New Urticaria Cure
Angioedema is caused by hereditary impairment of Cl-esterase inhibitor or acquired development of antibodies against it. The 17a-alkylated androgens, such as stanozolol and danazol, stimulate hepatic synthesis of the esterase inhibitor and thereby decrease the frequency of acute attacks. In women, virilization is a potential side effect. In children, virilization and premature epiphyseal
Snake bites Envenoming from snake bite is uncommon in the UK. Many exotic snakes are kept, some illegally, but the only indigenous venomous snake is the adder (Vipera berus). The bite may cause local and systemic effects. Local effects include pain, swelling, bruising, and tender enlargement of regional lymph nodes. Systemic effects include early anaphylactic symptoms (transient hypotension with syncope, angio-edema, urticaria, abdominal colic, diarrhoea, and vomiting), with later persistent or recurrent hypotension, ECG abnormalities, spontaneous systemic bleeding, coagulopathy, adult respiratory distress syndrome, and acute renal failure. Fatal envenoming is rare but the potential for severe envenoming must not be underestimated.
Acetaminophen usually is well tolerated. Erythematous or urticarial rash may occur and may be accompanied by drug fever and mucosal lesions. Patients who show hypersensitivity reactions to the salicylates only rarely exhibit sensitivity to acetaminophen. NAC functions by detoxifying NAPQI. It both repletes GSH stores and may conjugate directly with NAPQI by serving as a GSH substitute. Even in the presence of activated charcoal, there is ample absorption of NAC, and neither should activated charcoal be avoided nor NAC administration be delayed because of concerns of a charcoal-NAC interaction. Adverse reactions to NAC include rash (including urticaria, which does not require drug discontinuation), nausea, vomiting, diarrhea, and rare anaphylactoid reactions.
There are several cautions in the use of ACE inhibitors. Angioedema is a rare but potentially fatal adverse effect of the ACE inhibitors. Patients starting treatment with these drugs should be explicitly warned to discontinue their use with the advent of any signs of angioedema. Due to the risk of severe fetal adverse effects, ACE inhibitors are contraindicated during pregnancy, a fact that must be communicated to women of childbearing age.
Fibric acid compounds usually are well tolerated. Side effects, most often Gl-related, may occur in 5-10 of patients but most often are not sufficient to cause drug discontinuation. Other infrequent side effects include rash, urticaria, hair loss, myalgias, fatigue, headache, impotence, and anemia. Minor increases in liver transaminases and alkaline phosphatase have been reported. Clofibrate, bezafibrate, and fenofibrate reportedly can potentiate the action of oral anticoagulants by displacing them from their binding sites on albumin thus, monitoring of the prothrombin time and reduction in anticoagulant dosage may be appropriate.
Doses of chloroquine used for oral therapy of the acute malarial attack may cause GI upset, headache, visual disturbances, and urticaria. Pruritus also occurs, most commonly among dark-skinned persons. Prolonged medication with suppressive doses occasionally causes side effects such as headache, blurring of vision, diplopia, confusion, convulsions, lichenoid skin eruptions, bleaching of hair, widening of the QRS interval, and T-wave abnormalities. These complications usually disappear soon after the drug is withheld. Rare instances of hemolysis and blood dyscrasias have been reported. Chloroquine may cause discoloration of nail beds and mucous membranes.
The term pruritus is derived from the Latin prurire, which means to itch. Pruritus is a symptom unique to skin that occurs in a multitude of dermatologic disorders, including dry skin or xerosis, atopic eczema, urticaria, and infestations. Itching also may be a sign of internal disorders, including
Fibrin dissolution can be impaired by the administration of tranexamic acid, which inhibits fibrinolysis. It can be used to prevent bleeding or to treat bleeding associated with excessive fibrinolysis (e.g. in prostatectomy, bladder surgery, in dental extraction in patients with haemophilia, in conisation of the cervix, and in traumatic hyphaema) and in the management of menorr-hagia. Tranexamic acid may also be used in hereditary angioedema, epistaxis, and in thrombolytic overdose.
