angioedema/nausée

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Non-Surgical Management of Colo-Colonic Intussusception in Patients with Hereditary Angioedema.

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BACKGROUND Hereditary angioedema (HAE) is an autosomal disease caused either by deficiency or presence of a non-functioning C1 inhibitor. The lack or non-functionality of said inhibitors leads to activation of an inflammatory cascade, which result in cutaneous and mucosal edema. Most patients with

Ultrasound findings in an abdominal crisis of a patient with hereditary angioedema.

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ereditary Angioedema (HAE) is a rare autosomal-dominant disease caused by serum C1 inhibitor deficiency. This deficiency leads to an up-regulation of complement, activating the bradykinin pathway and causing vascular permeability and subsequent mucosal edema. Abdominal angioedema is a less

Gastrointestinal manifestations of hereditary angioedema diagnosed by ultrasound in the emergency department.

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Abdominal angioedema is a less recognized type of angioedema, which can occur in patients with hereditary angioedema (HAE). The clinical signs may range from subtle, diffuse abdominal pain and nausea, to overt peritonitis. We describe two cases of abdominal angioedema in patients with known HAE that

[Hereditary angioedema. A rare cause of acute abdominal pain with ascites].

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METHODS Since the age of 16 years a now 25-year-old woman had been known to have C1-inhibitor (C1-INH) deficiency. She presented herself at the emergency department because of acute severe lower abdominal cramps. A urinary infection had been treated with antibiotics for the previous 4 days. There

Successful resolution of bowel obstruction in a patient with hereditary angioedema.

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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

Hereditary angioedema: Validation of the end point time to onset of relief by correlation with symptom intensity.

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Time to onset of symptom relief in hereditary angioedema (HAE) is a common primary end point in clinical studies but it has never been validated by correlation with the course of HAE symptoms. This study was designed as a retrospective validation of the primary end point for a placebo-controlled

Acute pancreatitis due to hereditary angioedema.

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BACKGROUND Hereditary angioedema (HAE) is an infrequent disorder characterized by abnormalities in the levels and/or function of complement C1 esterase inhibitor. Clinical manifestations of HAE are due to recurrent episodic swelling of the subcutaneous or submucosal tissue. When swelling involves

Acute abdominal pain with a spontaneous resolution as a mark to the diagnosis of hereditary angioedema.

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Accurate and timely diagnostics of acute abdominal pain, a common emergency, is crucial in decreasing unnecessary surgical interventions. We present the case of a patient, Xh. M. aged 21, transported to emergency after being wakened from sleep by severe, acute abdominal pain. The pain was

[Hereditary angioedema by defict of C1 esterase. Our experience in 8 cases].

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Eight cases of hereditary angioedema, all of them with low values of C1-sterase inhibitor are analyzed. In 7 cases the C3 and C4 components of the complement were assessed; the results showed marked descent of C4. The 8 patients came from 4 different families; only 2 of them were males. Six patients

Intestinal angioedema mimicking Crohn's disease.

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Angioedema usually presents as episodic attacks of swelling of the face, airway and extremities, but it may also involve visceral tissues. A 58-year-old woman with repeated episodes of abdominal pain, nausea and vomiting had two laparotomies and was treated for Crohn's disease for two years before a

Migraine-like headache in a patient with complement 1 inhibitor deficient hereditary angioedema.

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We report on an angioedema patient with a genetic defect in complement 1 inhibitor, manifesting migraine-like episodes of headache, effective prophylaxis with Danazol, and triptan for a treatment of acute clinical episode. The patient was 44-yr-old Korean man with abdominal pain and headache, who

Fish allergy causing angioedema and secondary angle-closure glaucoma.

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A 56-year-old woman with a history of primary angle-closure glaucoma presented with acute generalised swelling, and facial angioedema following a fish meal. She complained of nausea, vomiting, headache, pain in both eyes and acute loss of vision. Her visual acuity was reduced and intraocular

ACE Inhibitor-Induced Angioedema of the Small Bowel.

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Angiotensin-converting enzyme (ACE) inhibitors are known to cause angioedema. Most ACE inhibitor-induced angioedema cases describe swelling in the periorbital region, tongue, and pharynx. We describe a case of a 62-year-old female with presumed angioedema of the small bowel after more than a 2-year

Small bowel angioedema induced by angiotensin converting enzyme (ACE) inhibitor: US and CT findings.

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Small bowel angioedema induced by angiotensin converting enzyme (ACE) inhibitors is a rare and often-unrecog- nized condition that presents with transient abdominal pain, nausea and vomiting. We report a case diagnosed in a 36 year-old female. Ultrasound and CT showed segmental small bowel wall

An unusual presentation of ACE inhibitor-induced visceral angioedema.

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ACE inhibitors (ACEi) are common anti-hypertensive drugs that can cause angioedema. Though classic, or facial angioedema is rare, visceral angioedema is even less common. When angioedema occurs, it typically presents early, within 30 days of initiating therapy. Visceral angioedema most commonly

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