Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a woman with a history of chronic alcohol abuse who was hospitalized with diarrhea, severe hypokalemia refractory to potassium infusion, nausea, vomiting, abdominal pain, alternations of high blood pressure with phases of hypotension, irritability and increased urinary 5-hydroxyindoleacetic acid and cortisol. Although carcinoid syndrome was hypothesized, abdominal computed tomography and colonoscopy showed non-specific inflammatory bowel disease with severe colic wall thickening, and multiple colic biopsies confirmed non-specific inflammation with no evidence of carcinoid cells. During the following days diarrhea slowly decreased and the patient's condition progressively improved. One year after stopping alcohol consumption, the patient was asymptomatic and serum potassium was normal. Chronic alcohol exposure is known to have several deleterious effects on the intestinal mucosa and can favor and sustain local inflammation. Chronic alcohol intake may also be associated with high blood pressure, behavior disorders, abnormalities in blood pressure regulation with episodes of hypotension during hospitalization due to impaired baroreflex sensitivity in the context of an alcohol withdrawal syndrome, increased urinary 5-hydroxyindoleacetic acid as a result of malabsorption syndrome, and increased urinary cortisol as a result of hypothalamic-pituitary-adrenal axis dysregulation. These considerations, together with the regression of symptoms and normalization of potassium levels after stopping alcohol consumption, suggest the intriguing possibility of a alcohol-related acute inflammatory bowel disease mimicking carcinoid syndrome.
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PMID:Acute inflammatory bowel disease complicating chronic alcoholism and mimicking carcinoid syndrome. 2294 95

Nausea and vomiting are common distressing symptoms with multiple etiologies. Serotonin and substance P can induce nausea and vomiting by binding to specific receptors (5-hydroxytryptamine3 [5HT3] and neurokinin-1 [NK-1] receptors respectively). Carcinoid tumors, which originate from enterochromaffin cells of the neuroendocrine system, secrete several biologically active amines and peptides, including serotonin and substance P, that are responsible for the distant effects of this tumor. The authors present an 88-year-old lady with metastatic carcinoid tumor, with evidence of carcinoid syndrome. She had nausea and vomiting that became unresponsive to 5HT3 receptor antagonists and other antiemetics. As substance P is released from carcinoid tumors and has a role in the pathogenesis of emesis, the NK-1 receptor antagonist aprepitant was trialed. This provided complete and sustained improvement of the nausea and vomiting until her death 2 months later. This case demonstrates the potential role and rationale of NK-1 receptor antagonists in the management of resistant emesis in patients with carcinoid tumors. Clinical trials are needed to evaluate the efficacy and toxicity of these drugs in the management of emesis in patients with carcinoid syndrome.
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PMID:Aprepitant for the management of refractory emesis in a patient with a small bowel carcinoid tumor. 2483 5

Neuromyelitis optica (NMO), or Devic's syndrome, is an autoimmune central nervous system demyelinating disorder primarily affecting the spinal cord and the optic nerves. It is characterized by the presence of NMO antibodies, alongside clinical and radiological findings. NMO and NMO-spectrum disorders (NMO-SD) have been reported in autoimmune disorders, and are infrequently described as a paraneoplastic syndrome with cancers of lung, breast, and carcinoid tumors of the thyroid. We report a patient who presented with severe vomiting, blurring of vision, vertigo, diplopia, left hemiparesis and hemisensory loss and ataxia. She was found to have a longitudinally-extensive demyelinating lesion extending from the medulla to the upper cervical spinal cord on MRI. Her gastric endoscopy revealed carcinoid tumor of the stomach, and classic paraneoplastic antibodies in the serum were negative. She had extremely high serum gastrin level and high titer of NMO IgG autoantibody. The patient made an excellent recovery with tumor resection and immunotherapy, with both clinical and radiological improvement. On rare instances, NMO or NMO-SD may present as a paraneoplastic neurological syndrome associated with carcinoid tumor of the stomach.
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PMID:Paraneoplastic neuromyelitis optica spectrum disorder associated with stomach carcinoid tumor. 2495 81

