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We stayed in the Dominica, and it was nearly perfect. Spotlessly clean. The decor style was sort of eclectic. Loved the large shower with great water pressure. We did not have the problem some others complained about of not enough hot water--we had plenty. There were wall-mounted dispensers of hand soap beside the sink and of soap and shampoo in the shower. We wouldn't have had to bring either of these. There were also the typical small bottles of lotion and bars of soap that you find in hotels. The bath towels were large and soft and there were also beach towels. The king-size bed was very comfortable. The unit was plenty large enough for the two of us. It had a very efficient central a/c. Good TV reception and also the internet worked great. The only thing I found to be missing in the unit was a dishwasher. We ate all of our meals out so that was not an issue for us, but if you plan to do a lot of cooking you should be aware of this. This unit is on the second level and it didn't actually have a balcony or deck. There are two small landings where you can sit in an upright chair but there's not enough room for a lounger. But who cares, with that gorgeous beach at the foot of your stairs?! Lots of shade from large Australian Pines. I have to be careful about getting too much sun because of sun poisoning, so this was perfect for me. There were plenty of chaise lounges, although to be honest, they weren't the most comfortable I've ever sat in. There is a swing hanging from one of the huge pine trees that is ideal for watching the beautiful sunsets from. There is also a hammock, but I never saw anyone use that while we were there. There is not a pool, but the ocean felt great and the water is so clear that we preferred it to a pool anyway. This place is very quiet. All of the guests I saw while we were there were at least middle-aged--no children or teens or even any young couples. Hmmm, wonder why no young couples? Richard, the owner is a very gracious host. When we checked in he offered us cold drinks and a fishing pole. He also offered to help carry our luggage up. He was usually out puttering around the property but he was never imposing. If we initiated conversation he was very friendly, but otherwise he just let us be. I only met his wife, Lynn, when we were checking out.
- Official Description (provided by the hotel):
- Angelinos Sea Lodge offers four beachfront cottages right on the Florida Gulf Coast, Anna Maria Island, Holmes Beach. Hidden in a quiet residential street, these beach vacation rentals are quaint, charming, and just a few steps to the white sand and turquoise ocean. All sea lodges have direct ocean views through a subtropical garden of swaying palms and whispering pines.To experience living on the beach and to feel life in harmony with nature at a price that's right for you, take the virtual tour of our beach, garden, and the interior of our four vacation rental units on the beach. ... more less
- Reservation Options:
- TripAdvisor is proud to partner with Travelocity and Hotels.com so you can book your Angelinos Sea Lodge reservations with confidence. We help millions of travelers each month to find the perfect hotel for both vacation and business trips, always with the best discounts and special offers.
- Also Known As:
- Angelinos Sea Hotel
- Angelinos Sea Lodge Anna Maria Island/Holmes Beach, FL


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The Power of Limits was inspired by those simple discoveries of harmony. The author went on to investigate and measure hundreds of patterns—ancient and modern, minute and vast. His discovery, vividly illustrated here, is that certain proportions occur over and over again in all these forms. Patterns are also repeated in how things grow and are made—by the dynamic union of opposites—as demonstrated by the spirals that move in opposite directions in the growth of a plant.
The joining of unity and diversity in the discipline of proportional limitations creates forms that are beautiful to us because they embody the principles of the cosmic order of which we are a part; conversely, the limitlessness of that order is revealed by the strictness of its forms. The author shows how we, as humans, are included in the universal harmony of form, and suggests that the union of complementary opposites may be a way to extend that harmony to the psychological and social realms as well.
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"In his lifetime, Gary has played music from many cultures. His integrity, humanity and humor have opened doors into personal and private worlds. The gift of songs and relationships with people from around the world has enriched Gary's life. These are gifts that Gary honors and remembers."
-Julie Cajune, Salish Montana educator
"I cannot imagine trying to come to terms with the history of this complicated country I have chosen to make my life's work without Gary's exquisite mastery and understanding of its many varied musical traditions. We don't leave home without him."
- Ken Burns, Florentine Films
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New Album Release: Old Songs, 2016
"Old Songs reflects a commitment I made back in 1996 when I first went to the Northern Plains of Dakota to study and record the songs of the American Indian. In 2015, I wanted to re-record my favorite melodies, which you hear on this recording. Many thanks go out to traditional American Indian flute makers Paul Thompson ~ Navajo and Bryan Akipa ~ Dakota. Without their flutes I could not have made this recording."
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- Author: Huamin Henry Li, MD, PhD, CPI; Chief Editor: Michael A Kaliner, MD more...
Practice Essentials
Angioedema is the swelling of deep dermis, subcutaneous, or submucosal tissue due to vascular leakage.[1, 2] Acute episodes often involve the lip, eyes, and face (see the image below); however, angioedema may affect other parts of body, including respiratory and gastrointestinal (GI) mucosa. Laryngeal swelling can be life-threatening.
Signs and symptoms
Angioedema may affect many organ systems. Visible swelling is common in peripheral angioedema. It is often associated with local burning sensation and pain without pronounced itchiness or local erythema. The most commonly involved areas are:
Peripheral swelling: skin and urogenital area (e.g., eyelids or lips, tongue, hands, feet, scrotum, etc.)
Abdomen: Abdominal pain (sometimes it can be the only presenting symptom of angioedema)
Larynx: Throat tightness, voice changes, and breathing trouble (indicators of possible airway involvement), potentially life-threatening.
See Presentation for more detail.
Examination in patients with suspected angioedema includes the following:
Dermatologic – Areas of swelling with or without erythematous skin, often with ill-defined margins; the face, extremities, and genitalia are most commonly affected [3]
GI – No specific findings may be present, even in severe cases of angioedema, or there may be abdominal distention and signs consistent with bowel obstruction; changes in bowel sounds and diffuse or localized tenderness may be present; the clinical picture may resemble that of an acute abdomen
Upper airway – Direct visualization of the uvula or tongue swelling; laryngoscopy is needed to assess laryngeal or vocal cord involvement; document swelling by means of physician notes, photographs, or both
Severe attacks of angioedema can herald the onset of systemic anaphylaxis, characterized initially by dyspnea. Many cases of angioedema occur in patients with urticaria.
Most mild cases of angioedema do not require laboratory testing. Suspected allergies to food, stinging insects, latex, and antibiotics can be screened and diagnosed. The value of aeroallergen screening for patients with angioedema is limited, except with regard to establishing atopic status.
