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)

A 44-year-old woman with C1q esterase inhibitor deficiency was seen in consultation for recurrent right upper quadrant abdominal discomfort, nausea, and vomiting. Each of these episodes was accompanied by concomitant peripheral edema. Initial diagnostic efforts were fruitless. In time, intermittent elevations in amylase and lipase developed, and a diagnosis of relapsing pancreatitis was made. We contend that the patient's recurrent acute pancreatitis is associated with her hereditary angioedema. Possible pathogenesis could involve intermittent intrapancreatic edema with partial ductal obstruction or loss of inhibition on the kallikrein-kinin system.
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PMID:Hereditary angioedema associated with pancreatitis. 143 59

Contrast media reactions may be classified as anaphylactoid, vasomotor, severe or life threatening, and fatal. Anaphylactoid reactions mimic immunoglobulin E-mediated hypersensitivity in that signs may consist of urticaria, angioedema, wheezing, dyspnea, hypotension, or shock. These reactions occur in 2% to 8% of all contrast media infusions. Vasomotor reactions occur in 5% to 8% of patients and consist of nausea, vomiting, flushing, and warmth. Severe reactions during which there is a concern for life occur about once per 1000 procedures. Fatalities have occurred in from 1:3000 procedures for intravenous cholangiography to between 1:10,000 to 1:100,000 procedures for intravenous urography. The pathogenesis of contrast media reactions is unknown, and various mechanisms may be associated with different clinical features. Radiocontrast media infusions can cause rises in plasma histamine and complement activation by either classic or alternate pathways or nonsequentially, yet adverse reactions may or may not occur. Abnormalities in the complement system or an increased conversion of prekallikrein to kallikrein has been demonstrated in some patients who have had anaphylactoid reactions. It is unknown if these mechanisms can explain the pathogenesis of anaphylactoid contrast media reactions. When patients who have had definite anaphylactoid reactions require a repeat procedure, the incidence of reactions ranges from 35% to 60% for intravascular infusion. Pretreatment with prednisone and diphenhydramine has been demonstrated to reduce this reaction rate to 9% in 465 procedures. Prednisone-diphenhydramine and ephedrine have further reduced the reaction rate to 3.1% in 192 procedures. These results are statistically significant (X2 = 5.4996, p = 0.019). Emergency equipment should be available should a severe reaction occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contrast media reactions. 649 Nov 7

This clinical entity described for the first time by Osler in 1888 presented a great therapeutic problem during many decades because of its severity. Landerman and later on Donaldson and Evans established the pathogenic mechanisms of this disease finding a deficiency in the inhibitor of the first activated component of complement, an alpha 2 aminoglycoprotein, to be the mechanism responsible of the same. More concretely, alterations in the plasmin, kinin and kallikrein systems are those that will lead to a change in vascular permeability with resultant tissue alterations. Four cases of hereditary angioneurotic edema are studied in female patients aged between 15 and 50 years and with family history consistent with angioneurotic familiar edema in which there were six cases of death due to edema of the glottis. Once the diagnosis had been made the patients were subjected to treatment with EACA at doses of 2.5 gm every 6 hours. The determinations of complement were similar in the four cases, with marked decreases in C4 and C1 inhibitor with a decrease in total complement in three cases. Regarding secondary effects, vomiting was found only in one cases, which as the dose was reduced did not necessitate termination of treatment. In summary, considering the results obtained in the cases above, we believe that due to its good tolerance and moderate cost, epsilon-amino-caproic acid at the abovementioned dosage is an excellent pharmacological agent in the treatment of Osler's hereditary angioneurotic edema.
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PMID:Epsilon-amino-caproic acid in the treatment of Osler's hereditary angioneurotic edema. 685 4

HFR is an integrated hemodiafiltration system that utilizes a double chamber filter to separate convection from diffusion. The ultrafiltrate is regenerated by passage through a sorbent cartridge made up of resin and activated carbon. A small percentage of patients using this technique had gastrointestinal symptoms that included nausea/vomiting, diarrhea and/or stomach cramps approximately 1-2 hours after the start of HFR. We undertook a series of investigations to try and elucidate the cause of these reactions. Since the majority of the patients were taking ACE inhibitors, attention was focused on contact phase activation. Healthy and uremic plasma were incubated with different components of the HFR circuit. The activated carbon caused a moderate activation of factor XII and production of kallikrein, while there was no activation for the lines, double filter or resin. Patients taking ACE inhibitors may be at risk for treatments involved with contact phase activation as ACE inhibitors also block the degradation of bradykinin. A new sorbent cartridge has now been developed that contains only resin.
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PMID:[Contact phase activation can occur with certain types of activated carbon]. 1574 7

Hereditary angioedema (HAE), a rare genetic disorder caused by a deficiency of the C1 esterase inhibitor, leads to an episodic, self-limiting increase in vascular permeability. Related symptoms commonly include recurrent, intractable abdominal pain, vomiting, and/or diarrhea. DX-88 (ecallantide), a 60-amino acid recombinant protein discovered through phage display technology, is a highly specific, potent inhibitor of human plasma kallikrein that has been used successfully in the treatment of patients experiencing acute HAE attacks. This case study involves a 65-year-old woman who presented with severe abdominal pain, cramping, and nausea. The study describes the use of a video obtained by capsule endoscopy for the direct imaging of bowel occlusion in a patient with HAE that resolved upon treatment with DX-88. After administration of DX-88, 80 mg intravenously, abdominal pain and nausea resolved within 30 min. Capsule endoscopy demonstrated a coincident resolution of the bowel wall edema, with a return to normal within approximately 1.5 h of DX-88 administration. This case study demonstrates that DX-88 can produce dramatic clinical benefits in a patient with an acute abdominal HAE attack, resolving both symptoms and pathologic signs. Furthermore, it illustrates the usefulness of videos obtained from capsule endoscopy in identifying the presence of bowel occlusion and demonstrating its subsequent rapid resolution upon administration of DX-88.
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PMID:Successful resolution of bowel obstruction in a patient with hereditary angioedema. 1846 21

Hereditary angioedema (HAE) is a rare autosomal dominant genetic disorder associated with a deficiency in C1 inhibitor. More than 200 mutations in this gene, located on chromosome 11, have been identified. Although HAE is often inherited, 20-25% of cases are from new spontaneous mutations and they have no family history of swelling. Decreased C1 inhibitor activity leads to inappropriate activation of multiple pathways, including the complement and contact systems and the fibrinolysis and coagulation systems. Reduced C1 inhibitor activity results in increased activation of plasma kallikrein-kinin system proteases and increased bradykinin levels. Bradykinin is felt to be the main mediator of symptoms in HAE. Patients with HAE have recurrent episodes of swelling of the extremities, abdomen, face, and upper airway. Angioedema involving the gastrointestinal tract can lead to intestinal wall edema, which results in abdominal pain, nausea, vomiting, and diarrhea. Laryngeal swelling is life-threatening and may lead to asphyxia. Common triggers of an attack include trauma, stress, infection, menstruation, oral contraceptives, hormone replacement therapy, and angiotensin-converting enzyme inhibitors. Laboratory testing including C4, C1 inhibitor level, and function is needed to confirm or rule out the diagnosis of HAE. The treatment of HAE has improved significantly in recent years with the availability of several safe and effective therapies. Several consensus guidelines have been created to further assist in the management of HAE patients. This review will provide an update on the classification, pathophysiology, clinical presentation, and diagnosis of HAE.
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PMID:Hereditary angioedema: classification, pathogenesis, and diagnosis. 2222 32