For formal reasons, side effects of aspirin might be divided into three categories first are the systemic effects due to acute and chronic overdosing or intoxication. To this category also belongs the bleeding tendency and toxic effects, in particular life situations, such as pregnancy or older age (Section 3.1). In addition to systemic effects, some organs, in particular, those with a preexisting injury or increased sensitivity, might be affected even by therapeutic doses of aspirin in the absence of systemic side effects. This involves the GI tract, liver, kidney, and the audiovestibular system (Section 3.2). Finally, there are no dose-related side effects that are due to a particular predisposition of the patient. These hypersensitivities might be inherent or acquired. This involves the Widal triad (aspirinsensitive asthma), allergic reactions at the skin or mucosa (urticaria), and Reye's syndrome with a still unclear relationship with aspirin (Section 3.3).
HA can produce a wide variety of powerful physiological changes as a result of activation of H1 receptors. Diseases involving mast cells such as urticaria pigmentosa or systemic mas-tocytosis also show many of these responses. Patients with allergies also experience many of these symptoms. It has been known for many years that HA is potent spasmogen on intestinal and bronchiolar smooth muscle, actions which are mediated predominantly by H1 receptors (Ash and Schild 1966). Asthmatics show exaggerated H1 bronchocontriction, but H1 antagonists are of little benefit for treating most patients. However, H1 receptors can induce coronary vasospasm, and may contribute to myocardial infarction (Gupta etal. 2001 Nakamura 2000). H1 effects on blood vessels consist of direct contractile actions on some
In contrast to the adjuvant properties described previously botanical polysaccharides have, in some cases, been reported to attenuate immune responses and have been proposed as promising agents for the treatment of IgE-dependent diseases (e.g., atopic dermatitis, asthma, atopic rhinitis, urticaria and food allergies). For example, Danilets and co-workers 297 studied the effects of water-soluble polysaccharides isolated from six different plants on anaphylactic shock and production of IgE and IgG1 by lymphocytes from mice immunised with OVA. They found that treatment with polysaccharides from coltsfoot, sweet flag, clover, Artemisia, marigold and elecampane reduced animal mortality after induction of anaphylactic shock. In addition, injection of these polysaccharides reduced serum concentrations of IgE and IgG1 297 . Likewise, pectins have been reported to exhibit antiallergic activity, resulting in a suppressed allergic asthmatic reaction in animals treated with doses of 5-12 mg kg...
Cyproheptadine possesses both antihistamine and anti-serotonin activity and is used as an antipruritic agent. It is indicated for the treatment of hypersensitivity reactions, perennial, and seasonal allergic rhinitis vasomotor rhinitis allergic conjunctivitis, uncomplicated allergic skin manifestations of urticaria and angioedema amelioration of allergic reactions to blood or plasma and cold urticaria. It is also used off-label for nightmares associated with posttraumatic stress disorder (PTSD), prevention of migraine, suppression of vascular headaches, and appetite stimulation. Sedation is the most prominent side effect, and this is usually brief, disappearing after 3 or 4 days of treatment.
Mild facial flushing and headache are the most common adverse effects associated with desmopressin. Allergic reactions ranging from urticaria to anaphylaxis may occur with desmopressin or vasopressin. Intranasal administration may cause local adverse effects in the nasal passages, such as edema, rhinorrhea, congestion, irritation, pruritus, and ulceration.
Drugs whose pharmacological action primarily involves antagonism of the action of histamine at its H2-receptors find therapeutic application in the treatment of acid-peptic disorders including heartburn, gastroesophageal reflux disease (GERD), erosive esophagitis, gastric and duodenal ulcers, and gastric acid pathologic hypersecretory diseases such as Zollinger-Ellison syndrome. They are also useful in combination with Hi-antihistamines for the treatment of chronic urticaria and for the itching of anaphylaxis and pruritis.59-62 The H2-antagonists are used to treat acid indigestion (an OTC application), GERD, peptic ulcers, and pathologic hy-persecretory disorders, as well as some of the symptoms of urticaria and anaphylaxis. Cimetidine, the original member of this drug class, was developed by a classical structure-activity study beginning with the endogenous agonist, hista-mine as shown in Table 23.4.64 Methylation of the 5-position of the imidazole heterocycle of histamine produced a...
