A 44-year-old Indian housewife presented with prolonged cough, intermittent fever, loss of weight and shortness of breath on exertion. Physical examination revealed a thin lady with fine crackles on both lungs. Marked eosinophilia and elevated erythrocyte sedimentation rate were noted on peripheral blood. Chest radiograph showed characteristic bilateral infiltrates affecting the periphery of both lungs. Treatment with corticosteroid resulted in dramatic improvement in symptoms, signs and radiographic changes within a few days.
Kimura's disease (KD) is an uncommon chronic inflammatory condition of unknown aetiology involving subcutaneous tissue, presenting as a tumor like lesion with a predilection for the head and neck region. Clinically it is often confused with parotid tumor with lymph node metastasis. It is difficult to diagnose before tissue biopsy. Fine needle aspiration cytology has only limited value. Unless the pathologists are aware of this entity, it might be misdiagnosed. Surgery, radiotherapy and steroid therapy have been tried but none is proved best and recurrence is common. Three cases of KD seen in our hospital and the problems encountered in them are presented.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/diagnosis*
Kimura disease (KD) is a rare benign chronic inflammatory disease that presents as a nodule mostly involving deep subcutaneous tissue of the head and neck region with frequent regional lymphadenopathy and peripheral blood eosinophilia. KD shares some clinical and histopathological similarity with angiolymphoid hyperplasia with eosinophilia (ALHE). Consequently, KD and ALHE were once considered variants of the same disease spectrum. We present here rare cases of Kimura disease and ALHE involving the eyelid and lacrimal gland and discuss their differential features.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/diagnosis*
Kimura's Disease (KD) is an uncommon, chronic inflammatory disorder of unknown etiology which is endemic in Orientals. It is characterized by painless, large solitary or multiple nodules in subcutis of head and neck region or the major salivary glands, associated with regional lymphadenopathy, blood eosinophilia and elevated IgE levels. Its treatment ranging from conservative observation in asymptomatic patient to surgical resection of the mass, corticotherapy and irradiation therapy for the symptomatic ones.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/diagnosis
Tropical pulmonary eosinophilia (TPE) is considered to be a variant of human filarial infection. The pulmonary manifestations of TPE have been well described. Extra-pulmonary features of the disease, although not commonly seen, have been reported previously. A 9-year-old Malay girl with a history of recurrent cough and wheezing was admitted because of cardiac failure. Physical examination revealed a very sick girl with tachypnoea, central cyanosis, finger clubbing, elevated jugular venous pulse, generalized crackles and rhonchi in the chest, a loud second heart sound and hepatosplenomegaly. A chest radiograph showed cardiomegaly and right pleural effusion. Laboratory investigations revealed hypochromic, microcytic anaemia with persistent blood eosinophilia (absolute eosinophil counts varied from 1.9 to 5.5 x 10(9)/1). The ELISA test for antifilarial IgG antibodies was strongly positive. She responded promptly to treatment with diethylcarbamazine. In summary, this is a patient with TPE who presented with cor pulmonale, probably due to late-stage interstitial pulmonary fibrosis. In order to prevent the long term morbidity of cardiorespiratory disability, the early signs of TPE should be recognized and the infection treated.
A 54-year-old Chinese man presented with ascites for 2 weeks. He had a preceding 2-year history of intermittent dysphagia, lethargy and general malaise. Blood investigations revealed leucocytosis with eosinophilia of 26.5%, whereas paracentesis showed turbid fluid with high protein content (45 g/L) and a high white blood cell count of 5580/µL, predominantly eosinophils (90%). An incidental assay of vitamin D showed a very low level of 13.5 ng/mL. No other cause of ascites was found. Gastroscopy was normal except for duodenitis. However, biopsies from lower oesophagus confirmed the presence of eosinophilic infiltration. Following vitamin D replacement, the patient experienced marked improvement in symptoms of dysphagia within 2 weeks and no recurrence of ascites after 3 months. The reason for the patient's vitamin D deficiency remains unclear. The marked improvement in the patient's health indicates a causative role of vitamin D deficiency in causing eosinophilic esophagogastroenteritis and associated eosinophilic ascites.
