Pucinischi V, Mennini M, Strisciuglio C, Iannicelli E, Giallorenzi MA, Furio S, Ferretti A, Parisi P, Di Nardo G
Ital J Pediatr 2024 Jan 23;50(1):13. doi: 10.1186/s13052-024-01592-2. PMID: 38263189Free PMC Article
Díaz AM, Rodríguez LF, de Gracia MM
Radiologia 2017 May-Jun;59(3):249-252. Epub 2017 Jan 6 doi: 10.1016/j.rx.2016.11.002. PMID: 28069255
Coremans L, Van Der Meersch F, Colle I, Van den Bossche B
Acta Gastroenterol Belg 2015 Jan-Mar;78(1):69. PMID: 26118584
Srygley FD, Gerardo CJ, Tran T, Fisher DA
JAMA 2012 Mar 14;307(10):1072-9. doi: 10.1001/jama.2012.253. PMID: 22416103
Kumar R, Mills AM
Emerg Med Clin North Am 2011 May;29(2):239-52, viii. doi: 10.1016/j.emc.2011.01.003. PMID: 21515178

Clinical prediction guides

Tsheten T, Clements ACA, Gray DJ, Adhikary RK, Furuya-Kanamori L, Wangdi K
Infect Dis Poverty 2021 Oct 9;10(1):123. doi: 10.1186/s40249-021-00908-2. PMID: 34627388Free PMC Article
Costable NJ, Greenwald DA
Clin Geriatr Med 2021 Feb;37(1):155-172. doi: 10.1016/j.cger.2020.09.001. PMID: 33213769
Wilkins T, Wheeler B, Carpenter M
Am Fam Physician 2020 Mar 1;101(5):294-300. PMID: 32109037
Díaz AM, Rodríguez LF, de Gracia MM
Radiologia 2017 May-Jun;59(3):249-252. Epub 2017 Jan 6 doi: 10.1016/j.rx.2016.11.002. PMID: 28069255
Srygley FD, Gerardo CJ, Tran T, Fisher DA
JAMA 2012 Mar 14;307(10):1072-9. doi: 10.1001/jama.2012.253. PMID: 22416103

Recent systematic reviews

Karlafti E, Tsavdaris D, Kotzakioulafi E, Protopapas AA, Kaiafa G, Netta S, Savopoulos C, Michalopoulos A, Paramythiotis D
Medicina (Kaunas) 2023 Aug 21;59(8) doi: 10.3390/medicina59081500. PMID: 37629790Free PMC Article
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Infect Dis Poverty 2021 Oct 9;10(1):123. doi: 10.1186/s40249-021-00908-2. PMID: 34627388Free PMC Article
Schizas D, Tomara N, Katsaros I, Sakellariou S, Machairas N, Paspala A, Tsilimigras DI, Papanikolaou IS, Mantas D
ANZ J Surg 2021 Mar;91(3):269-275. Epub 2020 Jul 20 doi: 10.1111/ans.16160. PMID: 32687691
Cappell MS, Stevens CE, Amin M
World J Gastroenterol 2017 Aug 14;23(30):5619-5633. doi: 10.3748/wjg.v23.i30.5619. PMID: 28852321Free PMC Article
Zullo A, Hassan C, Andriani A, Cristofari F, Cardinale V, Spinelli GP, Tomao S, Morini S
J Clin Gastroenterol 2010 May-Jun;44(5):340-4. doi: 10.1097/MCG.0b013e3181b4b1ab. PMID: 19745757

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