Angioedema In 0.1- 0.5 of patients, ACE inhibitors induce a rapid swelling in the nose, throat, mouth, glottis, larynx, lips, and or tongue. This untoward effect, called angioedema, apparently is not dose-related, and if it occurs, it does so within the first week of therapy, usually within the first few hours after the initial dose. Airway obstruction and respiratory distress may lead to death. Although the mechanism is unknown, angioedema may involve accumulation of bradykinin or inhibition of complement 1-esterase inhibitor. Once ACE inhibitors are stopped, angioedema disappears within hours meanwhile, the patient's airway should be protected, and if necessary, epi-nephrine, an antihistamine, and or a glucocorticoid should be administered. African Americans have a 4.5 times greater risk of ACE inhibitor-induced angioedema than do Caucasians. Although rare, angioedema of the intestine, characterized by emesis, watery diarrhea, and abdominal pain, also has been associated with ACE...
The skin reactions that are part of the type III hypersensitivity reaction caused by the local disposition of immune complexes are seen after treatment with monoclonal antibodies, which are used in relative high and repeated doses. These immune complexes may lead to anaphylactoid reactions and serum sickness-like symptoms. Skin reactions such as urticaria and rashes are common symptoms of this complication 14 . Monoclonal antibodies may also lead to local reactions at the injection site. However, as shown in Table 2, there is no relation between immunogenicity and local skin reactions. So these local reactions cannot be used as an early marker for more serious symptoms of immunogenicity.
Sulfonamides or sulfones usually account for most toxicity associated with coadministration of these antifolate drugs (see Chapter 43). The combination of pyrimethamine (25 mg) and sulfa-doxine (500 mg) (fansidar) causes severe and even fatal cutaneous reactions in up to 1 in 5000 people. This combination also has been associated with serum sickness-type reactions, urticaria, exfoliative dermatitis, and hepatitis. Pyrimethamine-sulfadoxine is contraindicated in individuals with previous reactions to sulfonamides, lactating mothers, and infants
The intravenous or intra-arterial injection of iodinated contrast material can lead to a diverse assortment of contrast reactions, most of which are minor and easily treated. Minor reactions include injection pain, a feeling of general body warmth and discomfort, mild nausea and vomiting, a strong metallic taste in the mouth, and mild urticaria (hives). Minor Intermediate or moderate reactions are those that require some form of therapy but are not life-threatening. These reactions include difficulty breathing, severe hives, severe nausea and vomiting, mild hypotension, wheezing, and other related reactions. Treatment ranges from administration of intravenous fluids to the use of intravenous diphenhy-dramine and or corticosteroids. Epinephrine may be administered, and atropine is used if there is a vasovagal reaction with hypotension and bradycardia. Severe reactions are those that are life-threatening. They include sudden cardiovascular collapse and death, as well as severe...
Within seconds of the intravenous injection of a histamine liberator, human subjects experience a burning, itching sensation. This effect, most marked in the palms of the hand and in the face, scalp, and ears, is soon followed by a feeling of intense warmth. The skin reddens, and the color rapidly spreads over the trunk. Blood pressure falls, the heart rate accelerates, and the subject usually complains of headache. After a few minutes, blood pressure recovers, and crops of hives usually appear on the skin. Colic, nausea, hypersecretion of acid, and moderate bron-chospasm also occur frequently. In urticaria pigmentosa (cutaneous mastocytosis), mast cells aggregate in the upper corium and give rise to pigmented cutaneous lesions that urticate (i.e., sting) when stroked. In systemic mas-tocytosis, overproliferation of mast cells also is found in other organs. Patients with these syndromes suffer a constellation of signs and symptoms attributable to excessive histamine release, including...
ADVERSE EFFECTS AND PRECAUTIONS Adverse effects of ACE inhibitors that result from inhibiting AngII-related functions also occur with ATJ receptor antagonists, including hypotension, hyperkalemia, and reduced renal function (especially associated with renal artery stenosis). Hypotension most often occurs in patients in whom the blood pressure is highly dependent on AnglI, including those with volume depletion (e.g., with diuretics), renovascular hypertension, cardiac failure, and cirrhosis in such patients initiation of treatment with low doses and attention to volume status is essential. Hyperkalemia may occur in conjunction with other factors, such as renal insufficiency, ingestion of excess K+, and the use of drugs that promote K+ retention. Cough is much less frequent with AngII receptor antagonists, and angioedema occurs very rarely. ATj receptor antagonists also should not be administered during pregnancy and should be discontinued as soon as pregnancy is detected.