An 8 yr old, intact male Shiba Inu was presented with loose stool, polydipsia, hematuria, vomiting, and anorexia. On abdominal ultrasonography, numerous nodules were detected in the hepatic parenchyma distributed diffusely throughout all lobes. Excisional biopsy of one of the nodules was performed via exploratory laparotomy. A histopathological diagnosis of the lesion was carcinoid, and the tumor cells stained positive to chromogranin A and gastrin. The serum gastrin level of the dog was 45,613 pg/mL (reference range: 160-284). In addition to medical treatment with omeprazole(c) and famotidine(e), suppression of gastrin secretion was attempted with octreotide acetate. A test dose of octreotide acetate significantly decreased the serum gastrin level to approximately one third of the baseline in 2 hr and the effect lasted approximately for 6 hr. On day 21, treatment with sustained-release formulation of octreotide acetate(a) (5 mg intramuscular, q 4 wk) was initiated. The serum gastrin concentration gradually decreased over 32 days and then progressively increased in parallel with the progression of the hepatic nodules. The dog gradually developed recurrence of initial clinical signs, and was lost to follow-up on day 510.
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PMID:Treatment of Gastrin-Secreting Tumor With Sustained-Release Octreotide Acetate in a Dog. 2653 61

Carcinoid tumors are rare neuroendocrine tumors that have been reported in a wide range of organs but most commonly involve the gastrointestinal tract (stomach, ileum, appendix, and colon), and rarely ovary and thymus. We present a case of a 56-year-old Nigerian man with a cecal carcinoid tumor that was surgically removed. A 56-year-old Nigerian man, presented to our hospital with a year history of right-sided lower abdominal fullness, audible bowel sounds, occasional diarrhea, nausea, vomiting, and epigastric pain. There was no history of hematochezia or passage of melena stool. Colonoscopy revealed a cecal mass occupying more than two-thirds of the cecal lumen. Histology confirmed carcinoid tumor (well-differentiated neuroendocrine tumor), which was surgically removed. Carcinoid tumors are slow growing rare neuroendocrine tumors. Mortality is low if it is diagnosed early.
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PMID:Cecal carcinoid tumor in a nigerian man: A case report and review of literature. 2851 26

Human adenovirus 41 (HAdV-41) causes acute gastroenteritis in young children. The main characteristics of HAdV-41 infection are diarrhea and vomiting. Nevertheless, the precise mechanism of HAdV-41-induced diarrhea is unknown, as a suitable small-animal model has not been described. In this study, we used the human midgut carcinoid cell line GOT1 to investigate the effect of HAdV-41 infection and the individual HAdV-41 capsid proteins on serotonin release by enterochromaffin cells and on enteric glia cell (EGC) activation. We first determined that HAdV-41 could infect the enterochromaffin cells. Immunofluorescence staining revealed that the cells expressed HAdV-41-specific coxsackievirus and adenovirus receptor (CAR); flow cytometry analysis supported these findings. HAdV-41 infection of the enterochromaffin cells induced serotonin secretion dose dependently. In contrast, control infection with HAdV-5 did not induce serotonin secretion in the cells. Confocal microscopy studies of enterochromaffin cells infected with HAdV-41 revealed decreased serotonin immunofluorescence compared to that in uninfected cells. Incubation of the enterochromaffin cells with purified HAdV-41 short fiber knob and hexon proteins increased the serotonin levels in the harvested cell supernatant significantly. HAdV-41 infection could also activate EGCs, as shown in the significantly altered expression of glia fibrillary acidic protein (GFAP) in EGCs incubated with HAdV-41. The EGCs were also activated by serotonin alone, as shown in the significantly increased GFAP staining intensity. Likewise, EGCs were activated by the cell supernatant of HAdV-41-infected enterochromaffin cells.IMPORTANCE The nonenveloped human adenovirus 41 causes diarrhea, vomiting, dehydration, and low-grade fever mainly in children under 2 years of age. Even though acute gastroenteritis is well described, how human adenovirus 41 causes diarrhea is unknown. In our study, we analyzed the effect of human adenovirus 41 infection on human enterochromaffin cells and found it stimulates serotonin secretion in the cells, which is involved in regulation of intestinal secretion and gut motility and can also activate enteric glia cells, which are found in close proximity to enterochromaffin cells in vivo This disruption of gut barrier homeostasis as maintained by these cells following human adenovirus 41 infection might be a mechanism in enteric adenovirus pathogenesis in humans and could indicate a possible serotonin-dependent cross talk between human adenovirus 41, enterochromaffin cells, and enteric glia cells.
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PMID:Interaction of Human Enterochromaffin Cells with Human Enteric Adenovirus 41 Leads to Serotonin Release and Subsequent Activation of Enteric Glia Cells. 2936 50