For angioedema without urticaria (especially those with recurrent episodes), diagnostic tests should include the following:
C4 level
C1 esterase inhibitor (C1-INH) quantitative and functional measurements
C1q level
Screening laboratory studies have limited value in most cases. For chronic or recurrent angioedema without a clear trigger, clinicians may consider the following tests:
CBC with differential
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level
D-dimer level
Comprehensive metabolic profile
Antinuclear antibody (ANA) testing
CH50 level
Thyroid studies, including levels of thyroid stimulating hormone, free T4, and thyroid autoantibodies (antimicrosomal and antithyroglobulin), particularly in women or in patients with a family history of thyroid disease or other autoimmune diseases
If the history and physical examination findings suggest specific problems, other tests that may be helpful include the following:
Stool analysis for ova and parasites
Helicobacter pylori workup
Hepatitis B and C virus workup
Rheumatoid factor
Cryoglobulin levels
Imaging studies
Imaging studies
Most angioedema patients do not need any imaging studies. However, when internal organ involvement is suspected, during acute attacks, the following studies can be performed:
Plain abdominal films – These may show a "stacked coin" or "thumbprint" appearance of the intestines [4]
Abdominal ultrasonography – This may show ascites.
Abdominal computed tomography – This may show severe edema of the bowel wall [1]
Chest radiography – This may show pleural effusion
Soft-tissue neck radiography – This may show soft-tissue swelling [5]
See Workup for more detail.
The primary goal of medical treatment for angioedema is to reduce and prevent swelling, as well as to reduce discomfort and complication.
Most medications used in treating urticaria and anaphylaxis are also used in the management of many types of angioedema. Epinephrine should be used when laryngeal angioedema is suspected. In addition, supportive care should be provided, regardless of the etiology.
Medications used in the management of angioedema include the following:
Alpha- and beta-adrenergic agonist agents (eg, epinephrine)
First-generation antihistamines (eg, diphenhydramine, chlorpheniramine, cyproheptadine, hydroxyzine hydrochloride)
Second-generation antihistamines (eg, cetirizine, desloratadine, fexofenadine, levocetirizine, loratadine)
Histamine H2 antagonists (eg, ranitidine, cimetidine)
Leukotriene receptor antagonists (eg, montelukast, zafirlukast)
Tricyclic antidepressants (eg, doxepin)
Corticosteroids (eg, prednisone, methylprednisolone, prednisolone)
Androgen derivatives (eg, danazol, oxandrolone), progesterone-based birth control pills.
Antifibrinolytic agents (eg, aminocaproic acid, tranexamic acid)
Immunomodulators (eg, cyclosporine, mycophenolate, methotrexate, )
Agents used in treating C1INH-HAE: C1 INH concentrates, ecallantide, and icatibant.
Surgical option
In severe cases of laryngeal edema, a surgical airway must be created via cricothyrotomy or tracheotomy.
See Treatment and Medication for more detail.
Angioedema, first described in 1586,[6] is usually defined by pronounced swelling of the deep dermis, subcutaneous or submucosal tissue, or mucous membranes as a result of vascular leakage.[3] Other terms, such as giant urticaria,[7] Quincke edema,[8] and angioneurotic edema,[9] have also been used in the past to describe this condition. Clinically, angioedema is usually nonpitting and nonpruritic. Involved skin often shows no change in color or may be slightly erythematous (see the image below).
Angioedema is most commonly observed affecting the lips and eyes (periorbital). Other commonly involved areas may include the face, hands, feet, and genitalia. However, this condition is not always visible, as in cases involving the gastrointestinal (GI) tract.[10] Depending on the area of swelling, pain can be absent or mild, as in most peripheral or facial swelling, or it can be very severe, as in GI angioedema. (See Presentation.)
Swelling that involves the tongue and upper airways is cause for greater concern than swelling involving other areas, owing to the potential of airway compromise.[11, 12] Laryngeal swelling is life-threatening and should be treated as a medical emergency.
Disfiguration, pain, and reduced function are common complaints in patients with angioedema, but this condition is also commonly associated with urticaria. When both angioedema and urticaria are evident during clinical presentation, the episode is primarily mast cell−mediated.[13] Affected patients describe subjective pruritus, sometimes associated with hypersensitivity to an offending agent (eg, a food or drug). However, the underlying triggers are often unidentifiable.
There are also a significant number of angioedema cases that present with angioedema alone. In such cases, the clinical presentation, trigger, cause, and response to treatment may be quite different from those in cases that present with both angioedema and urticaria; therefore, some experts believe that these patients may (at least in part) have different pathophysiologic mechanisms.[11] Many such cases do not respond to antihistamines. Vasoactive mediators other than histamine (eg, bradykinin) may be involved in the swelling.[11] (See Pathophysiology.)
Although angioedema can manifest as an episodic or self-limiting event, it can often be described as recurrent or chronic. Thus, classification is not always straightforward. Because most cases of angioedema are found to be associated with urticaria, those cases usually follow the classification of urticaria (ie, acute vs chronic or induced vs spontaneous).[14] For angioedema that is not associated with urticaria, other classifications have been suggested.[15, 11] (See Classification and Subtypes of Angioedema.) The most recent classification for recurrent angioedema without the presence of urticaria has also been proposed by an international angioedema work group.[16]
This article concentrates on angioedema without urticaria. For angioedema associated with urticaria, the treatment strategies are essentially the same as those for acute urticaria (see Acute Urticaria). Angioedema caused by decreased functional C1-esterase inhibitor (C1-INH) is covered elsewhere as well (see Hereditary Angioedema [HAE] and Acquired Angioedema [AAE]).
Angioedema is a result of the fast onset of an increase in local vascular permeability in subcutaneous or submucosal tissue. Histamine and bradykinin are the most recognized vasoactive mediators known to be critical in the pathologic process of angioedema; most cases of angioedema are primarily mediated by 1 of these 2 mediators, though some investigators indicate the possibility that both may be involved in certain cases.[17] (See Classification and Subtypes of Angioedema.)
Other vasoactive mediators are, at least in part, involved in the pathogenesis of various types of angioedema. Leukotrienes, for example, may play an important role in the onset of angioedema that is induced by nonsteroidal anti-inflammatory drugs (NSAIDs).[18] Thus, factors influencing histamine release, bradykinin metabolism, and endothelial cell function or permeability may directly or indirectly regulate the process of angioedema.
Histamine- and bradykinin-mediated angioedema
For histamine-mediated angioedema (histaminergic angioedema), mast cells and basophils are the primary sources of histamine. The activation of mast cells or basophils with subsequent histamine release may be either mediated or unmediated by immunoglobulin E (IgE). IgE-mediated mast cell activation and degranulation, key elements of an allergic reaction, often manifest as urticaria and angioedema. Type I hypersensitivity reactions, such as food or drug allergies, are typically IgE-mediated.