500 mg kg for Rh(NH3)5Cl Cl2 and RhCl(PPh3)3 , and 2000mg kg for Rh(acac)3. An examination of the frequencies of the positive prick test and patch test reactions to the chlorinated complexes of platinum-group metals revealed that the present concentration of these metals in the environment does not increase the incidence of reactions to these salts in patients with dermatitis and or urticaria.112 Rhodium complexes show relatively low mutagenicity. The Ames tests indicate that the Rh2(RCOO)2(N-N)2(H2O)2 (RCOO)2 complexes (R H, Me, Et, Ph N-N bpy, phen, dmpq) at MIC (minimal inhibitory concentration) do not show any mutagenic activity.45 Rhodium trichloride, at a concentration 300 mM, induced mutations in V-79 cells.113 Apart from the test of Ames, the bacterial SOS chromotest is used for the assessment of genotox-icity. The latter is a rapid test giving results within hours. In this assay, the lacZ gene of the tester strain E. coli PQ37 is fused to the bacterial sfiA SOS operon and...
(1) Local allergic reactions, which are of three types. The commonest is the late-phase reaction, a biphasic IgE reaction characterized by immediate burning and pruritus with a wheal and flare at the injection site. It may resolve or become indurated, with pruritus continuing for hours to days. Two rarer forms are the Arthustype reaction, producing a pruritic painful nodule 6-8 h after injection, and the delayed hypersensitivity reaction, which is similar but appears 12-24 h after injection. The local reactions are characterized by swelling, erythema, pruritus and lipoatrophy at injection sites they usually disappear with continued treatment. Generalized allergy may produce urticaria, angioedema and, very rarely, anaphylactoid reactions if continued therapy with insulin is essential, desensitization procedures may need to be performed (Wintermantel et al., 1988). Local allergy was extremely common in the 1960s with the use of impure insulins, but the reported prevalence in patients...
Intravenous immunoglobulin (IVIG) is prepared from fractionated pooled human sera derived from thousands of donors with various antigenic exposures (see Chapter 52). At the present time it is unclear if IVIG therapy is beneficial for treatment of dermatoses. Reports of successful use of IVIG in the treatment of autoimmune and inflammatory dermatoses are anecdotal. IVIG has been used to treat toxic epidermal necrolysis, dermatomyositis, chronic recalcitrant urticaria angioedema, atopic dermatitis, systemic lupus erythematosus, and autoimmune blistering disorders.
NOTE See also antihypertensive combinations. Hyperkalemia possible, especially If used concomitantly with other drugs that increase K+ (including K+ containing salt substitutes) and in patients with heart failure, diabetes mellitus, or renal impairment. Monitor closely for hypoglycemia, especially during first month of treatment when combined with insulin or oral antidiabetic agents. ACE inhibitors are contraindicated during pregnancy. Contraindicated with a history of angioedema. Renoprotection and decreased cardiovascular morbidity mortality seen with some ACE inhibitors are most likely a class effect.
Epi is the drug of choice to reverse the manifestations of serious acute hypersensitivity reactions (e.g., from food, bee sting, or drug allergy). A subcutaneous injection of Epi rapidly relieves itching, hives, and swelling of lips, eyelids, and tongue. In some patients, careful intravenous infusion of Epi may be required to ensure prompt pharmacological effects. This treatment may be life saving when edema of the glottis threatens airway patency or when there is hypotension or shock in patients with anaphylaxis. In addition to its cardiovascular effects, Epi activates b receptors that suppress the release from mast cells of mediators such as histamine and leukotrienes. Although glucocorticoids and antihistamines frequently are administered to patients with severe hypersensitivity reactions, Epi remains the mainstay.
Currently used antihypertensive medications (e.g., ACE inhibitors, angiotensin receptor blockers, (3-blockers and aldosterone antagonists) are not universally effective and do not reach the therapeutic goal (130 80 mm Hg) in about 70 of those treated. Some of them cause side effects. All ACE inhibitors, including enalapril (see page 69), cause serious airway inflammation, cough and angioedema in 15-20 of individuals due to the concurrent inactivation of bradykinin. ACE inhibition does not prevent the conversion of angiotensin I to angiotensin II by other proteases.
