Atypical respiratory complications of dengue fever

In last decade, dengue has emerged as one of the most important vector born disease. With increasing cases, uncommon presentations and complications are now commonly recognized. Here, we report two cases of rare pattern of respiratory involvement in dengue: acute respiratory distress syndrome and bronchiolitis with respiratory failure.     

Spontaneous Coronary Artery Dissection

Spontaneous coronary artery dissection is an important etiology of nonatherosclerotic acute coronary syndrome, myocardial infarction, and sudden death. Innovations in the catheterization laboratory including optical coherence tomography and intravascular ultrasound have enhanced the ability to visualize intimal disruption and intramural hematoma associated with SCAD. Formerly considered “rare,” these technological advances and heightened awareness suggest that SCAD is more prevalent than prior estimates. SCAD is associated with female sex, young age, extreme emotional stress, or extreme exertion, pregnancy, and fibromuscular dysplasia. The clinical characteristics and management strategies of SCAD patients are different than for atherosclerotic heart disease and deserve specific consideration. This review will highlight recent discoveries about SCAD as well as describe current efforts to elucidate remaining gaps in knowledge.     

Role of tissue harmonic imaging in focal hepatic lesions: comparison with conventional sonography

Background: The purpose of the present study was to compare iissue harmonic imaging (THI) and conventional sonography in focal hepatic lesions. Methods: Fifty patients with focal hepatic lesions were enrolled for study. Conventional grayscale and THI was performed in all the patients and two sets of images of the lesions were recorded (one each for THI and conventional) and assessed for fluid–solid differentiation, detail and overall image quality. These images were compared with conventional sonographic images and graded better, same or worse as per the case. Lesions were confirmed by fine‐needle aspiration cytology (FNAC)/surgery/other modalities such as computed tomography (CT) or magnetic resonance imaging (MRI). Results: Out of 50 patients with focal hepatic lesions, 21 patients had metastatic lesions (two single; 19 multiple) five patients had hepatocellular carcinoma (HCC), five patients had hydatid cysts, nine had simple hepatic cyst whereas five patients had liver abscess, three had focal fatty infiltration; and lymphoma and hemangioma were seen in one patient each. The first observer ranked THI better than standard sonography in 40 patients (80%) for fluid–solid differentiation, in 38 (76%) for detail and in 39 (78%) for overall image quality. The second observer ranked THI better than standard sonography in 39 patients (78%) for fluid–solid differentiation, in 40 (80%) for detail and in 42 (84%) for overall image quality. Tissue harmonic imaging provided additional information in eight patients (16%) and resulted in treatment alteration in three patients (6%). Conclusion: Tissue harmonic imaging was significantly better than conventional sonography for fluid–solid differentiation, detail and total image quality in focal hepatic lesions, especially in obese patients and patients with poor acoustic window.     

Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function

Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report). A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC- gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC- delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function.     

Human platelet signaling defect characterized by impaired production of inositol-1,4,5-triphosphate and phosphatidic acid and diminished Pleckstrin phosphorylation: evidence for defective phospholipase C activation

Signal transduction on platelet activation involves phosphoinositide- specific phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositides and formation of inositol-1,4,5-triphosphate [I(1,4,5)P3], which mediates Ca2+ mobilization, and diacylglycerol (DG), which activates protein kinase C (PKC) to phosphorylate a 47-kD protein (Pleckstrin). We studied these events in two related patients previously reported (Blood 74:664, 1989) to have abnormal aggregation and 14C-serotonin secretion, and impaired intracellular Ca2+ mobilization in response to several agonists. Thrombin-induced I(1,4,5)P3 and phosphatidic acid formation were diminished. Pleckstrin phosphorylation was impaired on activation with thrombin, platelet- activating factor, and ionophore A23187, but was normal with PKC activator 1,2-dioctonyl-sn-glycerol (DiC8). Ca2+ mobilization induced by guanosine triphosphate (GTP) analog guanosine 5'-0-(3 thiotriphosphate) (GTP gamma S) was diminished. Pretreatment with either A23187 or DiC8 did not correct the impaired adenine diphosphate- induced secretion; however, upon stimulation with A23187 plus DiC8, pleckstrin phosphorylation and secretion were normal, indicating that both PKC activation and Ca2+ mobilization are essential for normal secretion. We conclude that these patients have a unique inherited platelet defect in formation of two key intracellular mediators [I(1,4,5)P3 and DG] and in the responses mediated by them due to a defect in postreceptor mechanisms of PLC activation.