Non–IgE-mediated mast cell activation or mediator release may explain certain autoimmune-mediated and idiopathic angioedema.[19] Numerous inflammatory mediators and cytokines and chemokines are known to influence histamine release and activation of mast cells and basophils. In addition, C3a and C5a are known to activate mast cells or basophils via an IgE-independent pathway.
Mast cells can also be activated by other non–IgE-mediated processes, such as the binding of IgG antibodies to IgE receptors on mast cells or basophils, leading to spontaneous mast cell activation and histamine release. Another example of non–IgE-mediated mast-cell activation is the reaction induced by intravenous (IV) contrast material.
Plasma and tissue factors, such as bradykinin, and certain components in the contact system or the fibrinolytic system are also found to play an important role in certain forms of angioedema.[20, 21] For angioedema without evidence of histamine involvement, bradykinin is likely the most important mediator.[11]
Hereditary angioedema (HAE), angiotensin-converting enzyme (ACE) inhibitor–induced angioedema, and certain idiopathic angioedemas are examples of bradykinin-mediated angioedema; bradykinin levels are elevated during an episode of angioedema.[13] Accumulation of bradykinin, either from overproduction or from decreased breakdown, accounts for the pathogenesis of these types of angioedema.[20]
C1-INH is a serine protease that is involved in the regulation of bradykinin, a potent vasoactive substance. Low levels of this protease (either hereditary or acquired) results in unchecked activation of the kallikrein-kinin system, which leads to the overproduction of bradykinin (see the image below).[22] (See Hereditary Angioedema.)
Other mediators
Besides mast cells, many other cellular components (eg, macrophages, dendritic cells, lymphocytes, monocytes, eosinophils, and endothelial cells) are involved in the pathogenesis of angioedema.[3, 23] These contribute to the generation, maturation, and activation of mast cells and basophils and thereby exert an influence on histamine release.[24] Release of vasoactive substances causes vasodilatation of endothelial cells, as well as smooth muscle bowel contraction,[25] ultimately manifesting in the common clinical presentation of the disease.
Urticaria and angioedema
Urticaria is often discussed together with angioedema. In many cases, the 2 conditions are remarkably similar, both in their underlying etiologies and in the clinical management strategies employed to treat them. However, angioedema is also quite different from urticaria, in that it usually involves a deeper layer of skin (reticular dermis) or subcutaneous or submucosal tissue, whereas urticaria affects a more superficial layer of skin (papillary dermis and mid-dermis). In fact, mucosal involvement is observed only in angioedema but not in urticaria.
In addition, pruritus is the most prominent complaint in urticaria, but it is less troublesome or absent in angioedema. Furthermore, pain or tenderness is uncommon in urticaria but frequent or even severe in angioedema. Addressing these differences is necessary for successful treatment of angioedema.
Angioedema with and without urticaria
Angioedema associated with urticaria may represent hypersensitivity to an offending agent. Histamine is released into the bloodstream, resulting in increased endothelial cell permeability. Angioedema, generalized urticaria, and, in severe cases, anaphylaxis will occur.[26] The allergen binds to the mast cell, causing degranulation and histamine and tryptase release. Degranulations of mast cells have also been shown to be a direct result of anesthetics, contrast media, and opiates.[26]
Autoantibodies against the mast cell IgE receptor or mast cell−bound IgE (or basophils) are another common cause of histamine release. Additionally, proteases may activate the complement cascade associated with C3a, C4a, and C5a, which are considered anaphylactoids, and result in increased capillary permeability and extravasation of fluid.[25]
With respect to pathophysiology, angioedema without urticaria may differ substantially from angioedema with urticaria. In many cases, histamine is not involved or only minimally involved. Bradykinin is known to be the major mediator for HAE, acquired angioedema (AAE), ACE inhibitor–induced angioedema, and certain idiopathic angioedemas.
HAE and AAE
The following 3 types of HAE have been identified:
Type I – C1-INH deficiency
Type III – Normal C1-INH concentration and function with C1-esterase dysfunction [31] ; often seen in women with factor XII gene mutations. [20, 32, 33]
There are no reliable diagnostic tests to establish the diagnosis of type III HAE; rather the patient's family history and clinical presentation are key diagnostic components. Originally described as affecting women only, type III HAE was subsequently reported in a few men as well.[34] Orofacial involvement seems to be the most common presentation for type III HAE, but abdominal attacks are seen less frequently in this variant. The new classification has proposed to combine HAE Type I and II and name it as C1-IHN HAE, whereas HAE Type III is to be differentiated into FXII-HAE and U-HAE.[16]
AAE (now preferred to be named as C1-INH-AAE) is classified as either type I or type II.[13]
C1-INH-AAE Type I is associated with B-cell proliferative disorders and is characterized by hypercatabolization of C1-INH. Immune complexes are formed between antibodies and abnormal immunoglobulins on the cell surface of B cells. The complement cascade hyperreacts, producing large amounts of C1. C1-INH is then consumed in attempts to prevent the activation of the continuously activated C1. As a result, levels of serum C1q are decreased in patients with C1-INH-AAE, but not in those with C1-INH-HAE (see Laboratory Studies).
The relative deficiency of C1-INH causes increased activation of the kallikrein-kinin system.[35, 25] Enzymatic cleavage by kallikrein is increased with consumption of kininogen, and subsequently, the production of bradykinin increases. The end result of this intricate molecular cascade is vasodilation meditated by the interaction of kinins with the endothelial cell receptors B1R and B2R.[36]
Type II AAE is associated with autoantibodies (IgG, and less often, IgM) directed against the C1-INH molecule.[25] Depletion of C1-INH results in the production of large amounts of bradykinin and other vasoactive substances, which causes the signs and symptoms of angioedema.
More than 40% of chronic angioedema is idiopathic. Trauma, surgical procedures, and stress are common nonspecific triggers for angioedema attacks.
Angioedemas with identifiable etiologies include those caused by the following:
Hypersensitivity (eg, food, drugs, or insect stings)
Physical stimuli (eg, cold or vibrations)
Autoimmune disease or infection
ACE inhibitors
C1-INH deficiency (hereditary and acquired)
Angioedemas with unidentifiable etiologies include idiopathic angioedema (histaminergic or nonhistaminergic).
