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Comparative efficacy of H1blocker, H2blocker, and corticosteroid individually and in combination in resolution of sign and symptoms of acute Urticaria



Objective: To compare the efficacy of H1 blocker, H2 blocker, corticosteroid in combination or individually in resolution of the sign and symptoms of acute urticaria. Study Design: Randomized control trial Place and Duration of Study: This study was carried out at Medical Department, Naseer Teaching Hospital, Peshawar, Khyber Pakhtunkhwa (KPK) for the period of six months (July 2012 through December 2012). Materials and Methods: In this study 140 adult patients of both gender with acute urticaria were treated with either Hi blocker (group A), H2 blocker (group B) or in combinations of H1 blocker + H2 blocker (group C), H, blocker + H2 blocker + dexamethasone (group D), Hi blocker + dexamethasone (Group E), H2 blocker + dexamethasone (Group F) or Dexamethasone (group G) alone. The end points were resolution of sign and symptoms in each group of patients (minimum 3 hours after treatment). Pregnant females, anemic and Patients with cardiac disease were excluded. Results: H1+ H2blockers + dexamethasone found to be most effective therapeutic combination (95% of patients) in resolution of sign and symptoms of acute urticaria, followed by H( blocker + dexamethasone (90%) and H1+ H2 blockers (85%). Conclusion: This study concludes that the combination of H1+H2 blockers + dexamethasone is more effective in relieving the patient from the sign and symptom of acute urticaria as compared to H1 blocker or H2 blocker or dexamethasone given alone or in combination of any two.
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Objective The aim of the study is to assess various reflux sites in patients with varicose veins by using duplex scan. Patients and Methods This prospective observational study was done at Department of Diagnostic Radiology, Holy Family Hospital, Rawalpindi in collaboration with Department of Surgery, Social Security Hospital, Islamabad from January 2007 to December 2010. All the patients diagnosed as having varicose veins by the surgeon and referred to the department of radiology underwent duplex scanning of the venous system of the affected lower limb. The patients having recurrent varicose veins, history of limb trauma, previous venous surgery, sclerotherapy, and deep venous thrombosis were excluded from the study. The long and short saphenous systems were assessed, together with the deep veins and perforators along the medial aspect of the thigh and calf. Reflux was defined by retrograde flow lasting longer than 0.5 s after manual calf compression. Results A total of 128 lower limbs of 114 patients were included in the study. 71 (62.28%) were males and 43 (37.72%) were females. Mean age was 44.67 years (range 22-63). Mean age of male was 42.06 years and that of females was 48.53 years. Of the 128 lower limbs assessed, 68 were right, 60 were left and 14 patients had bilateral varicose veins. Isolated sapheno-femoral junction incompetence was found in 46 (35.9%) cases whereas isolated sapheno-popliteal junction incompetence was seen in 30 (23.4%) patients, 32 (25%) had both sapheno-femoral and sapheno-popliteal incompetence. Conclusion Saphenofemoral junction was the most common site of reflux in the varicose veins. As colour duplex scan is non-invasive, repeatable, and readily accepted by the patients, it should be the investigation of choice for patients presenting with varicose veins.
This is a study of one hundred patients of epistaxis who reported to the Department of ENT at Services Hospital, Lahore during the year 1993- 1994. A thorough evaluation of these patients for a possible cause revealed 'trauma' to be the commonest (45%). Next in frequency was the idiopathic group (24%). Other aetiological factors like hypertension (9%), neoplasia (9%), acute nasal infection (7%), bleeding disorders (4%) and miscellaneous (2%) formed the rest of this bulk.
