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 ISSN: 0973- 3809 

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Editorial : Future of Asthma Therapy

Dr.P.Ravindran ,Senior Consultant Pulmonologist, Cosmopolitan Hosital, Trivandrum

           Inspite of decades of research the cure of asthma still eludes us. Advances in molecular biology, immunology and biochemistry have only made the understanding of asthma more complex and the treatment complicated. To the clinician, asthma remains the same. He finds each patient with a different clinical picture and differing response to therapy, which perplexes him. He consoles himself, thinking that each individual is different and the way he manifests any disease also will be different. This is true in the case of asthma, as it is a multi-gene defect and hence the disease manifests differently from patient to patient. Number of research groups have put forward different classifications and guidelines for management of asthma. A practicing clinician will soon recognize that these are only guidelines but are convenient for day to day management of asthma.

Review Article : Tropical Eosinophilia

Dr.V.K.Vijayan,Director, VP Chest Institute, University of Delhi. 

          Tropical eosinophilia (TE) is an occult form of filariasis and is characterized by cough, dyspnoea and nocturnal wheezing, diffuse reticulo-nodular infiltrates in chest X-rays and marked peripheral blood eosinophilia. The syndrome results from immunologic hyperresponsiveness to human filarial parasites, Wuchereria bancrofti and Brugia malayi. Frimodt-Moller and Barton in 1940 described a group of sanatorium patients in South India who had fever, cough, chest pain and weight loss in association with massive blood eosinophilia. These patients had extensive bilateral military mottling in chest X-rays and were wrongly diagnosed as military tuberculosis. However, they were in good physical condition and were not associated with high mortality observed in military tuberculosis. They described this entity as “pseudo-tuberculosis condition associated with eosinophilia”. The name “Tropical Eosinophilia” to this syndrome was coined by Weingarter in 1943. He described 81 patients with severe spasmodic bronchitis, lecuocytosis and very high eosinophilia and disseminated mottlings of both lungs. These patients were successfully treated with neoarsphenamine, by the accidental observation that one of his patients with concurrent syphilis was cured of his TE on being given neoarsphenamine for syphilis. Tropical eosinophilia is endemic in the Indian subcontinent, South East Asia and South pacific islands.

Special Articles: 

Preventive and Management Strategies of Nosocomial Bacterial   Pneumonias in Critical Care Units 

Dr.P.Ravindran,Former Director & Professor of Respiratory  Medicine,Medical College, Trivandrum. 

          Nosocomial pneumonia is one of the dreaded complications of patients managed in critical care units. In spite of very powerful antibiotics available to us mortality ranges from 50 to 70%. For the purpose of definition nosocomial pneumonia is diagnosed if it occurs 48 hours after admission to hospital, 48 hour after admission to critical care unit or 48 hours after putting on ventilator. The incidence is variously reported (10 to 40%) from institution to institution. However opinion differ in attributing pneumonia as the direct cause of death for these patients. These patients also have multi organ dysfunction and that could be the reason for the higher mortality. However, when the organism is pseudomonas or acinectobacter the mortality is definitely high.

Pulmonology – A success by evolution

Dr.K.P.Govindan,Former Professor & Head,Institute of Chest Diseases, Medical College,Calicut.

Health Effects of Passive Smoking

Dr.A.K.Abdul Khader 

Smoking is the largest single cause of preventable premature death. Smoking accounts for more than a third of all death in middle age. Now adverse health effects of environmental tobacco smoke is an issue of enormous interest. Passive smoking causes high incidence of acute and chronic respiratory illness in children. The number of people injured by involuntary tobacco smoke is much more than any environmental agent that is regulated like asbestos and lead. It is reported that 63% of population has some daily exposure.

Environmental tobacco smoke is derived from 2 sources, that is mainstream smoke and side stream smoke.

The particles in SSS has smaller size than in MSS and more likely to be deposited in the most distant alveolar portions of the lung. 85% of the smoke generated while smoking is from side stream.

When a smoker takes in 16mg CO, the spread to atmosphere via side stream smoke is 40mg, while smoking a cigarette. But this is more when he smokes a beedi.

Allergic Bronchopulmonary Aspergillosis 

Dr.C.Ravindran,Associate Professor,Institute of Chest Diseases, Medical College, Calicut. 

          Allergic bronchopulmonary aspergillosis (ABPA) is a complex disease occurring in 1-2% of patients involving hypersensitivity to Aspergillus sp. This was initially reported by Hinson et al in 1952 and is characterized by recurrent chest roentgenographic infiltrates, peripheral blood and sputum eosinophilia and asthma. This clinical entity is often underdiagnosed since it mimics many other common diseases such as bronchi- ectasis, pulmonary tuberculosis and tropical pulmonary eosinophilia. So, high index of suspicion is needed for an early diagnosis and treatment.

          Aspergillus fumigatus, in common with other fungi such as the harvest moulds. Alternaria tenius and Cladosporium herbarum, can stimulate IgE antibody production and cause asthma. A.fumigatus alone also causes:

-         Pulmonary eosinophilia (eosinophilic consolidation)

-         Proximal bronchiectasis (localized bronchial wall damage)

-         Bilateral upper lobe fibrosis.

The probable explanation of this difference in pathological effect is that hyphal growth of  inhaled spores of A.tenuis and C.hebarum does not occur at body temperature. The spores are rapidly cleared from the airways; their allergens are the soluble proteins which are eluted from the surface of spores before they are cleared. A.fumigatus spores are capable of hyphal growth at body temperature. The hyphae persist in the airway as an insoluble particulate stimulus leading to:

-         B lymphocyte, IgE and IgE production

-         T lymphocyte dependent release of eosinophilic chemetactic factors (eg.IL 5) which recruit eosinophils in to the airways and adjacent alveoli to cause eosinophilic consolidation (pulmonary eosinophilia)

Release of tissue damaging basic proteins (major basic protein and cationic protein) is probably responsible for localized tissue damage