Angioedema has also been associated with certain conditions or syndromes, such as the following:
Cytokine-associated angioedema syndrome (ie, Gleich syndrome or episodic angioedema with eosinophilia) [37]
Well syndrome or eosinophilic cellulitis (ie, granulomatous dermatitis with eosinophilia) [38]
Hypersensitivity angioedema
Hypersensitivity (allergic) angioedema is often associated with urticaria. It is typically observed within 30 minutes to 2 hours after exposure to the allergen. Mast cell–mediated angioedema or urticaria may be triggered by food, drugs, animal bites, stings (eg, from Hymenoptera), preservatives, or food coloring.[13] Food coloring and preservatives may cause angioedema with or without urticaria.[25]
Allergic angioedema may be associated with urticaria and anaphylaxis. In an Australian study of all anaphylaxis presentations to an adult emergency department (ED) in a single year, angioedema was present in 40% of the 142 cases (49.3% of those with urticaria).[39] In a Korean study, 69.4% of 138 patients who had anaphylaxis were found to have angioedema.[40]
Pseudoallergic angioedema
"Pseudoallergic" angioedema (PAE) is not mediated by IgE; that is, the angioedema is caused by a nonallergic or nonimmunologic reaction. However, its clinical course and presentation are very similar to those of allergic angioedema. Typical examples are angioedema induced by NSAIDs and that induced by intravenous (IV) contrast material; aspirin (ASA) is the most common culprit.
True IgE-mediated reactions to ASA or other NSAIDs are uncommon. The angioedema (with or without urticaria) reflects the pharmacologic properties of the drugs. By inhibiting cyclooxygenase (COX), ASA and NSAIDs cause overproduction of proinflammatory and vasoactive leukotrienes. COX-2 inhibitors and acetaminophen (APAP) do not usually cause angioedema.
Nonallergic angioedema
Nonallergic angioedema does not involve IgE or histamine and is generally not associated with urticaria. The 5 types of nonallergic angioedema are as follows[20] :
Renin-angiotensin-aldosterone system (RAAS)-blocker-induced angioedema (RAE)
Hereditary angioedema
HAE, a rare autosomal dominant disorder, is perhaps the prototype of nonallergic angioedema.[27] Most patients report a family history of disease, but approximately 20–25% of cases are the result of spontaneous mutations. More than 150 mutations in the C1 INH gene on the long arm of chromosome 11 have been associated with HAE.[41] As noted (see Pathophysiology), 3 types of HAE have been identified.
Acquired angioedema
Acquired angioedema, now known as C1-INH-AAE is a rare disorder caused by accelerated consumption of C1-INH or the production of autoantibodies to C1-INH. Onset is usually in the fourth decade of life. C1-INH-AAE is often associated with autoimmune diseases and lymphoproliferative disorders.[25]
ACE inhibitor–induced angioedema (ACEI-AAE or AIIA)
ACE inhibitors can precipitate attacks of angioedema by directly interfering with the degradation of bradykinin, thereby potentiating its vasoactive effect. ACE inhibitor–induced angioedema (AIIA or ACEI-AAE) is bradykinin-mediated, as in cases of HAE and AAE. ACEI-AAE occurs when ACE inhibitors interfere with the degradation of bradykinin, a potent vasoactive nonapeptide.
In a multicenter study, ACEI-AAE accounted for almost one-third of angioedema cases treated in the ED; however, it remains a rare ED presentation.[42] Most ACEI-AAE is observed in the first week after starting the medicine; in as many as 30% of cases, however, onset occurs after months, or even years, of taking the medicine.[30, 42] In later-onset cases, the ACE inhibitor can easily be overlooked as a cause of angioedema.
The most common sites of ACEI-AAE are the face, lip, and tongue, but abdominal involvement has been reported as well.[3] Abdominal computed tomography (CT) can be informative in cases with GI involvement.[2]
Genetic screening for ACE polymorphism may help identify the population at risk for ACEI-AAE. In 0-9.2% of cases, patients with ACEI-AAE may develop angioedema when switching to an angiotensin II receptor blocker (ARB).[30]
Physically induced angioedema
Physically induced angioedema is caused by physical agents, such as cold, heat pressure, vibration, and ultraviolet radiation.[25] This manifestation may occur with or without urticaria. Cold-induced angioedema and urticaria have been reported in association with cryoglobulins, cold agglutinin disease, cryofibrinogenemia, and paroxysmal cold hemoglobinuria. (See Anaphylaxis, Urticaria, and Acute Urticaria.)
Idiopathic angioedema
The causes of IAE are, by definition, not identifiable. Furthermore, the exact mechanisms are unclear, though nonspecific mast cell activation and degranulation are suspected.[43, 26] On the basis of responses to medication, some cases are thought to be mediated by mast cell activation, albeit independent of IgE. Some cases may be associated with urticaria. Common triggers include heat, cold, emotional stress, and exercise.
Other causes
The link between infection and angioedema is vague at best. Helicobacter pylori infection has been found to be associated with HAE exacerbation, and treatment of H pylori infection has led to clinical improvement of chronic urticaria and angioedema.[28] Systemic viral, bacterial, or parasitic infection may stimulate the immune system and cause improper activation or inflammatory changes.
C1-INH functions normally in estrogen-dependent angioedema.[44] This has been proposed as HAE type III. The exact mechanism of angioedema in these patients is still unclear.[31] In some of the affected patients, factor XII (FXII) point mutation results in a gain of function that can potentially affect the metabolism of bradykinin.[45]
Patients with Gleich syndrome exhibit elevated eosinophil levels with angioedema. Gleich syndrome, which responds well to corticosteroids, is thought to be related to hypereosinophilic syndrome.[46] In addition to the elevated eosinophil count, immunoglobulin G (IgG) autoantibody against endothelial cells has been identified.
Thyroid autoantibodies are found in 14-28% of patients with chronic urticaria or angioedema, and IgG autoantibodies to either the high-affinity receptor for IgE (FceRI) or to IgE are found in 30-50% of these patients.[43, 28] In affected individuals, autoantibody (IgG) has been found to crosslink FceRI on mast cells, resulting in mast cell activation and release of histamine, cytokines, and other proinflammatory mediators. Immunomodulatory drugs may be beneficial for this type of angioedema.[47]
United States statistics
The reported incidence or prevalence of angioedema varies depends on the study population and the method of study (eg, patient reported vs physician diagnosed). The World Allergy Organization (WAO) notes that urticaria and angioedema affects up to 20% of the population.[14] It is estimated that approximately 10-20% of population may experience at least 1 episode of angioedema during their lifetime.[43, 26]
Approximately 40-50% of patients with chronic spontaneous urticaria have angioedema, and about 10% have angioedema alone.[13, 14] Up to 1% of the population has chronic urticaria.[43] With these data in mind, up to 0.5% of the population is estimated to have chronic or recurrent angioedema.