We report a 20-year-old college student presents with bilateral ankle edema associated with hypereosinophilia following a history of traveling in a rural area. Physical examinations and investigations failed to diagnose any underlying cause. She was treated with antihelminth medication and the edema subsided within a week and the eosinophil counts normalized within two weeks.
Angiostrongylus cantonensis is the most frequent cause of eosinophilic meningitis in humans in Thailand and worldwide. Because of difficulty of recovering the Angiostrongylus larvae from infected patients, detection of parasite-specific antibodies is used to support clinical diagnosis. This study tested serum samples from eosinophilic meningitis patients and individuals at risk of infection with A. cantonensis to evaluate a recently developed simple and rapid dot-immunogold filtration assay (DIGFA) for detection of specific antibodies against A. cantonensis. Purified 31-kDa glycoprotein of A. cantonensis and protein A colloidal gold conjugate were employed to detect the 31-kDa anti-A. cantonensis antibody in patients sera from the parasite endemic areas of northeast Thailand. The results were compared with those obtained by dot-blot enzyme-linked immunosorbent assay (ELISA) with 31-kDa A. cantonensis antigen. The overall positivity rate of DIGFA and dot-blot ELISA for A. cantonensis infection in 98 clinically diagnosed cases from three highly endemic districts in Khon Kaen province were 39.79% and 37.75%, respectively. Among 86 sera of subjects at risk of infection with A. cantonensis, 24.41% were positive by DIGFA and 23.25% by dot-blot ELISA. There were good correlation between the visual grading of DIGFA and dot-blot ELISA in both groups of defined sera. DIGFA is as sensitive and specific as dot-blot ELISA for confirming eosinophilic meningitis due to A. cantonensis infection, with advantages of simplicity, rapidity and without the use of specific and expensive equipment, and can be used in field settings.
The principal etiologic agent of human eosinophilic meningitis, Angiostrongylus cantonensis, was first detected in rats in Canton, China in 1933. The first human case was detected on Taiwan in 1944. Epidemic outbreaks were noted on Ponape (E. Caroline Is.) from 1944 to 1948. The disease may present as transient meningitis or a more severe disease involving the brain, spinal cord and nerve roots, with a characteristic eosinophilia of the peripheral blood and CSF. Since 1961 it has been known that human infections are usually acquired by purposeful or accidental ingestion of infective larvae in terrestrial mollusks, planaria and fresh-water crustacea. There is no effective specific treatment. The African land snail, Achatina fulica played an important role in the panpacific dispersal of the organism: it will be important in Africa in the future as well. Rats were, and will continue to be the principal agents of expansion of the parasite beyond the Indopacific area. During and just after WWII the parasite was introduced, and/or spread passively from South and Southeast Asia into the Western Pacific islands and eastward and southward through Micronesia, Melanesia, Australia and into Polynesia, sequestered in shipments of war material and facilitated by post-war commerce. In the 1950s numerous cases were identified for the first time on Sumatra, the Philippines, Taiwan, Saipan, New Caledonia, and as far east as Rarotonga and Tahiti. Then cases were detected in Vietnam, Thailand, Cambodia, Java, Sarawak, the New Hebrides, Guam and Hawaii during the 1960s. Subsequently in the Pacific Basin the disease has appeared on Okinawa, other Ryukyu islands, Honshu, Kyushu, New Britain, American Samoa and Western Samoa, Australia, Hong Kong, Bombay, India, Fiji and most recently in mainland China. The parasite in rats now occurs throughout the Indopacific Basin and littoral. Beyond the Indopacific region, the worm has been found in rodents in Madagascar (ca 1963), Cuba (1973), Egypt (1977), Puerto Rico (1984), New Orleans, Louisiana (1985) and Port Harcourt, Nigeria (1989). Human infections have now been detected in Cuba (1973), Réunion Island (1974) and Côte d'Ivoire (1979) and should be anticipated wherever infected rats of mollusks have been introduced. Caged primates became infected in zoos in Hong Kong (1978) and New Orleans and Nassau, Bahamas (1987). The use of mollusks and crustacea as famine foods, favored delicacies and medicines has resulted in numerous outbreaks and isolated infections. Economic and political instability, illicit trade, unsanitary peridomestic conditions and lack of health education promote the local occurrence and insidious global expansion of parasitic eosinophilic meningitis.(ABSTRACT TRUNCATED AT 400 WORDS)