Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five patients with ulcerative colitis were treated between 1959 and 1986 at the Mount Sinai Hospital, with severe gastrointestinal hemorrhage as their major complaint. Twenty-two patients required operation, while three patients were treated medically. Total proctocolectomy with ileostomy was carried out in 5 patients, and subtotal colectomy accompanied by mucous fistula (14), Hartmann closure (2), or ileosigmoidostomy (1) was performed in 17 patients. Eleven of the patients who underwent operation had emergency colectomies, while the remaining 11 had semielective procedures. Subtotal colectomy was performed in 10 of the 11 emergency cases. Indications for emergency surgery were massive hemorrhage alone in seven patients and severe hemorrhage complicated by toxic megacolon in four patients. One patient died postoperatively of a perforated duodenal ulcer following emergency subtotal colectomy. There were two late deaths from leukemia in one surgically treated patient and one medically treated patient at 9 and 18 months, respectively. All 4 of the 25 patients with remaining intact rectums were alive and well at 3- to 12-year follow-up. Subtotal colectomy can be undertaken in patients with massive hemorrhage from ulcerative colitis for whom subsequent ileoanal anastomosis is planned, provided that one recognizes and is prepared for the approximately 12% risk of continued rectal hemorrhage.
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PMID:Management of severe hemorrhage in ulcerative colitis. 234 80

This is the first report of doxorubicin (Adriamycin) interacting with whole-body electro-beam irradiation to produce generalized toxic epidermal necrolysis. The patient was a 32-year-old woman with acute myelomonocytic leukemia and leukemia cutis. The severe dermatitis obscured clinical recognition of concomitant pseudomembranous colitis and contributed to the patient's death during management of toxic megacolon. Suggestions are made for minimizing this occurrence in future patients treated in a similar fashion.
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PMID:Doxorubicin-enhanced skin reaction after whole-body electron-beam irradiation for leukemia cutis. 677 13

A 43 year old woman in remission from acute myeloid leukaemia developed abdominal pain, severe melaena, diarrhoea and gram-negative septicaemia whilst severely pancytopenic following consolidation chemotherapy. Subsequently, serial abdominal X-rays showed a progressive toxic megacolon. Conservative management was attempted but, because of radiological evidence of increasing colonic dilatation and incipient perforation, an emergency defunctioning colostomy was performed. The patient recovered and 2 months later the caecostomy was reversed and a right hemicolectomy performed. This first described case of toxic megacolon following leukaemia treatment is compared with three previously described cases following cytotoxic chemotherapy for other conditions.
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PMID:Toxic megacolon complicating chemotherapy for acute myeloid leukaemia. 787 Jun 42

This article reviews a variety of specific colonic disorders that may have been an acute clinical presentation. Less common causes of colonic obstruction include volvulus, intussusception, and hernias. Nonobstructive colonic dilatation is most often due to pseudo-obstructions and toxic megacolon. Several miscellaneous disorders discussed include colonic perforation, complications of leukemia that may affect the colon, and pseudomembranous colitis. The pathogenesis and clinical aspects of these disorders are reviewed, but the radiologic features are emphasized.
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PMID:Specific acute colonic disorders. 808 1

Primary gut involvement by Aspergillus is an exceedingly rare and often a fatal complication of intensive chemotherapy in patients with acute leukaemia. We report a 46-yr-old patient with granulocytic sarcoma of the testis. He received acute myeloid leukaemia type treatment with ADE chemotherapy (Cytosine Arabinoside, Daunorubicin and Etoposide). While neutropenic he presented with pyrexia, abdominal pain and massive abdominal distention. He was treated with intravenous antibiotics and antifungals according to our usual institutional protocol without any response. He was found to have toxic megacolon on plain X-ray and subsequently underwent total colectomy and ileostomy. The colon histology showed Aspergillus fungal hyphae infiltrating the bowel wall. There was no any evidence of pulmonary, hepatic, splenic or renal lesions on the computerised tomography scan. Following colectomy, he was treated with 2 wk of antifungal treatment. He recovered well and was discharged home. The increased awareness, high degree of clinical suspicion of unusual presentation and early surgical intervention with aggressive antifungal treatment, has a key role in the management of these rare and often fatal cases.
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PMID:Invasive aspergillosis localised to the colon presenting as toxic megacolon. 1732 84

Over the last 40 years, cryptosporidium has increasingly been recognized as a cause of acute self-limiting diarrhea in normal hosts. In the immunocompromised patient, cryptosporidium may cause severe illness with prolonged diarrhea and malabsorption. Pharmacologic therapy of cryptosporidium relies on adequate delivery of drug metabolites to the colon. Here we describe a patient who developed toxic megacolon during induction therapy for leukemia, requiring ileostomy formation to proceed with leukemia treatment. Although the megacolon resolved promptly, the resulting isolation of the colon from the fecal stream prevented luminal delivery of active metabolites of anti-protozoal drugs, resulting in persistent cryptosporidiosis. Refeeding of the ileostomy output into the colon effectively eradicated cryptosporidium from the colon and permitted closure of the ileostomy.
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PMID:Eradication of cryptosporidium from a defunctionalized colon limb by refeeding stoma effluent. 2010 71

Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previously MEN2A) due to mutations of a tyrosine kinase receptor encoded by the rearranged during transfection (RET) protoncogene; MEN3 (previously MEN2B) due to RET mutations; and MEN4 due to cyclin-dependent kinase inhibitor (CDNK1B) mutations. Each MEN type is associated with the occurrence of specific tumors. Thus, MEN1 is characterized by the occurrence of parathyroid, pancreatic islet and anterior pituitary tumors; MEN2 is characterized by the occurrence of medullary thyroid carcinoma (MTC) in association with phaeochromocytoma and parathyroid tumors; MEN3 is characterized by the occurrence of MTC and phaeochromocytoma in association with a marfanoid habitus, mucosal neuromas, medullated corneal fibers and intestinal autonomic ganglion dysfunction, leading to megacolon; and MEN4, which is also referred to as MENX, is characterized by the occurrence of parathyroid and anterior pituitary tumors in possible association with tumors of the adrenals, kidneys, and reproductive organs. This review will focus on the clinical and molecular details of the MEN1 and MEN4 syndromes. The gene causing MEN1 is located on chromosome 11q13, and encodes a 610 amino-acid protein, menin, which has functions in cell division, genome stability, and transcription regulation. Menin, which acts as scaffold protein, may increase or decrease gene expression by epigenetic regulation of gene expression via histone methylation. Thus, menin by forming a subunit of the mixed lineage leukemia (MLL) complexes that trimethylate histone H3 at lysine 4 (H3K4), facilitates activation of transcriptional activity in target genes such as cyclin-dependent kinase (CDK) inhibitors; and by interacting with the suppressor of variegation 3-9 homolog family protein (SUV39H1) to mediate H3K methylation, thereby silencing transcriptional activity of target genes. MEN1-associated tumors harbor germline and somatic mutations, consistent with Knudson's two-hit hypothesis. Genetic diagnosis to identify individuals with germline MEN1 mutations has facilitated appropriate targeting of clinical, biochemical and radiological screening for this high risk group of patients for whom earlier implementation of treatments can then be considered. MEN4 is caused by heterozygous mutations of CDNK1B which encodes the 196 amino-acid CDK1 p27Kip1, which is activated by H3K4 methylation.
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PMID:Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4). 2393 18