It is likely that the great majority of cases of chronic or recurrent angioedema are idiopathic.[43, 26] HAE has an estimated prevalence of 1:10,000 to 1:50,000.[48] The prevalence of AAE is very low; until 2006, only about 136 cases had been reported in the literature.[29] The reported incidence of ACE inhibitor–induced angioedema ranges from 0.1% to 6%.[30]
International statistics
International occurrence rates are believed to be similar to those reported in the United States. However, in a Danish population survey, the lifetime prevalence of angioedema was 7.4%, and approximately 50% of cases were chronic angioedema (non-HAE).[35] In this study, 35.5% of angioedema patients had urticaria. The basis for the inconsistency between these findings and those of other studies is not clear.
Age-related demographics
Angioedema can affect people of all ages. Persons who are predisposed to angioedema have an increase in frequency of attacks after adolescence, with the peak incidence in the third decade of life. There is a continuous increase in the rate of hospital admissions for angioedema (3.0% per year).[14] The rate of hospitalization is highest in persons aged 65 years and older.[14]
Allergic reactions to food are more common in children. For patients with HAE, the onset of symptoms is often around puberty. The average age for angioedema induced by ACE inhibitors is 60 years. IAE is more common among persons aged 30-50 years than among other age groups.[43]
Sex-related demographics
Estrogen may exacerbate certain forms of angioedema. In HAE, affected women tend to have more frequent attacks and run more severe clinical courses. Oral contraceptives containing estrogen are often linked to exacerbation of swelling attacks. Chronic idiopathic angioedema is more common in females than in males.[43] Other types of angioedema do not show a strong sex preponderance.
Race-related demographics
No specific racial predilection exists for angioedema. However, black individuals are more susceptible to angioedema induced by ACE inhibitors. Compared with white persons, the adjusted relative risk for black persons is about 3.0 to 4.5.[30] Other forms of angioedema have no clear association between race and the disease frequency or severity.
The prognosis for patients with angioedema depends on the etiology and varies as follows:
Angioedema with identifiable causes – If the trigger(s) can be identified and avoided, angioedema can be prevented
Angioedema without identifiable causes – There is a tremendously variable clinical course, ranging from mild to severe and a few days to many years; the response to conventional treatment is less unpredictable
HAE – Lifelong treatment is often required
AAE – Outcome depends on the treatment of underlying lymphoproliferative or autoimmune disorders
Patient Education
Individuals with allergies to food, venom, or medications need to be educated regarding allergen avoidance. Patients must also be educated regarding the indications for and proper technique of epinephrine autoinjector use and the need to seek further medical assistance afterward.
For patient education information, see the Allergies Center and the Skin Conditions and Beauty Center, as well as Hives and Angioedema, Severe Allergic Reaction (Anaphylactic Shock), Food Allergy, and Drug Allergy.
Other recommended Websites include the following:
World Allergy Organization (WAO)
American Academy of Allergy, Asthma and Immunology (AAAAI)
American College of Allergy, Asthma and Immunology
Joint Council of Allergy, Asthma, and Immunology (JCAAI)
Food Allergy Research and Education (FARE) (formerly Food Allergy and Anaphylaxis Network [FAAN])
US Hereditary Angioedema Association (HAEA)
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Bossi F, Fischetti F, Regoli D, et al. Novel pathogenic mechanism and therapeutic approaches to angioedema associated with C1 inhibitor deficiency. J Allergy Clin Immunol. 2009 Dec. 124(6):1303-10.e4. [Medline]. [Full Text].
Banerji A, Weller PF, Sheikh J. Cytokine-associated angioedema syndromes including episodic angioedema with eosinophilia (Gleich's Syndrome). Immunol Allergy Clin North Am. 2006 Nov. 26(4):769-81. [Medline].
Ferreli C, Pinna AL, Atzori L, Aste N. Eosinophilic cellulitis (Well's syndrome): a new case description. J Eur Acad Dermatol Venereol. 1999 Jul. 13(1):41-5. [Medline].
Brown AF, McKinnon D, Chu K. Emergency department anaphylaxis: A review of 142 patients in a single year. J Allergy Clin Immunol. 2001 Nov. 108(5):861-6. [Medline].
Yang MS, Lee SH, Kim TW, et al. Epidemiologic and clinical features of anaphylaxis in Korea. Ann Allergy Asthma Immunol. 2008 Jan. 100(1):31-6. [Medline].
Kalmár L, Hegedüs T, Farkas H, Nagy M, Tordai A. HAEdb: a novel interactive, locus-specific mutation database for the C1 inhibitor gene. Hum Mutat. 2005 Jan. 25(1):1-5. [Medline].
Banerji A, Clark S, Blanda M, LoVecchio F, Snyder B, Camargo CA Jr. Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Ann Allergy Asthma Immunol. 2008 Apr. 100(4):327-32. [Medline].
Frigas E, Park M. Idiopathic recurrent angioedema. Immunol Allergy Clin North Am. 2006 Nov. 26(4):739-51. [Medline].
Hentges F, Hilger C, Kohnen M, Gilson G. Angioedema and estrogen-dependent angioedema with activation of the contact system. J Allergy Clin Immunol. 2009 Jan. 123(1):262-4. [Medline].
Cichon S, Martin L, Hennies HC, et al. Increased activity of coagulation factor XII (Hageman factor) causes hereditary angioedema type III. Am J Hum Genet. 2006 Dec. 79(6):1098-104. [Medline]. [Full Text].
Gleich GJ, Leiferman KM. The hypereosinophilic syndromes: current concepts and treatments. Br J Haematol. 2009 May. 145(3):271-85. [Medline].
Morgan M, Khan DA. Therapeutic alternatives for chronic urticaria: an evidence-based review, Part 2. Ann Allergy Asthma Immunol. 2008 Jun. 100(6):517-26; quiz 526-8, 544. [Medline].
Bouillet L, Longhurst H, Boccon-Gibod I, Bork K, Bucher C, Bygum A, et al. Disease expression in women with hereditary angioedema. Am J Obstet Gynecol. 2008 Nov. 199(5):484.e1-4. [Medline].
Sánchez-Borges M, Asero R, Ansotegui IJ, Baiardini I, Bernstein JA, Canonica GW, et al. Diagnosis and treatment of urticaria and angioedema: a worldwide perspective. World Allergy Organ J. 2012 Nov. 5(11):125-47. [Medline].
Joint Taskforce on Practice Parameters Website. Available at http://www.allergyparameters.org/. Accessed: June 5, 2013.
Joint Taskforce on Practice Parameters. Angioedema practice parameters: 2013 update. J Allergy Clin Immunol. [in press] June 2013.
Cugno M, Zanichelli A, Bellatorre AG, Griffini S, Cicardi M. Plasma biomarkers of acute attacks in patients with angioedema due to C1-inhibitor deficiency. Allergy. 2009 Feb. 64(2):254-7. [Medline].