Unfortunately, despite low systemic concentrations, the risks of side effects are not eliminated by topical NSAIDs.19 The most common side effects are skin reactions such as urticaria, pruritus, irritation, and contact dermatitis. These occur in approximately 2 per cent of
Side-effects Side-effects of the aminosalicylates include diarrhoea, nausea, vomiting, abdominal pain, exacerbation of symptoms of colitis, headache, hyper-sensitivity reactions (including rash and urticaria) side-effects that occur rarely include acute pancreatitis, hepatitis, myocarditis, pericarditis, lung disorders (including eosinophilia and fibrosing alveolitis), peripheral neuropathy, blood disorders (including agranulo-cytosis, aplastic anaemia, leucopenia, methaemoglobin-aemia, neutropenia, and thrombocytopenia see also recommendation above), renal dysfunction (interstitial nephritis, nephrotic syndrome), myalgia, arthralgia, skin reactions (including lupus erythematosus-like syndrome, Stevens-Johnson syndrome), alopecia.
The principal catabolizing enzyme in the lung and other vascular beds is kininase II, or ACE (Figure 24-2) (see Chapter 30). Removal of the C-terminal dipeptide abolishes kinin-like activity. Neutral endopeptidase 24.11 or neprilysin also inactivates kinins by cleaving off the C-terminal dipeptide. A slower-acting enzyme, carboxypeptidase N (lysine carboxypeptidase, kininase I), releases the C-terminal EF residue, producing des-Arg9 bradykinin and des-Arg10 kallidin (Table 24-3 and Figure 24-2), which are themselves potent B1-kinin receptor agonists. Car-boxypeptidase N is expressed constitutively in blood plasma, where its concentration is about 10-7 M. A familial carboxypeptidase N deficiency has been described in which affected individuals with low levels of this enzyme display angioedema or urticaria.
The use of infliximab as a biologic response modifier raises several important considerations. Both acute (fever, chills, urticaria, or even anaphylaxis) and subacute (serum sickness like) reactions may develop after infliximab infusion. Anti-double-stranded DNA antibodies develop in 9 of patients, but a frank lupus-like syndrome occurs only rarely. Antibodies to infliximab can decrease its clinical efficacy strategies to minimize the development of these antibodies (e.g., treatment with glucocorticoids or other immunosuppressives) may be critical to preserving inflix-imab efficacy for either recurrent or chronic therapy.
Frequent adverse effects include headache ( 15 of patients), GI symptoms (e.g., nausea, vomiting, diarrhea, heartburn, flatulence), and rash. More serious reactions include hepatotoxicity, serum sickness reaction, angioedema, and hematologic effects (e.g., leukopenia, neutropenia, punctate basophilia, and monocytosis). Blood studies should be checked weekly during treatment. Estrogen-like effects have been observed in children.
60 mL minute 1.73 m2 Pregnancy see notes above Breast-feeding see notes above Side-effects see notes above also flatulence, hyper-triglyceridaemia, arthralgia, rhinitis rarely headache, asthenia, anaemia, hypersensitivity reactions (including rash, pruritus, urticaria) very rarely nausea Dose
Occasional individuals show marked hypersensitivity to intravenous administration of iodide or organic preparations of iodine. Angioedema is the cardinal manifestation, and laryngeal edema may lead to suffocation. Later, a serum sickness-like reaction may develop. These reactions to radiographic contrast agents are not due to the iodine per se.
Cautions see above also monitor activated partial thromboplastin time or other appropriate blood clotting parameters increased risk of allergic reaction to protamine (including previous treatment with prot-amine or protamine insulin, allergy to fish, men who are infertile or who have had a vasectomy) Side-effects nausea, vomiting, lassitude, flushing, hypotension, hypertension, bradycardia, dyspnoea, rebound bleeding, back pain hypersensitivity reactions (including angioedema, anaphylaxis) and pulmonary oedema reported Dose
Measurement of serum calcitonin is used diagnostically to detect medullary thyroid cancer, especially in the setting of multiple endocrine neoplasia, type 2. Therapeutically, it is used in the acute management of hypercalcemia. It also is approved for Paget's disease, generally by subcutaneous injection because of limited bioavailability of the intranasal form, and for the therapy of osteoporosis. After initial therapy at 100 units day, the dose typically is reduced to 50 units three times a week. Side effects include allergic reactions, nausea, hand swelling, urticaria, and rarely intestinal cramping.
