Combined Allergic Bronchopulmonary Aspergillosis and Tropical Pulmonary Eosinophilia: A Rare Co-occurrence

Allergic bronchopulmonary aspergillosis (ABPA) and tropical pulmonary eosinophilia (TPE) are common lung diseases presenting with peripheral blood eosinophilia. Although these have been widely reported both from India and outside, simultaneous co-occurrence of the two diseases has not been reported so far. We hereby present a case of an elderly male, a known case of asthma, who was diagnosed to have concurrent ABPA and TPE. Partial clinical response as well as the persistence of eosinophilia after ABPA treatment raised the suspicion that subsequently led to the diagnosis of TPE. The concurrent treatment of both conditions led to satisfactory clinical and serological improvement.

A Comparative Clinical Study On The Efficacy Of Vishwadi Leha And Bharangydi Leha In The Management Of Vataja Kasa W.s.r Tropical Pulmonary Eosinophilia

Vataja Kasa (presented by Shushka Kasa, Prasakta Vega, Shirah Shoola, Hrit Shoola, Parshwa Shoola, Swara Bheda and kshamana) has an increasing prevalence overtime due to the external influences such as industrialisation, urbanisation, environmental pollution and population explosion. Since it’s a demanding health concern, Vataja Kasa was taken up for the present clinical study and was approximately co-related to Tropical Pulmonary Eosinophilia (TPE) which is an immune hyper-responsiveness to microfilariae trapped in the lungs, characterised by paroxysmal nocturnal cough, breathlessness, wheezing, chest pain, scanty sputum production and eosinophilia. The study was conducted with the prime aim of assessing the efficacy of the trial drugs Vishwadi Leha and Bharangyadi Leha in the management of Vataja kasa – TPE. The Clinical trial included 40 patients of Vataja Kasa categorized into two groups (20 in each). In Group A-Vishwadi Leha (3 gms) and in Group B- Bharangyadi Leha (3 gms) were administered thrice daily along with quantity sufficient warm water after food for 30 days. The findings were recorded, assessed and graded accordingly on the 14th and 30th day. The results were analysed statistically for ‘p’ value using student’s paired t-test before and after treatment. Significant results (p<0.001) were observed in both groups. Comparative study between percentages of improvement in Group A showed 5% (based on subjective parameters) and 7% (based on objective parameters) more improvement than that of Group B. Based on the results, it was concluded that Vishwadi Leha has a slightly better result than Bharangyadi Leha in the management of Vataja Kasa-TPE.

A Case of Chronic Cough with Progressive Breathlessness in a 32 Year-old Male Health worker- Tuberculosis?, Allergic Bronchitis? Asthma?

Introduction: Although tuberculosis is hyper-endemic in India and is responsible for a huge proportion of respiratory morbidity, adequate workup should be conducted to rule out other differential diagnosis wherever applicable. Case Report: A 32 year old male health worker was suffering from productive cough and gradually increasing breathlessness since three months. The investigations conducted were a sputum analysis and a chest x-ray, both of which were normal and hence he was treated as a case of allergic bronchitis. Subject presented to us after three months with no relief. We further investigated him and found severe eosinophilia in the peripheral blood, a positive anti-filarial antibody and a negative triple stool test for ova and parasites. He was treated with diethylcarbamazine and albendazole+ivermectin combination. The patient responded well and had no complaints at the end of the 4 week treatment. Discussion and Conclusion: The subject should have been evaluated by conducting a basic investigation like a complete blood count. Delay in treatment of cases of tropical pulmonary eosinophilia can lead to permanent respiratory morbidity.

Tropical pulmonary eosinophilia - A review.

Tropical pulmonary eosinophilia (TPE) is a syndrome of wheezing, fever and eosiniphilia seen predominantly in the Indian subcontinent and other tropical areas. Its etiological link with Wuchereria bancrofti and Brugia malayi has been well established. The pathogenesis is due to an exaggerated immune response to the filarial antigens which includes type I, type III and type IV reactions with eosinophils playing a pivotal role. Peripheral blood eosinophilia is usually striking with levels over 3000/μl being common. High serum levels of IgE and filarial-specific IgE and IgG are also found. The pathology may vary from an acute eosinophilic alveolitis to histiocytic infiltration depending on the stage of the disease. While earlier studies had suggested that the disease runs a benign course, more recent work has shown that untreated TPE could result in a fair degree of respiratory morbidity. Pulmonary function tests may show a mixed restrictive and obstructive abnormality with a reduction in diffusion capacity. The bronchoalveolar lavage (BAL) eosinophil count has a negative correlation with the diffusion capacity. Treatment consists of diethylcarbamazine (DEC) for at least three weeks. Despite treatment with DEC, about 20 per cent of patients may relapse. Steroids have shown to have a beneficial effect but the exact dose and duration is yet to be confirmed by randomized controlled trials. A specific and easily available marker is required for TPE in order to distinguish it from other parasitic and non-parasitic causes of pulmonary eosinophilia.

Tropical Pulmonary Eosinophilia : Masquerading as Eosinophilic Leukaemia.

Benign conditions like Tropical Pulmonary Eosinophilia(TPE) can present with very high total count and Absolute Eosinophil Count (AEC) and can mimick malignancy. Diagnostic work up for TPE should be done in any patient presenting with pulmonary symptoms and eosinophilia. Though most case series on TPE report AEC in range of 3000 to upto 20,000, very rarely AEC can rise beyond 50,000. The following case is of TPE presenting with absolute eosinophil count of >70,000. Rapid response to Diethyl carbamazine is the rule in a confirmed case of TPE.

Acquired alpha 1-antitrypsin deficiency in tropical pulmonary eosinophilia.

Background & objectives: Observation of an increased frequency of an intermediate deficiency of serum alpha1-antitrypsin (α1-AT) in patients with Tropical Pulmonary Eosinophilia (TPE) was earlier reported. Though the possibility of existence of an acquired deficiency was suggested, without phenotyping a hereditary α1-AT deficiency in TPE could not totally be ruled out. In this study, we have done Pi (Protease inhibitor) phenotyping to investigate the possibility of association of any heterozygous (or homozygous) α1-AT deficiency in patients with TPE. Methods: Serum a1antitrypsin (α1-AT) was measured in 103 patients (Group A) with TPE, 99 patients with pulmonary eosinophilia who had associated intestinal worm infestation (Group B) and 43 healthy volunteers who served as controls. In 19 α1-AT deficient patients (9 of Group A and 10 of Group B), α1-AT level was measured before and after treatment. In 58 patients with TPE and in 5 controls, phenotyping was done. Results: Fifteen patients of Group A and 16 from Group B showed intermediate α1-AT deficiency (150 mg % or less. None of the control subjects had α1-AT deficiency (<200 mg%). After treatment with DEC and/or deworming, in 19 patients there was a significant (P < 0.001) rise in α1-AT levels. Results of phenotyping showed that all had M1 or M2 allele and none had S or Z variant (either homozygous or heterozygous) thus ruling out any underlying genetic cause for the observed α1-AT deficiency. Interpretation & conclusions: The observed α1-AT deficiency may be due to the chronic inflammation in TPE and associated oxidative stress. However, in such α1-AT deficient patients with TPE and those with worm infested pulmonary eosinophilia, faecal α1-AT concentration and faecal α1-AT clearance should be routinely estimated to rule out the possibility of any intestinal protein loss.