To the Editor: Foreign body aspiration presenting as isolated pleural effusion without an underlying pneumonia is rare. So far only one case has been reported [1].An 11-mo-old boy presented with a history of sudden onset of fast breathing and retractions since last 4 h. He was hemodynamically stable with 95 % saturation under hood oxygen. Auscultation revealed decreased air entry on the left side. Chest radiography showed pleural effusion with collapse lung on left side with ipsilateral mediastinal shift. Ultrasound chest showed left sided pleural fluid of 6 mm depth. Diagnostic pleural tap showed a transudative fluid with no pus cells or bacteria. Total blood WBC count was 18,600 with 78 % polymorphs. The child had a fever spike of 101°F 2 h after admission. Hence, a possibility of community acquired pneumonia with synpneumonic effusion was kept and child was started on intravenous ceftriaxone.After 48 h of treatment, the child's respiratory distress did not improve and air entry was persistently decreased on the left. Blood culture and pleural aspirate culture were sterile, no further fever spikes. Repeat chest radiography showed a partially expanded lung with only minimal blunting of costophrenic angle on the left and hyperinflated lung on the right. Hence, on clinical grounds, a diagnostic fibreoptic bronchoscopy was done which revealed a Bengal gram piece in the left intermediate bronchus. Urgent rigid bronchoscopy was done and two pieces of Bengal gram were removed from the left intermediate bronchus. Post procedure the child was treated with intravenous steroids and adrenaline nebulisation. The child showed dramatic improvement, respiratory distress settled. Repeat chest radiography 12 h later was normal. Blood counts normalised to a total count of 10,600 with 63 % polymorphs and the child was discharged after 48 h.
To the Editor: Dubowitz syndrome (DS) is an autosomal recessive disorder of growth retardation, microcephaly, mental retardation, and eczema [1] with a variable phenotypic spectrum. It also involves the skin, eyes, teeth, musculoskeletal, urogenital, cardiovascular, and A 3½ month male was the first born to healthy unrelated parents at term gestation. The antenatal period was uneventful. At birth the child had a weight of 3 kilogram (kg) (z-score À0.73), Occipitofrontal circumference (OFC) was 36 centimeter (cm) (z-score 1.21) and the length was 50 cm (z-score 0.06). At 3 1/2 months the weight was 3.5 kg (z-score À4.62), length 55 cm (z-score À3.17) and OFC 39 cm (z-score À1.30). There was no significant family history. The child had a high sloping forehead, sparse eyebrows, hypertelorism, telecanthus, blephropimosis, left sided ptosis, left nasolacrimal duct blockage, flat and broad nasal bridge ( Figure 1A), low set posteriorly angulated ears, high arched palate, left hand simian crease, clinodactyly, bilateral partial cut syndactyly of second/third toes with overlapping crowded toes ( Figure 1B). The systemic examination including joints, skin, and genitalia were normal. The diagnosis of DS was considered on the basis of the phenotypic features. Thyroid function tests, lipid profile, karyotype, and FISH analysis were within normal limits. Five millimeter osteum secundum ASD was detected on echocardiography. Chromosomal breakage studies did not show any spontaneous or induced breaks. At 5 months of age there was increasing pallor and hepatosplenomegaly. The hemoglobin was 5.5 g peripheral smear showed microcytic hypochromic anemia, teardrop cells and nucleated RBC's. MCV was 57 fl. Hemoglobin electrophoresis by HPLC (high performance liquid chromatography) was suggestive of TM (HbF ¼ 78%; HbA2 ¼ 3%; HbA ¼ 19%). Both parents were found to have thalassemia trait with presence of 619 bp deletion in the father and IVS 1-5 in the mother. The child was a compound heterozygote with both the mutations.Our patient had typical findings of DS. Absence of eczema and cryptorchidism does not rule out DS since this is seen in only 60% and 18% cases, respectively [1]. There is no laboratory confirmatory test for DS. Neither the gene location nor the pathogenesis is yet known. Chromosomal breakage (spontaneous or after clastogenic stress) [7] and defects in cholesterol biosynthetic pathway or transport have also been reported [8]. Sister chromatid exchanges have been shown to be normal [1]. Whether this represents a chance association in a family with high carrier rate of thalassemia or is an associated gene defect is unclear.
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