New Treatment Of Urticaria
In this condition itching red weals develop they resemble the effects of stinging nettle (Urtica dioica) on the skin. The condition may be associated with allergic reactions, infection, or physical stimuli, but in most patients no cause can be found. Similar lesions may precede, or be associated with, vasculitis (urticarial vasculitis), pemphigoid, or dermatitis herpetiformis. The physical urticarias, which account for about 25 of cases, include dermatographism and the pressure, cold, heat, solar, cholinergic, and aquagenic urticarias. Dermatogyaphism is an exaggerated release of histamine from stroking the skin firmly with a hard object, such as the end of a pencil. Pressure urticaria is caused by sustained pressure from clothing, hard seats, and footwear it may last some hours. Cold urticaria varies in severity and is induced by cold, particuarly by cold winds or by the severe shock of bathing in cold water. It appears early in life in infancy in the rare familial form. In a few...
Of 91 patients studied, one male subject developed new anti-ISIS 2302 IgG IgM antibody by d 82 at a 1 10 titer without clinical sequelae. ISIS 2302 was well tolerated (Table 1). Medically important adverse events were limited to hypersensitivity reactions in a small proportion of patients (3 , including urticaria in six patients and two drug reactions).
Evaluation of food allergies have recently been published as a medical position statement by the American Gastroenterological Association (Sampson et al, 2001). It is essential to obtain a careful history correlating symptoms with specific foods. Most immediate hypersensitivity reactions to food include a set of symptoms that consistently occur minutes to hours after ingesting certain foods. In some individuals, other factors, such as medications or exercise, may modulate the reaction to a specific food. Specificity of the reaction does not always imply a food allergy because patients with anaphylactoid reactions or lactose intolerance report defined reactions to specific foods. However, the nature of the reaction will help differentiate lactose intolerance (gas, bloating, diarrhea) from an allergy to cow's milk protein (often urticaria, swelling of the lips and oral mucosa, and or asthmatic symptoms occur in addition to GI symptoms).
Features range from mild skin rashes to severe urticaria, hypotension, broncho-spasm, abdominal pain, diarrhoea, a 'feeling of impending doom' and cardiovascular collapse. Initial hypotension is largely related to profound vasodilation, which is followed by leakage of intravascular fluid into the interstitium. Cardiac depression (thought to be caused by circulating inflammatory mediators) may also contribute to hypotension. The cardiovascular effects are exacerbated by aortocaval compression.
Prodromal symptoms of flushing, itching, facial swelling, urticaria, abdominal pain, diarrhoea, wheeze, and stridor may precede shock or may be the only manifestations of anaphylaxis. The presence of these additional symptoms confirms anaphylaxis as the cause of shock in a child. Most patients will have a history of previous attacks and some may have a medic-alert bracelet.
Immediate management of severe reactions consists of intravenous adrenaline 100 mg boluses and fluids, with management of the airway and administration of oxygen. Aortocaval compression must be avoided at all times. Any potential for adrenaline to cause uteroplacental vasoconstriction and uterine hypotony is outweighed by the restoration of cardiac output. Intravenous chlorphenamine 10 mg and hydrocortisone 200 mg may be given to reduce the effects of subsequent inflammatory mediator release. For less severe reactions (e.g. urticaria only), chlorphenamine alone may suffice.
Known history of anaphylaxis to latex. It does not always occur to patients that their rubber allergy might be of relevance to the anaesthetist. Two patients who denied allergies developed delayed responses of intraoperative hypotension and flushing. Both had increases in tryptase levels (10.4 mgl-1 and 8.5 mgl-1 normal 2 m gl-1), and positive skin prick tests to latex. Only at this stage did each patient declare their cutaneous reactions to latex (Fisher 1997).Another had hives after the use of gloves and sneezing during vaginal examinations (Ballantine & Brown 1995). She had undergone IVF for infertility, which involved regular use of a latex-covered vaginal probe.
CBPV mainly attacks adult bees and causes two forms of paralysis symptoms in bees (Bailey, 1975). The most common one is characterized by an abnormal trembling of the body and wings, crawling on the ground due to the flight inability, bloated abdomens, and dislocated wings. The other form is identified by the presence of hairless, shiny, and black-appearing bees that are attacked and rejected from returning to the colonies at the entrance of the hives by guard bees. Both forms of symptoms can be seen in bees from the same colony. The variation in the disease symptoms may reflect differences among individual bees in inherited susceptibility to the multiplication of the virus (Kulincevic and Rothenbuhler, 1975 Rinderer et al, 1975).
Patients may present with acute upper airway compromise from laryngeal oedema (Jensen & Weiler 1998). Emergency tracheostomy may be needed (Hamilton et al 1977). Severe postoperative angioedema occurred in a 61-year-old man after cervical surgery, performed because osteophytes were thought to be causing dysphagia and choking episodes (Krnacik & Heggeness 1997). Fatal obstruction occurred in a 27 year old on ITU, whilst preparations for tracheostomy were being made (Nielsen et al 1995).
