Measuring nasal nitric oxide in allergic rhinitis patients.

OBJECTIVE: This study aimed to compare two sampling methods for nasal nitric oxide in healthy individuals and allergic rhinitis patients, and to examine the within-subject reliability of nasal nitric oxide measurement. METHODS: The study included 23 allergic rhinitis patients without concomitant asthma and 10 healthy individuals. For all participants, nitric oxide levels were measured non-invasively from the lungs through the mouth (i.e. the oral fractional exhaled nitric oxide) and the nose. Nasal nitric oxide was measured by two different methods: (1) nasal aspiration via one nostril during breath holding and (2) single-breath quiet exhalation against resistance through a tight facemask (i.e. the nasal fractional exhaled nitric oxide). RESULTS: Compared with healthy participants, allergic rhinitis patients had significantly higher average oral and nasal nitric oxide levels. All methods of nitric oxide measurement had excellent reliability. CONCLUSION: Nasal nitric oxide measurement is a useful and reliable clinical tool for diagnosing allergic rhinitis in patients without asthma in an out-patient setting.

[Angioedema caused by angiotensin-converting enzyme inhibitors]. / Angioedem izazvan lekovima inhibitorima enzima ACE.

Angioedema is a rare, but important effect of arterial hypertension treatment with drugs which inhibit angiotensin-converting enzyme. Usually, it develops in the first week of therapy, but some atypical cases of the development of angioedema after several months to few years after the onset of the therapy have been reported. Undesired reactions caused by these drugs are probably not allergic, but they are caused by pharmacological effect of these drugs in persons with risk of allergic reaction. In this paper we present some patients with angioedema.

[T lymphocytes in allergic inflammation]. / Limfociti T u alergijskoj inflamaciji.

T lymphocytes are the crucial cells in immunopathogenesis of allergic diseases since they regulate the occurrence of allergic sensitisation, synthesis of immunoglobulin E and allergic inflammation. The importance of lymphocyte T is reflected on the fact that after activation by a specific antigen they are able to produce different cytokines responsible for activation and aggregation of specific inflammatory cells in target tissues, promoting the occurrence and maintenance of allergic inflammation. Discovery of functional dichotomy of activated lymphocytes T CD4+ capable of suppressing synthesis of immunoglobulin E (Th1) or stimulate immunoglobulin E and allergic inflammation (Th2) is an important element in elucidation of pathogenesis of allergic inflammation and inadequate synthesis of immunoglobulin E. The immunoglobulin synthesis is regulated by a complex combination of factors and signals where lymphocytes CD4+ play the central regulatory role.

[Leukotrienes in allergic inflammatory reactions]. / Leukotrijeni u reakcijama alergijske inflamacije.

Production of leukotrienes, lipooxygenase products of arachidonic acid metabolism, plays an important role in inflammatory reactions, particularly well studied in bronchial asthma. Lipooxigenase-5 and lipooxygenase-activating protein-5 are crucial in the production of leukotrienes with potent biological activities. Leukotriene B4 is a leukocytic chemoattractant and it induces aggregation and adherence of leukocytes to endothelial vasculature. Sulfidopeptid leukotrienes (C4, D4 and E4) are potent bronchoconstrictors, producing mucous secretion in the airways and increasing vascular permeability. Leukotrienes participate in the process of inflammation, as well as in early and late asthmatic responses. They are found in the blood, liquid obtained upon bronchoalveolar lavage as well as in the urine, irrespectively whether bronchospasm developed spontaneously or it was induced by an allergen. Administration of the specific leukotriene receptor antagonists or leukotriene synthesis inhibitors ameliorates the symptoms and signs of bronchial asthma.

[The role of prostaglandins in allergic inflammation]. / Uloga prostaglandina u alergijskoj inflamaciji.

Prostaglandins likewise leukotriens are proinflammatory mediators resulting from metabolic degradation of the arachidonic acid originating from membrane phospholipids. The most important products of enzyme cyclooxygenation of arachidonic acid are prostaglandins D2, E2, F2a, tromboxane A2 and prostacyclin. Prostaglandins express their tissue effects via the five basic receptor types. Within the allergic inflammation activated mast cell synthesizes prostaglandin D2 (first lipid mediator) which has bronchoconstrictive and vasodilating effects and attracts neutrophilic leukocytes. Moreover, it also participates in the late phase reactions, six hours subsequent to the exposure to the allergen. This mediator is also important in pathogenesis of urticaria, allergic rhinitis and allergic bronchial asthma. In addition to prostaglandin D2, prostaglandin F2a and tromboxane A2 also have bronchoconstrictive actions, while prostacyclin and prostaglandin E have bronchodilating effects. Inhalation of prostaglandin E prevents asthmatic attacks caused by allergens, strain, metabisulfite and ameliorates attacks of aspirin asthma, which confirms the hypothesis that aspirin asthma is based on cyclooxigenase inhibition and increased leukotriene production. In patients with atopic dermatitis, prostaglandin E has suppressive effects on Interferon gamma production by Th1 helper cells and increases production of Interleukin 4 by the Th2 cells. Tromboxane A2 plays a certain role in the development of bronchial hyperreactivity and late asthmatic response. Prostaglandins are also important mediators in the pathogenesis of allergic conjunctivitis. Most of nonsteroidal antiinflammatory drugs inhibit the enzyme cyclooxygenase and thus also prostaglandin biosynthesis and release.

[Sjogren's syndrome]. / Segrenov sindrom.

Sjogren's syndrome is a chronic inflammatory disease of unknown aethiology. It is characterized by decreased secretion of salivary and lacrimal glands, which induces keratoconjunctivitis sicca and xerostomia. Sjogren's syndrome is a central autoimmune disease, and it has characteristics of both organ-specific and generalized autoimmune diseases. It can exist as a primary disease or is associated with other autoimmune diseases (most freyuently with systemic lupus erythematosus or rheumatoid arthritis) and is classified as a secondary Sjogren's syndrome. The aethiology is multifactorial, and it has not yet been completely explained. In the pathogenesis of the disease the important role have genetic predisposition, chronic oestrogen stimulation, end viral infections, especially of the herpes virus group (EBV, CMV, HHV6) and retroviruses. In the clinical picture xerostomia, xerophtalmia and non-erosive arthritis are the most common features, with the whole spectrum of extraglandular manifestations of respiratory, gastrointestinal, skin, and haematologic, neurologic and endocrinologic disturbances. Pathohistological findings of minor labial salivary gland lymphocyte infiltration is the most specific and the most sensitive diagnostic criterion of Sjogren's syndrome. The diagnosis of keratoconjunctivitis sicca is made by Schrimer's test, Rose bengal dye staining and by the "tear break up time". Differential diagnosis of Sjogren's syndrome includes an extremely large number of various pathologic states. The treatment of Sjogren's syndrome consists of symptomatic treatment of dry mucosas (artificial tears, etc.) and also of antiinflammatory drugs, glucocorticoids, immunosuppressive drugs. Plasmapheresis and intravenous administration of immunoglobulins are used for immunosuppression in these patients.

[Risk factors for allergic bronchial asthma]. / Faktori rizika za nastanak alergijske bronhijalne astme.

The paper deals with the current data on aetiological factors of allergic bronchial asthma. The cause of allergic bronchial asthma is unknown. In general, endogenous and environmental factors are though to play a certain role in its development. Early contact with allergic agents, air pollution, tobacco smoking and infective agents (viruses), are considered to be environmental factors. Endogenous factors are heredity of allergic diseases and special susceptibility for bronchial asthma.