I. Acute urticaria/angioedema. A recent episode of urticaria/angioedema lasting less than 6 weeks is characterized as acute, while lesions recurring for more than six weeks are termed chronic. In acute urticaria/angioedema, the etiology may be readily apparent to both the patient and the physician. For example, the patient who presents with acute urticaria after drug administration, insect sting, or repetitive physical triggers will often note an association. The longer the urticaria persists the more difficult it is to determine a specific etiology. Urticaria should be considered when the patient presents with pruritic (and sometimes painful or burning), erythematous, circumscribed (or coalescent) wheals. Urticarial lesions commonly involve the extremities and trunk but may appear on any part of the body. In contrast to urticaria, angioedema presents as deeper subcutaneous swelling. Less circumscribed than the lesions of urticaria, angioedema has a predilection to areas of loose connective tissue such as the face or mucous membranes involving the lips or tongue. If angioedema involves the upper respiratory tract, life-threatening obstruction of the laryngeal airway may occur. Hereditary or acquired angioedema associated with C1 esterase inhibitor deficiency are particularly prone to this presentation, although other forms of angioedema can present either with laryngeal or glossopharyngeal edema causing hoarseness and difficulty in swallowing. The etiology of urticaria/angioedema can often be deduced by a detailed history. The patient should be asked about recent use of medications (including herbals and supplements), food exposures, physical triggers, viral infections, contactants, occupational and natural allergen exposures or systemic diseases which can manifest as acute urticaria. The physical examination should include the skin, lymph nodes, eyes, ears, throat, neck, joints, lungs, heart, and abdomen in an effort to detect an underlying causal condition. Findings ascertained by history or physical examination may direct attention towards an identifiable trigger or cause of urticaria/angioedema. Given the vast number of potential urticarial triggers and the difficulty in identifying them, any clues uncovered by history and physical may be extremely important. Evaluation of a suspected cause of acute urticaria/angioedema is often based on a clear temporal relationship between onset of symptoms and exposure to a specific food, insect sting or drug. If IgE-mediated penicillin-induced hives is suspected, predictive diagnostic skin tests are available. Allergy skin testing and/or in vitro tests may be useful in determining whether anaphylactogenic foods or inhalants are the cause of urticaria. Viral diagnostic studies may be helpful in confirming the association of hives with viral infections (eg, the Epstein-Barr virus). On the other hand, a complex evolving process may develop in patients with acute urticaria/angioedema. Initial evaluation may not provide definitive diagnosis and further management becomes empiric. In the absence of historical information or physical signs suggesting an underlying cause, therapeutic intervention should be implemented. The immediate treatment of acute urticaria/angioedema that occurs as a component of anaphylaxis necessarily takes precedence over diagnostic considerations. Patients may improve after removal of factors that augment or induce urticaria/angioedema (eg, aspirin, NSAIDs, or alcohol ingestion). The cornerstone of treatment for acute urticaria/angioedema not associated with anaphylaxis is the use of H1 antihistamines. Second generation H1 antihistamines are usually preferred. When these fail, first generation antihistamines, such as hydroxyzine or diphenhydramine may be effective, although caution about the sedating side effects of these agents should be emphasized. The use of glucocorticosteroids in the treatment of patients with acute urticaria/angioedema is rarely necessary. If they are required, short courses of oral glucocorticosteroids rather than depot parenteral preparations are preferred to lessen the duration of systemic effects. If known triggers or causes for urticaria/angioedema are not discovered within the first six weeks of the onset of symptoms, further evaluation and management of this chronic process becomes more complex. At this point, referral to an allergist/immunologist is appropriate, especially if the etiology has not been determined. II. CHRONIC URTICARIA. Urticarial lesions are defined as chronic if manifestations persist or recur beyond six weeks. Persistent symptoms may be daily or episodic. Diurnal patterns are often reported but these are highly variable from patient to patient. It is not possible to predict the duration of chronic urticaria/angioedema. Spontaneous remissions often occur within 12 months but many patients continue to have symptoms at least periodically for years. Conditions that can masquerade as urticaria include erythema multiforme minor, nonspecific maculopapular