Flushing is the subjective sensation of warmth accompanied by visible cutaneous erythema occurring throughout the body with a predilection for the face, neck, pinnae, and upper trunk where the skin is thinnest and cutaneous vessels are superficially located and in greatest numbers. Flushing can be present in either a wet or dry form depending upon whether neural-mediated mechanisms are involved. Activation of the sympathetic nervous system results in wet flushing, accompanied by diaphoresis, due to concomitant stimulation of eccrine sweat glands. Wet flushing is caused by certain medications, panic disorder and paroxysmal extreme pain disorder (PEPD). Vasodilator mediated flushing due to the formation and release of a variety of biogenic amines, neuropeptides and phospholipid mediators such as histamine, serotonin and prostaglandins, respectively, typically presents as dry flushing where sweating is characteristically absent. Flushing occurring with neuroendocrine tumors accompanied by gastrointestinal symptoms is generally of the dry flushing variant, which may be an important clinical clue to the differential diagnosis. A number of primary diseases of the gastrointestinal tract cause flushing, and conversely extra-intestinal conditions are associated with flushing and gastrointestinal symptoms. Gastrointestinal findings vary and include one or more of the following non-specific symptoms such as abdominal pain, nausea, vomiting, diarrhea or constipation. The purpose of this review is to provide a focused comprehensive discussion on the presentation, pathophysiology, diagnostic evaluation and management of those diseases that arise from the gastrointestinal tract or other site that may cause gastrointestinal symptoms secondarily accompanied by flushing. This review is divided into two parts given the scope of conditions that cause flushing and affect the gastrointestinal tract: Part 1 covers neuroendocrine tumors (carcinoid, pheochromocytomas, vasoactive intestinal polypeptide, medullary carcinoma of the thyroid), polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, skin changes (POEMS), and conditions involving mast cells and basophils; while Part 2 covers dumping syndrome, mesenteric traction syndrome, rosacea, hyperthyroidism and thyroid storm, anaphylaxis, panic disorders, paroxysmal extreme pain disorder, and food, alcohol and medications.
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PMID:Flushing Disorders Associated with Gastrointestinal Symptoms: Part 1, Neuroendocrine Tumors, Mast Cell Disorders and Hyperbasophila. 2965 May 25

A 67-year-old man presented with abdominal distention and vomiting.Computed tomography revealed bowel obstruction due to a cecal tumor.We performed laparoscopic ileocecal resection after decompression with an ileus tube. Intraoperative findings included multiple disseminated nodules on the mesenterium surrounding the cecal tumor.The histopathologic diagnosis was poorly differentiated adenocarcinoma, which consisted of glandular proliferation of atypical epithelial cells and dispersed infiltration of goblet cells. Immunohistochemistry showed positively stained neuroendocrine markers, such as CD56, chromogranin, and synaptophysin.The patient was diagnosed with goblet cell carcinoid of the appendix and treated with combination chemotherapy of bevacizumab, fluorouracil, folinic acid, and oxaliplatin.He remained free from progression for over 1 and half years with this treatment.Subsequent chemotherapy was ineffective, and he passed away.There is no established chemotherapy regimen for goblet cell carcinoid, which has the aspects of both adenocarcinoma and neuroendocrine tumors.However, the present case suggested the efficacy of the mFOLFOX6 regimen in combination with bevacizumab for appendiceal goblet cell carcinoid.
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PMID:[Appendiceal Goblet Cell Carcinoid Successfully Treated with Bevacizumab plus mFOLFOX6 Regimen-A Case Report]. 3240 32

Mesenteric panniculitis (MP) is a rare, benign, and idiopathic disorder characterized by chronic inflammation of the mesenteric adipose tissue of the small intestine. The exact etiology of MP is unknown and its associations with underlying malignancies continues to be poorly understood. In this case report, we describe a rare case of acute exacerbations of MP in a middle-age female with a known past medical history of non-Hodgkin's lymphoma in remission and small bowel resection for a localized carcinoid tumor. The patient was diagnosed with MP 4 years ago and started on tamoxifen therapy with adequate control of her symptoms. Last year, she reported to the emergency department with multiple episodes of sudden-onset, severe, and localized right upper quadrant abdominal pain and nausea without vomiting. She was diagnosed with an acute exacerbation of MP and a decision was made to add 60 mg prednisone daily in addition to her tamoxifen regimen. She remained symptomatically stable for the next 6 months after the start of dual therapy with tamoxifen and prednisone. However, for the past 6 months, the patient reported to the emergency department on an average of 2 times/month with the same recurrent symptoms despite high compliance with tamoxifen and prednisone therapy. She was admitted for her pain management and her dose of prednisone was increased and she was subsequently discharged home with improvement of her symptoms. Her tamoxifen was switched to mycophenolate on her follow-up visit with gastrointestinal clinic, and her disease has remained stable for the past 2 months. Our case report discusses in-depth the literature on MP and its management. We also detail the steps in management of a rare case of recurrent acute exacerbations of MP despite the patient being on immunosuppressive therapy.
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PMID:Acute Recurrent Exacerbations of Mesenteric Panniculitis With Immunosuppressive Therapy: A Case Report and a Brief Review. 3313 61


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