Lang DM, Aberer W, Bernstein JA, Chng HH, Grumach AS, Hide M, et al. International consensus on hereditary and acquired angioedema. Ann Allergy Asthma Immunol. 2012 Dec. 109(6):395-402. [Medline].
Powell RJ, Leech SC, Till S, Huber PA, Nasser SM, Clark AT. BSACI guideline for the management of chronic urticaria and angioedema. Clin Exp Allergy. 2015 Mar. 45(3):547-65. [Medline].
Craig T, Pürsün EA, Bork K, Bowen T, Boysen H, Farkas H, et al. WAO Guideline for the Management of Hereditary Angioedema. World Allergy Organ J. 2012 Dec. 5(12):182-199. [Medline].
Zuberbier T, Asero R, Bindslev-Jensen C, Walter Canonica G, Church MK, Giménez-Arnau A, et al. EAACI/GA(2)LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria. Allergy. 2009 Oct. 64(10):1417-26. [Medline].
Ferrer M, Sastre J, Jáuregui I, Dávila I, Montoro J, del Cuvillo A, et al. Effect of antihistamine up-dosing in chronic urticaria. J Investig Allergol Clin Immunol. 2011. 21 Suppl 3:34-9. [Medline].
Handa S, Dogra S, Kumar B. Comparative efficacy of cetirizine and fexofenadine in the treatment of chronic idiopathic urticaria. J Dermatolog Treat. 2004 Jan. 15(1):55-7. [Medline].
Potter PC, Kapp A, Maurer M, Guillet G, Jian AM, Hauptmann P, et al. Comparison of the efficacy of levocetirizine 5 mg and desloratadine 5 mg in chronic idiopathic urticaria patients. Allergy. 2009 Apr. 64(4):596-604. [Medline].
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Hindmarch I, Johnson S, Meadows R, Kirkpatrick T, Shamsi Z. The acute and sub-chronic effects of levocetirizine, cetirizine, loratadine, promethazine and placebo on cognitive function, psychomotor performance, and weal and flare. Curr Med Res Opin. 2001. 17(4):241-55. [Medline].
Asero R, Tedeschi A, Lorini M. Leukotriene receptor antagonists in chronic urticaria. Allergy. 2001 May. 56(5):456-7. [Medline].
Maurer M, Rosén K, Hsieh HJ, Saini S, Grattan C, Gimenéz-Arnau A, et al. Omalizumab for the treatment of chronic idiopathic or spontaneous urticaria. N Engl J Med. 2013 Mar 7. 368(10):924-35. [Medline].
Spector SL, Tan RA. Advances in allergic skin disease: omalizumab is a promising therapy for urticaria and angioedema. J Allergy Clin Immunol. 2009 Jan. 123(1):273-4. [Medline].
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Riedl MA, Hurewitz DS, Levy R, Busse PJ, Fitts D, Kalfus I. Nanofiltered C1 esterase inhibitor (human) for the treatment of acute attacks of hereditary angioedema: an open-label trial. Ann Allergy Asthma Immunol. 2012 Jan. 108(1):49-53. [Medline].
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'Grateful Dead from the Mars Hotel' Single Cover, 'U.S. Blues'. Grateful Dead Records. Artwork: Kelley/Mouse Studios
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The summer of 1974 was a real good time! I certainly enjoyed the release of Mars hotel, the Dead's new music (Scarlet!) and the wonderful show in Louisville, KY at Freedom Hall.
"Red and white, blue suede shoes. I'm Uncle Sam, how do you do?!"


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Online Exclusive » The steep price of downsizing the Washington press corps
By Bill Walsh Walsh is a former Washington reporter for New Orleans Times-Picayune.
Bill Walsh, a former Washington reporter for New Orleans' Times-Picayune, delivered these remarks Monday evening as he accepted the National Press Club's Robin Goldstein Award for Washington Regional Reporting:
I feel a bit odd accepting this award for being a Washington correspondent because I no longer am one. In fact, I'm no longer in journalism. After 22 years, I left in May to take a job as a healthcare strategist at a large non-profit in Washington, D.C. Given the state of the newspaper industry, I suspect that had I not left voluntarily I wouldn't have had a choice eventually. The slot I left hasn't been filled.
The number of bloggers commenting on the news out of Washington has exploded. The number of reporters actually digging up the news has dwindled. Washington bureaus are hemorrhaging reporters or closing altogether. In tight times, papers see their Washington operations as luxuries. That's misguided.
The result is that members of Congress, except for the leaders, are getting less scrutiny than ever. Even before I left, I was so busy covering the daily stories that I had little time to do what I was sent here to do: Dig into what local members of Congress were up to, find out who was influencing them and figure out if they were truly representing the folks back home.
In the long run there is a public cost. I see us, fundamentally, as explainers cutting through the complexities of Washington and telling our readers what it means to them. Lacking that, the public grows ever-more cynical and detached from an increasingly complicated government they seem to understand less and less. At a time when members of Congress have gotten remarkably sophisticated at manipulating their images, there are fewer reporters around cutting through the spin, putting it in context, explaining it.
We think of ourselves as watchdogs, integral parts of a healthy democracy, but we have become expendable. Why? If I don't report that a senator has introduced legislation to curry favor with an influential constituent, or that FEMA has decided not to give hurricane assistance to college students, or that Democrats are using racially tinged comments to demean a rising star in the Republican Party, who happens to be non-white, it's as if those things never happened. We literally don't know what we're missing.
If we don't miss it, was it worth knowing?
Of course it was.
It's our job to tell people what they need to know about their government before they know they need it. People are too busy to sort out the machinations of Congress and the federal agencies. That's what we do. But the explainers are losing their jobs, or leaving them.
I loved journalism. And there are few jobs in journalism better than being a Washington correspondent. The work seemed important and vital. It was and it always will be. The public as well as our editors and publishers need to understand that. Now more than ever.
Walsh is a senior strategic adviser at AARP. In introducing him at the National Press Club's Journalism Awards presentation Monday night, club President Sylvia Smith quoted the contest judges, saying, "He has an excellent command of Congress and federal agencies that he communicates clearly to his readers. He has served as watchdog for his state."
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Very large crowds and very big events especially around football. More than almost to a fault.
You don't need to have a computer, Its easy enough to find one even during crunch times. Good luck finding one you can play games or watch YouTube videos on though. If you have an ethernet cable the internet connection is fast and pretty reliable, but the WiFi cuts in and out a bit, depending on where you are.
Hard to find good spaces, because a lot of people leave their cars in the overnight lots, but there are usually open spots somewhere
The weather is phenomenal here, it is beautiful here pretty much all year around. The only slight exception would be during winter, it gets pretty cold and it has been cold and rainy lately, but it is rare to see this much rain this time of year. Other than that the winter has been beautiful, drop dead gorgeous out!!