Inactive proteins sequentially activate each other. The complement cascade is initially activated by either the classical or alternate pathways. It is normally kept under control by inhibitors, or when activated, by the spontaneous decay of the active component.The kinin-generating and fibrinolytic systems are also involved, and the oedema appears to result from the generation of a peptide that causes increased capillary permeability.The C1 inhibitor gene has been mapped to chromosome 11, and many different mutations can be responsible.Two types have been identified.Type I has no C1 EI, whereas type II has normal levels of protein, but it is dysfunctional (Cicardi & Agostini 1996).The hereditary form is responsible for only a small proportion of cases of angioedema.
This may be a familial (see Hereditary angioneurotic oedema) or, more rarely, an acquired disorder involving the complement system.The acquired form is mostly associated with a B-lymphocyte malignancy, and antibodies have been detected against abnormal immunoglobulins present on the malignant B-cells. Reaction between the two cause C1 activation, which in turn produces a secondary reduction in the concentrations of C1, C2 and C4 and a reduced functional activity of C1 esterase inhibitor (Geha et al 1985).This form must be distinguished from the physical forms of angioedema that occur in response to food, drugs or insect bites, or in association with connective tissue disorders. Recently, a number of patients have developed angioedema in response to treatment with ACE inhibitors, particularly enalapril and captopril (Barna & Frable 1990). Substantial increases in plasma bradykinin have been demonstrated during attacks of hereditary, acquired, and captopril-induced angioneurotic oedema...
Everything inside a living cell is continually moving and changing, forming and breaking down. At any instant, many or most of the cell's elementary machines - the protein molecules - are busily engaged in specialised individual activities. The proteins themselves are continually being produced and destroyed ( turned over ). At any instant, each mitochondrion, lysosome and segment of endoplasmic reticulum, every little region in the nucleus and in the cytoplasm, is buzzing with activity, each of its numerous proteins pursuing its appointed task. To describe the cell as a hive of industry would be to understate reality. The cell is a hive of hives of industry.
Two prominent classes of antihypertensive drugs, the ACE inhibitors, e.g. benazepril, and the ARBs, e.g. valsartan, function by blocking the RAS. Despite the demonstrated efficacy of these drugs in controlling hypertension and reducing endorgan damage, both mechanisms of action have some disadvantages 10 . Complete inhibition of ACE does not prevent the conversion of Ang I to Ang II by other peptidases, including chymase. Indeed, in cardiac tissue, most Ang II is produced by enzymes other than ACE. In contrast, inhibition of bradykinin cleavage by ACE causes the side effects of coughing and angioedema in a substantial number of patients. Although the ARBs prevent binding of Ang II to AT1, high levels of Ang II and its cleavage products remain in circulation and are available to activate AT2, AT3 and AT4. Renin is anticipated to be a superior target for antihypertensives 31,32 .
Thus, immunoglobulins are responsible for all types of diseases caused by immunreaction type I, II and III according to the classification of Coombs & Gell. As the pattern of immune responses initiated by immunoglobulins strictly depends on the immunoglobuline isotype, the diseases caused by immuno-globulins depend not only on the antigen they recognize. The clinical spectrum of diseases initiated by autoantibodies ranges from urticaria, through cytopathic tissue damage leading to cytopenia, inflammatory tissue destruction following the deposition of immunoglobulins and complexes at membranes till to severe necrosis, as a consequence of acute vascular infarction.
Red itchy marks at injection sites after starting insulin are also rare, and if they do occur usually disappear spontaneously. If they are very troublesome, adding hydrocortisone to the insulin bottle so that each dose contains about 1 mg eliminates the problem. Insulin allergy causing urticaria still occurs from time to time though it is certainly a very infrequent event investigation by skin testing and desensitisation may be needed. Abscesses at injection sites are also remarkably rare.
Symptoms are variable, and can include episodic attacks of itching, urticaria, dermographia, headache, flushing, syncope, palpitations, abdominal pain, diarrhoea, nausea, and vomiting.The flush is bright red and lasts for 3. Skin lesions vary in type and colour, but small, reddish brown maculopapular lesions are common.A positive Darier's sign may be demonstrated. Light stroking of the affected skin with a blunt, but pointed, object produces dermographia (secondary to localised urticaria), and a flare.
Erythema toxicum neonatorum (urticaria neonatorum) on the back of a term infant. This is the most common rash noted in the normal term infant. It is not seen in preterm and rarely seen in post-term infants. It usually appears on the 2nd or 3rd day of life (rarely in the first 24 hours) and is seldom seen after the age of 14 days. It affects about 40 to 50 of full term infants and the condition is self-limiting. Lesions may be minimal or extensive. Figure 1.23. Erythema toxicum neonatorum (urticaria neonatorum) on the back of a term infant. This is the most common rash noted in the normal term infant. It is not seen in preterm and rarely seen in post-term infants. It usually appears on the 2nd or 3rd day of life (rarely in the first 24 hours) and is seldom seen after the age of 14 days. It affects about 40 to 50 of full term infants and the condition is self-limiting. Lesions may be minimal or extensive.
