Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A procedure for processing-independent quantitation of procholecystokinin (proCCK) and its products has been applied to plasma. The procedure is based on tryptic cleavage after Lys61 and Arg71 with subsequent monospecific radioimmuno-analysis of fragment 62-71 of human proCCK, which again corresponds to fragment 1-10 of CCK-22. The detection limit of the analysis was 0.2 pmol/l. Plasma was extracted with ethanol. In plasma from 13 healthy volunteers the basal concentration with the above-mentioned radioimmunoassay was 1.1 +/- 0.1 pmol/l (mean +/- S.E.M.) before, and 13.7 +/- 0.6 pmol/l after, incubation with trypsin. Two hours after ingestion of a mixed meal, the plasma concentration was 2.0 +/- 0.1 pmol/l before, and 21.7 +/- 1.2 pmol/l after tryptic cleavage. With a conventional CCK radioimmunoassay specific for the C-terminally amidated and O-sulfated bioactive epitope, the concentration was 1.0 +/- 0.1 pmol/l in the basal state and 4.2 +/- 0.4 pmol/l 2 h after a meal. Tryptic cleavage did not increase the concentrations of amidated, bioactive CCK peptides. In plasma from 37 patients with the carcinoid syndrome, the basal concentration of proCCK and its products was 14.1 (2.8-150.4) pmol/l (median (range)), compared with 0.3 (0-18.8) pmol/l for carboxyamidated CCK. Only two patients had significantly elevated CCK concentrations. We conclude that processing-independent analysis is useful for quantitation of proCCK and its products in plasma, since it quantitates CCK cell secretion more accurately than conventional CCK assays.
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PMID:Quantitation of procholecystokinin and its products in plasma by processing-independent analysis. 755 93

A 35-year-old woman was scheduled for laparoscopic removal of an ovarian tumor. Intravenous metamizol was administered and when pneumoperitoneum was performed she developed severe hypotension and bronchospasm. Anaphylactic reaction was suspected, all drugs were suspended, and 2 doses of intravenous adrenalin (0.2 and 1 mg) were injected followed by continuous perfusion. Because response was slow and given the unknown origin of the tumor, the possibility of a carcinoid crisis was considered. When an intravenous bolus dose of octreotide was administered, pressure recovered, patient was extubated and could be transferred asymptomatic to the recovery ward. Tests later ruled out carcinoid syndrome, whereas tryptase levels in blood extracted during surgery and allergy tests confirmed an anaphylactic reaction to metamizol. Carcinoid crisis can be difficult to distinguish from anaphylactic reaction because the clinical pictures are similar. Anesthetic management of carcinoid crisis has been facilitated by administration of octreotide. Less is known about the use of octreotide to treat hypotension in patients with autonomic neuropathy based mainly on the drug's ability to produce splanchnic vasoconstriction. This is probably the reason why octreotide resolved our patient's shock in a context of systemic vasodilation caused by the anaphylactic reaction.
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PMID:[Anaphylactic reaction versus carcinoid crisis: the role of octreotide as a vasoconstrictor]. 1549 39

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely but if elevated in the absence of anaphylaxis, should suggest alternative diagnoses including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential because they do not usually accompany any of the aforementioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year or two or more episodes in 2 months are classified as IA-frequent (IA-F). Patients who experience fewer episodes are classified as IA-infrequent (IA-I). This distinction is important because IA-F patients initially will require prednisone as disease-modifying therapy whereas most IA-I patients will not. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Chapter 25: Idiopathic anaphylaxis. 2279 98

Anaphylaxis is a systemic, life-threatening disorder triggered by mediators released by mast cells and basophils activated via allergic (IgE-mediated) or nonallergic (non-IgE-mediated) mechanisms. It is a rapidly evolving, multisystem process involving the integumentary, pulmonary, gastrointestinal, and cardiovascular systems. Anaphylaxis and angioedema are serious disorders that can lead to fatal airway obstruction and culminate in cardiorespiratory arrest, resulting in hypoxemia and/or shock. Often, these disorders can be appropriately managed in an outpatient setting; however, these conditions can be severe enough to warrant evaluation of the patient in the ED and in some cases, hospitalization, and management in an ICU. Reports suggest that underdiagnosis and undertreatment of anaphylaxis are common. Several new syndromes have been described recently including bird-egg, pork-cat, delayed allergy to mammalian meat and a diverse group of mast cell activation disorders. Conditions such as postural orthostatic tachycardia syndrome, carcinoid syndrome, Munchausen stridor, and factitious anaphylaxis can present similarly and need to be included in the differential diagnosis. Anaphylaxis is a clinical diagnosis, but plasma tryptase and urinary histamine levels are often elevated, allowing diagnostic confirmation; however, diagnostic testing should not delay treatment as results may not be immediately available. The sine qua non of treatment is avoidance of any known triggers and epinephrine, which should never be delayed if this disorder is suspected. Secondary treatments include fluids, bronchodilators, antihistamines, and glucocorticoids. Patients with cardiopulmonary arrest or airway or vascular compromise require mechanical ventilation, vasopressors, and other advanced life support in the ICU.
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PMID:Anaphylaxis. 2880 Aug 65

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely, but, if elevated in the absence of anaphylaxis, should suggest alternative diagnoses, including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema or acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential diagnosis because urticaria does not usually accompany any of the above-mentioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year, or two or more episodes in 2 months are classified as having IA-frequent (IA-F). Patients who experience fewer episodes are classified as having IA-infrequent (IA-I). This distinction is important because patients with IA-F will initially require prednisone as disease-modifying therapy, whereas most patients who with IA-I will not require prednisone. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Idiopathic anaphylaxis. 3169 Mar 94