exanthemata, mast cell releasibility syndromes such as urticaria pigmentosa and urticarial vasculitis. The skin lesions of urticarial vasculitis differ from urticaria in that they are palpable, purpuric, and persist 24 hours or longer. Resolution of these lesions is prolonged and they often leave residual pigmented changes in the skin. If skin lesions have the appearance of urticarial vasculitis, a skin biopsy should be performed. Routine histopathology reveals the presence of leukocytoclastic vasculitis while immunofluorescence may demonstrate the presence of fibrinogen, various immunoglobulins, and complement within the vascular lesions. Systemic collagen vascular diseases should also be considered in the differential diagnosis of urticarial vasculitis. Treatment of this condition may require various anti-inflammatory agents such as glucocorticosteroids, colchicine, dapsone, hydrochloroquine, or other cytotoxic agents. Commonly, chronic urticaria and angioedema coexist; however, some patients may develop chronic angioedema without urticaria. Etiologic triggers of chronic angioedema without urticaria may be the same as those observed in acute urticaria and include medications, occupational exposures, insect sting, physical hypersensitivity disorders, delayed pressure angioedema, and C1 esterase inhibitor deficiencies. Drugs such as ACE inhibitors or aspirin/NSAIDs may induce or aggravate angioedema. If this relationship is suspected, the drug should be withdrawn as soon as possible. Of particular importance is the family history, because of the possibility of hereditary C1 esterase inhibitor deficiency. The episodes of swelling in patients with this disease are often precipitated by trauma. Screening C4 levels should be obtained in all patients with chronic angioedema without urticaria. C4 levels are usually decreased during and between attacks while C2 levels are reduced only during attacks. Fifteen percent of patients with hereditary C1 esterase inhibitor deficiency have normal quantitative levels of C1 esterase inhibitor protein that is dysfunctional. Chronic angioedema due to C1 esterase inhibitor deficiency may also be acquired as a manifestation of a systemic connective tissue disease, a lymphoproliferative disorder or as a de novo autoantibody to C1 esterase inhibitor protein. The treatment choices for recurrent, life-threatening attacks of C1 esterase inhibitor deficiency are limited and supportive. Plasma infusions or C1 esterase inhibitor concentrates (available only on an experimental basis) may offer short-term palliative benefit. Should these measures fail, intubation or tracheostomy may be necessary. To prevent recurrent episodes of angioedema due to C1 esterase inhibitor deficiency, prophylactic management with anabolic steroids may be helpful. It is very unusual to find an exogenous cause for chronic urticaria/angioedema. Nevertheless, every effort should be made to determine the etiology of these symptoms by redirecting attention to a detailed medical history and review of systems. Triggers such as foods, drugs, physical factors, insect bites, occupational exposures, and contactant exposures should have been ruled out during the initial workup of acute urticaria. The differential diagnosis of chronic urticaria/angioedema should include complement-mediated disorders, malignancies, cutaneous or systemic mastocytosis, mixed connective tissue diseases and cutaneous blistering disorders (eg, bullous pemphigoid and dermatitis herpetiformis). Only a few screening laboratory tests are possibly helpful in detecting etiology at this stage of the workup. These include a complete blood count with differential, erythrocyte sedimentation rate, urinalysis, and liver function tests. Since thyroid autoantibodies may be present in up to 28% of patients with urticaria/angioedema, particularly women with chronic urticaria/angioedema, some clinicians advocate that these tests be obtained regardless of the patient's thyroid status. Evaluation of the patient for autoantibodies to high affinity IgE receptor (FcεR1) should also be considered. If not previously obtained, a punch skin biopsy should also be performed in patients with difficult-to-manage chronic idiopathic urticaria. Two groups of patients with chronic urticaria have been identified based on the histopathology of the skin lesions: (1) perivascular lymphocyte-predominant urticaria and (2) perivascular polymorphonuclear-predominant urticaria.
1. Breech malposition and hormonal joint laxity produce atraumatic posterior dislocations in the hip joints of young rabbits. 2. Experimental studies were shown to cause the development of a limbus and other softtissue changes similar to those found in human congenital dislocations. 3. The development of femoral retroversion and anteversion in the presence of joint laxity is described. 4. The co-existence of breech malposition and hormonal joint laxity in utero, and their importance as prime factors in the etiology of congenital dislocation of the hip, are discussed.