These drugs are used in urticaria and acute allergic (type I immediate hypersensitivity) reactions. The newer long acting and non-sedating antihistamines are useful for treatment during the day and can be combined with one of the sedating type at night if pruritus is preventing sleep.
Polymorphic eruptions also present with pruritis with urticaria papules and plaques (the PUPP syndrome). It usually occurs on the abdomen in the third trimester and then becomes widespread. There may be a postpartum flare up. It can be a distressing condition for the mother but the baby is not affected, and it rarely recurs in subsequent pregnancies. Topical steroids can be used, but systemic steroids should be avoided.
A rare group of diseases in which there is overproliferation and abnormal aggregations of mast cells within the skin, and in other organs (Austen 1992).The disorders range from cutaneous mastocytosis, through systemic mastocytosis to mast-cell leukaemia (Golkar & Bernhard 1997).When the skin alone is involved, the condition is known as urticaria pigmentosa.This mostly occurs in infants and children, may be associated with mastocytomas, and is relatively benign (Coleman et al 1980). In the systemic diseases, bone, liver, spleen and lymph nodes are most commonly affected.
Familial amyloidosis involving the kidneys has been reported by Ostertag 19 and others 20-22 . Families with apolipoprotein A1 mutation, as well as mutations in the fibrinogen a-chain gene, have been recognized. On presentation, patients with renal involvement exhibit hypertension and mild renal insufficiency that progresses to endstage renal failure. The amyloid deposits have mutations in the fibrino-gen a-chain gene. This form of amyloidosis is autosomal dominant. No peripheral neuropathy develops, and the onset of renal disease occurs in the fifth to seventh decades of life. The mutation consists of the substitution of glutamic acid for valine at position 526 of the fibrinogen chain. A mutation in fibrinogen has been described at position 554 23,24 . A rare form of inherited secondary amyloidosis produces nephropathy, deafness, and urticaria. This form has been referred to as the Muckle-Wells syndrome 25 . (Adapted from Kyle and Gertz 26 .)
A general term applied to the development of acute oedema in the subcutaneous or submucous tissues.Anaesthetic help may be sought during an attack, when oedema of the lips, tongue or larynx may cause respiratory problems. Angioedema may be secondary to release of histamine, or a number of other vasoactive substances such as the bradykinins, prostaglandins or leukotrienes. It is thought that paediatric and adult angioedemas differ. Children are less likely to required intubation or tracheostomy than adults (Ishoo et al 1999, Shah & Jacobs 1999). Recent work in adults has shown substantial increases in plasma bradykinin during attacks of hereditary, acquired or captopril-induced angioedema (Nussberger et al 1998).The development of oedema may be 4. A known side effect of a drug. Recently, there have been a number of cases of angioedema reported, usually involving the tongue, floor of the mouth, epiglottis and aryepiglottic folds, secondary to treatment with ACE inhibitors (Gannon & Eby...
This is a lesion of bullous mastocytosis (urticaria pigmentosa) that presented at birth in this infant as a solitary bullous lesion on the sole of the right foot. Note the area of redness surrounding the lesion (dermatographism) following examination of the lesion. Spontaneous remission of the skin lesions usually occurs. It is rare for lesions to appear after the age of 3 years. Differential diagnosis includes bullous impetigo, epidermolysis bullosa, incontinentia pigmenti, and bullous congenital ichthyosiform erythroderma.
Alopecia, erythema, macules, papules, pruritis, and urticaria have been seen rarely with lamivudine (65). Hypersensitivity reactions. A serious and potentially lethal hypersensitivity reaction to abacavir is seen in 2-5 of patients (106-110). Clinical presentation includes fever to 39-40 C, macules, papules, and urticaria, fatigue, malaise, nausea, vomiting, diarrhea, abdominal pain, arthralgias, cough, and or dyspnea. These clinical presentations may be associated with increased creatine phosphokinase (CPK), elevated liver function tests, and lymphopenia. These findings usually occur within the first six weeks of therapy. The hypersensitivity reaction usually resolves with cessation of abacavir, but a rechallenge of the drug after this reaction can be fatal. All physicians and patients should be aware of this potentially serous side effect. Therefore, patients taking ABC who develop a skin eruption associated with fever, gastrointestinal symptoms, cough, dyspnea,...
Inflammation associated with immune complexes in the capillaries and small blood vessels is part of the pathological changes of many of the conditions described above. The term vasculitis is also used clinically to describe a variable clinical picture with red macules and papules and with necrosis and bruising in severe cases. In children purpura is more prominent and these cases are classified as Henoch-Schonlein purpura. The legs and arms are usually affected. Skin signs are preceded by malaise and fever with arthropathy and there may be associated urticaria. As a high proportion of cases are associated with systemic lesions, it is essential to check for renal, skeletal, gastrointestinal, and central nervous system disease. In children with Henoch-Schonlein purpura nephritis is common.
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