Campus Housing:
All of the dorms are centralized on the campus, allowing for a sense of ease getting from the dorm to class.
I'm sure parking is difficult at all schools, but it's pretty hard to find a spot. I'd consider walking or riding a bike if possible.
Greek Life:
Greek life is an amazing opportunity for networking and meeting new people. However, I've seen a lot of people get sucked into the lifestyle; partying, too concerned with looks, thinking non-greeks aren't good enough. If you can keep your head on your shoulders and are interested in meeting new people it's worth considering.
Health & Safety:
While not the safest area, the school takes our safety very seriously. With the safe bus, a bus that drives around campus at night so you don't need to walk, and emergency signals within eye sight of any place on campus, I do feel at peace.
Campus Quality:
FSU's campus is great! It is aesthetically beautiful and makes for an easy walk to class every day. There are new buildings and nice, clean facilities. Landis is great for killing time in the sun between class and there is always something fun and exciting going on!
Drug Safety:
I have not really seen any drugs on campus. I thought I smelled someone smoking pot once on campus, but that is it. Off campus is a different story. There will always be people who drink and smoke out of school.
Campus Food:
There are many places on campus to find food. We have a food court that has Papa Johns, Pollo Tropical, a Sushi place, and Freshens. We also have a Chilis and a Subway in our Union. They are very delicious and not a far walk. The dining halls are pretty nice.They normally have almost the same everyday, but a couple menu items are different. Even if you want to go off campus for a meal, there are many places that are very easy to walk to.
Guys & Girls:
Most guys are very cute, and they dress pretty nice. The girls are very pretty and dress comfortably most of the time. You will be able to tell who is in a frat or sorority and who is not.
Campus Housing:
The majority of dorms on campus are pretty old and have a lot of wear and tear. However, they're not too bad considering how long they've been around.
The transportation at Florida State is great, but it could be better. The buses are usually either extremely hot, or extremely cold. In addition, there should be more buses because during certain times where there's a lot of students trying to ride the bus, there's not enough space and I'll usually have to wait for the next bus.
The various schools at this university are among the best in the country. I have met various alumni who are right where they want to be in life.
There are so many different kinds of people here that I never could have imagined seeing and meeting. Students from other countries, of other beliefs, speaking other languages, but all identifying as part of the same community.
I am very happy with my decision to major in human resource management and management information systems. My previous major was engineering; it was not a good fit for me. My success coach helped me find a major that I liked, and she did a great job. If I could do it over again, I would pick hr management as my first major. I woul also look into minors and certificates. My goal is to graduate before I'm 21 and work in a company. I want to eventually be an hr director. I do have a little bit of a concern findin a job in my field, but I feel that if I add certificates and other majors then I will make myself more marketable
The fall semester when I received aid event smoothly. No problems, and everything went the way it was supposed to. However, in spring, I didn't want to accept an unsubsidized loan. This was a lengthy process which included me running everywhere on campus and it took 4-5 hours out of my day.
I'm a current student at FSU majoring in human resources management and management information systems. My minor will be computer science. I love all my classes, and I feel like they will adequately help me later in life. The Rovetta school of business faculty is helpful! So far I had had no problems with anything.
I have not had an internship yet, but I definitely plan to get one. An internship offers you so much. You can work on communication skills, get hands on experience, and network within that company. I don't worry about getting an internship because I have a 3.6 GPA and the career center at Fsu can help me find one. Don't just rely on the career center though, you should definitely keep actively searching for an internship though.
Party Scene:
There are a lot of clubs to get in to if you are 18 and older. I have had so much fun going out and i am only 18.The strip is fun, with bars and clubs. The clubs like Lit and Bajas are really fun too!
Health & Safety:
My friend got hurt on campus and help came to her within 5 or ten minutes. The police were very helpful.
Local Area:
There's no beaches but there are parks and recreation places. There are a variety of nightclubs, and plenty social house parties, and frat parties.
Guys & Girls:
FSU is very diverse, and you would find all types of people with different styles and religions. It is a fun comfortable environment.
I received a scholarship just for being in the top percent of freshmen in my high school class.
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You would be hard-pressed to find a graduate of Florida State University who doesn't have fond memories of the years they spent on campus. Current students will also agree that they are happy with their decision to attend school here. There is something for everyone, from athletics to academia, and you would have a hard time finding a more comfortable setting than Tallahassee. It has so much to offer, from exciting nightlife to beautiful weather.
Although it bears the reputation of a party school, FSU also has a growing reputation for turning out some of the best and brightest graduates in the entire nation. The school is now turning its focus on research, which should appeal to those interested in science and mathematics. But never fear, FSU also emphasizes the arts through their award-winning film and theater departments. From math and science, to the arts, FSU offers a vast array of eclectic degrees, which will be nothing but helpful later in your life. Choosing which college to attend is not an easy decision, but if you're looking for the perfect combination of a good education and a good time, you can't do much better than Florida State University.
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Originally posted on Fox Sports Kansas City | Last updated 6/11/13
KANSAS CITY, Mo. It all started when a new shipment of designated hitter Billy Butler's "Hit it a TON" barbecue sauce arrived in the Royals' clubhouse six days ago. That's when Royals right-hander Jeremy Guthrie began passing bottles of the sauce around the dugout during the game, rewarding Royals for getting big hits. The television cameras began taking note, and now the story is close to going viral: There are bottles of Billy's barbecue sauce everywhere in the dugout, and players from Guthrie to Alex Gordon to Eric Hosmer to David Lough to Sal Perez have been shown grabbing the bottles and flashing them before the cameras after each Royals score. And don't expect the fun to end all that soon: The Royals have won six straight for the first time in two years and seemingly righted their season, and it all coincides with Guthrie unleashing the power of the sauce. "It started exactly when the streak started," Butler said. "Baseball players are superstitious. We all know that. It's not going to change. I like it. "We got a new shipment in right before that first win of the streak. Jeremy has been getting us going ever since." Although Butler launched his line of barbecue sauce over two months ago, the added television exposure from the dugout shots apparently has boosted sales in the last week. "We sold out of some grocery stores already in the last couple of days," Butler said. Guthrie said he isn't sure why he started grabbing bottles of the sauce and passing them out in the dugout after a score. "When that shipment came in I just thought, 'Hey, we need to hit it a ton, too,' " Guthrie said. "And we started to." Win No. 6 in a row came Monday night as Guthrie and the Royals battled to a tight 3-2 win over the division-leading Detroit Tigers. Guthrie survived though he gave up a two-run homer to Miguel Cabrera in 6 13 innings of work. "Actually, I threw a few barbecue balls myself today," Guthrie said, smiling. "But we won anyway." Hosmer has been in on the "promotion" as well, and when the television cameras found him after Monday's win in the clubhouse, he launched into his best TV sales pitch voice. "Hey, you'll do anything to score a run and get some barbecue sauce," Hosmer said, smiling and holding up a bottle of "Hit it a TON" sauce. "And if you taste this sauce, you'll run the bases like me." The idea for Billy's barbecue sauce came during the offseason and stemmed from Butler's relationship with Kansas City's Zarda barbecue, which along with Original Juan helped develop the sauce. All proceeds from the sauce go to Butler's "Hit-It-A-Ton" foundation, which supplies food to needy families in the Kansas City area. You can follow Jeffrey Flanagan on Twitter @jflanagankc or email him at email@example.com.