From a clinical standpoint in using these Hi antagonists in the treatment of allergic rhinitis, urticaria in the early part of the pollen season (when the count is still low), these drugs seem highly effective with little or no adverse effects. As the pollen count rises and the period of exposure becomes protracted, symptoms are not as well controlled for instance, the rhinorrhea, nasal itching, nasal obstruction, and sinus congestion increase. The earlier low doses of antihistamines satisfactorily performed a balancing act between antagonizing the effects of moderate levels of released histamine and the unwanted drowsiness (and mucosal dryness). As the level of released histamine increases (due to greater allergic challenge), those low doses become inadequate. Simply increasing these doses is not satisfactory since the adverse anticholinergic and sedative effects may reach unacceptable levels the balance of effects achieved before is lost. A partially successful solution is the...
Structural or histological causes of menorrhagia, or fibroids causing distortion of the uterine cavity, before initiating treatment) regular liver function tests in long-term treatment of hereditary angioedema Contra-indications thromboembolic disease Renal impairment reduce dose consult product literature for details Pregnancy no evidence of teratogenicity in animal studies manufacturer advises use only if potential benefit outweighs risk crosses the placenta Breast-feeding small amount present in milk anti- Hereditary angioedema, 1-1.5 g 2-3 times daily Epistaxis, 1 g 3 times daily for 7 days
Cutaneous clotrimazole occasionally may cause stinging, erythema, edema, vesication, desquamation, pruritus, and urticaria. When it is applied to the vagina, 1.6 of recipients complain of a mild burning sensation, and rarely of lower abdominal cramps, a slight increase in urinary frequency, or skin rash. The sexual partner may experience penile or urethral irritation. By the oral route, clotrimazole can cause GI irritation. In patients using troches, the incidence of this side effect is 5 .
Aspirin produces irreversible platelet aggregation, a concern if surgery is anticipated in the near future. Other salicylates (e.g., choline magnesium tri-salicylate, salsalate) have fewer GI side effects and less effect on bleeding time. Reye's syndrome is associated with aspirin use in children who have a viral illness (varicella). Aspirin hypersensitivity is of two types one involving respiratory reactions (observed in patients with rhinitis, asthma, or nasal polyps), and the second involving rapid development of urticaria, angioedema, hypotension, shock, or syncope.
Of metastatic or progressive prostate cancer at a usual initial dose of 10-16 mg kg daily in 3 or 4 divided doses. Following oral administration, at least 75 of a dose of estramustine is absorbed from the GI tract and rapidly dephosphorylated. Estramustine is found in the body mainly as its oxidized 17-keto analog isomer, estromustine both forms accumulate in the prostate. Some hydrolysis of the carbamate linkage occurs in the liver, releasing estradiol, estrone, and the normustine group. Estramustine and estromustine have plasma t1 2 of 10-20 hours, respectively, and are excreted with their metabolites, mainly in the feces. In addition to myelosuppression, estramustine also possesses estrogenic side effects (gynecomastia, impotence, and elevated risk of thrombosis, and fluid retention) and is associated with hypercalcemia, acute attacks of porphyria, impaired glucose tolerance, and hypersensitivity reactions including angioedema.
Therapeutic uses FDA-approved dermatological uses of hydroxychloroquine include treatment of discoid and systemic lupus erythematosus. Unapproved but first-line uses include treatment of dermatomyositis, porphyria cutanea tarda, polymorphous light eruption, sarcoidosis, eosinophilic fasciitis, lymphocytic infiltrate of Jessner, lymphocytoma cutis, solar urticaria, granuloma annulare, and some forms of panniculitis.
Indications hyperlipidaemias of types IIb and IV in patients who have not responded adequately to diet and other appropriate measures Contra-indications peptic ulcer Renal impairment reduce dose if eGFR 30-60 mL minute 1.73 m2 avoid if eGFR less than 30 mL min-ute 1.73m2 Pregnancy manufacturer advises avoid Breast-feeding manufacturer advises avoid Side-effects vasodilatation, flushing, itching, rashes, urticaria, erythema heartburn, epigastric pain, nausea, diarrhoea, headache, malaise, dry eyes rarely angioedema, bronchospasm, anaphylaxis Dose
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