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, Volume 6, Issue 6, pp 676-695
First online:
Automatizing Parametric Reasoning on Distributed Concurrent Systems
- Paola InverardiAffiliated withI.E.I. - C.N.R.
- , Corrado PriamiAffiliated withDipartimento di Informatica, Universita di Pisa
- , Daniel YankelevichAffiliated withDepartment of Computer Science, NC State University
Rent the article at a discountRent now
* Final gross prices may vary according to local VAT.Get Access
There can be different views of a concurrent distributed system, depending on who observes it. The final user may just want to know how the system behaves in terms of its possible sequences of actions, while the designer may want to know what are the sequential components of a system or how are they distributed in space. In other words, there is not a widely accepted single semantic model for concurrent systems. This paper describes a parametric verification tool for process description languages. It performs a symbolic execution of processes at different levels of abstraction and verifies deadlock and reachability properties. The tool also provides facilities to check behavioural equivalences. In addition to the classical interleaving semantics, truly concurrent approaches based on the notion of causality and locality are considered. This allows us to compare the expressive power of different models within the same environment. In this respect, we have verified many of the examples given in the literature using our tool.
KeywordsConcurrent systems Specification Verification
Reference tools
- Title
- Automatizing Parametric Reasoning on Distributed Concurrent Systems
- Journal
Formal Aspects of Computing
Volume 6, Issue 6 , pp 676-695
- Cover Date
- 1994-12
- Print ISSN
- 0934-5043
- Online ISSN
- Publisher
- Springer London
- Additional Links
- Topics
- Keywords
- Concurrent systems
- Specification
- Verification
- Industry Sectors
- Authors
- Paola Inverardi (1)
- Corrado Priami (2)
- Daniel Yankelevich (3)
- Author Affiliations
- 1. I.E.I. - C.N.R., Via S. Maria, 46, I-S6100, Pisa, Italy
- 2. Dipartimento di Informatica, Universita di Pisa, Pisa, Italy
- 3. Department of Computer Science, NC State University, Raleigh, NC, USA


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Nec 2690 Question & Help
Started Dec 23, 2007 | Discussions thread
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Jim Campbell • Senior Member • Posts: 1,880
Nec 2690 Question & Help
Dec 23, 2007
I would like to get a 2690. I assume I will need a new video card to get the max resolution as right now I have the Geo Force FX5200.
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Mark Allen McGrath
Position: WR
5-11, 175lb (180cm, 79kg)
Born: December 17, 1957 in San Diego, CA
College: Montana St.
Weighted Career AV (100-95-...): 1 (13070th overall since 1960)
High School: Shorecrest (WA)
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Cilantro Lime Chicken
Total Time
Prep 5 mins
Cook 15 mins
My husband has recently declared my kitchen a cilantro-free zone :( so unfortunately I haven't yet tried this dish, but I am posting it because it sounds good to me and thought it might appeal to others as well. The recipe comes from Ainsley Harriott, a British chef, and he cautions not to marinate the chicken longer than two hours as the lime juice will break down the chicken to the point that it will fall apart. Preparation time does not include marinating time.
Ingredients Nutrition
- 6 cloves garlic, chopped
- 4 tablespoons chopped cilantro leaves, plus extra to garnish
- 2 teaspoons black peppercorns, coarsely ground
- 2 teaspoons sugar
- 2 limes, juice only
- 2 teaspoons Thai fish sauce (nam pla)
- 1 tablespoon light soy sauce
- 1 tablespoon sunflower oil
- 4 boneless skinless chicken breasts
- Make the marinade of garlic, cilantro, ground peppercorns, sugar, lime juice, fish sauce, soy sauce and sunflower oil.
- Blend well.
- Place chicken breasts with marinade in a shallow dish or resealable plastic bag, coating them well, and set in the refrigerator at least 1 hour and no more than 2, turning them from time to time.
- Preheat a ridged griddle pan or heavy non-stick frying pan and cook the chicken for 7-8 minutes each side until the chicken is cooked through.
- Serve hot or cold, garnished with cilantro leaves.
Most Helpful
This was good! I doubled the marinade because I wanted to make sure there was plenty to cover the chicken while marinading. We had it with rice and a black bean and corn medley.
Replace with fish sauce with Tequila. Nix the sugar, and you have one of my favorite chicken dishes. Some caramalized onions never hurt, either.
OMG, this was sooo delicious it was almost ridiculous! I used worchestershire sauce in place of the fish sauce and I used bone-in breasts rather than skinless, boneless cuz that's all I happened to have on-hand. I also had to use 2 key limes instead of regular limes and filled in with lemon juice for what I lacked in lime juice. I let the chicken marinate in the fridge for an hour and then I baked it in the oven in a shallow pan @ 425 degrees covered in foil for the first 30 mins and then removed the foil, flipped the breast and cooked @ 450 uncovered for 20 minutes and it was soooo delicious. The marinade reduced and made a lovely sauce for dipping hunks of white meat into. Simply gorgeous. A new house favorite! Thanks for sharing!


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What will they think of next? This is an app called Motor Recall, and if you're at all like us, it's pretty much the equivalent of any nighttime car ride as a kid - see a pair of headlights or taillights, pick out the make, model and if you're lucky/good, the year. Now, the clever folks at Case By Case Studios have turned that time-honored way of surviving a long drive into an app.
Motor Recall game
- Volvo shoots for self-drivers by 2021
- Jeep spends $1 billion on factories
- Find Parts & Accessories for your vehicle!
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- Compare Volvo XC90 and Lincoln MKX


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Home > News > Village explores upgrades
December 17th, 2003
Citizens and government officials in Deerfield are taking more steps toward improvements in the village. According to Village Supervisor Jim Hyder, the village is running tests to determine the feasibility of implementing a pilot program called "nano-filtration" at Deerfield's water filtration plant. He said the new system will help the village meet new state requirements for drinking water that become effective Jan. 1.
Lenawee Connection
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