The DOTS strategy for treatment of paediatric pulmonary tuberculosis in South Delhi, India.

SETTING: Paediatric Pulmonology Department, TB Institute, New Delhi, India. OBJECTIVE: To evaluate the outcome of the DOTS strategy for paediatric pulmonary tuberculosis (TB). DESIGN: Retrospective analysis of 1098 children. RESULTS: The mean age of the children included in the study was 11.2 years, with more females (61.7%) than males (38.3%). In the 0-5, 6-10 and 11-14 year age groups, the percentage of patients was respectively 18.3%, 26.6% and 55.1%. Patients were registered as new cases (87.7%), relapses (1.9%), failures (1.0%), defaulters (5.0%), transferred in (0.9%) and others (3.5%). Of the total number of cases, 414 were smear-positive and 404 smear-negative, while sputum status was not known for 280 patients. Sputum positivity increased with age. Category I, II and III regimens were started by respectively 50.6%, 10.5% and 38.9% patients. The cure rate was 92.4% (302/327) for new and 92% (80/87) for retreatment cases (chi(2)(1) = 0.02, P = 0.901), but the treatment completion rate was significantly higher for new cases (97%, 636/656) than retreatment cases (53.6%, 15/28) (chi(2)(1) = 100.8, P < 0.001). The overall success rate was 95.4% and 82.6% for new and retreatment cases, respectively (chi(2)(1) = 30.35, P < 0.001). Overall, the rates for default, failure and death in the study were respectively 3%, 1.9% and 1%. CONCLUSION: DOTS appears to be a highly efficacious treatment strategy.     

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.     

Evaluation of retinopathy of prematurity screening in reverse Kangaroo Mother Care: a pilot study

Purpose

To evaluate retinopathy of prematurity (ROP) screening practice in reverse Kangaroo Mother Care (R-KMC) with respect to stress and pain to the infant.

Methods

In a pilot study we evaluated ROP screening practice in R-KMC in 20 babies at risk of ROP. The R-KMC differed from the conventional KMC with respect to the baby position where the baby lay supine on mother''s chest. With the mother lying supine and the baby in R-KMC position, screening examinations were done with indirect ophthalmoscope. The outcome measures included stress (quantified by pulse, respiration, and oxygen saturation) and pain to the baby by observing facial expression (eye squeezing, crying, and brow bulge). The heart rate, respiratory rate, and SpO2 (%) were compared before and immediately after the procedure using paired t-test.

Result

Mean (±SD) gestational age and birth weight were 30.8±2.3 weeks and 1362.5±253.9 g, respectively. During examination in R- KMC position 8 babies (40%) were completely relaxed (no eye squeezing and crying), 10 (50%) were partially relaxed (no brow bulge) and 2 babies (10%) were not relaxed. A change in heart and respiration rate both by 10 per minute was recorded in 12 (60%) and 10 (50%) babies, respectively. Five babies (25%) had reduction in blood oxygen concentration below 92%. The majority of the mothers (19 of 20) were relaxed.

Conclusion

ROP screening in R-KMC can be a baby friendly screening practice with respect to stress and pain to the infant and needs further evaluation in a larger cohort.     

Acquired granular pool defect in stored platelets

Platelets stored as concentrates (PC) for 72 h at 22 degrees C develop a functional defect. Alterations in adenine nucleotides of platelets have been shown to affect platelet function. Adenine nucleotide content of platelets was measured before and after storage and a decrease of 27.1 /+- 1.7% (mean /+- SE) in ATP and 39.1 /+- 2.6% in ADP were found in 34 PC stored with final volume of 50 ml. In 11 PC with 30 ml volume. ATP and ADP decreased by 39.4 /+- 3.2% and 49.4 /+- 2.1%, respectively. The mean ATP to ADP ratio of stored platelets was significantly higher than of fresh platelets in both groups, suggesting a relatively greater decrease in granular than metabolic pool nucleotides. Levels of low affinity platelet factor 4 measured by radioimmunoassay in plasma from 0.86 /+- 0.08 microgram/ml in the fresh PC to 8.59 /+- 0.39 microgram/ml in stored PC, indicating a concomitant alpha-granular secretion. Labeling of metabolic pool with 14C-adenine revealed a mean decrease in the adenylate energy charge of 2.0 /+- 0.4% in 12 of 16 stored PC, with a lower ATP and higher hypoxanthine labeling in stored as compared to fresh platelets. These observations suggest that stored platelets develop an acquired defect in both dense and alpha granules and in their ability to maintain ATP homeostasis.     

Retrieval of fractured dialysis catheter through phlebotomy of internal jugular vein: a case report

A central venous catheter is the most common access for initiating hemodialysis. Prolonged access through a central venous catheter increases the risk of infection and dysfunction of the catheter with potential development of catheter-induced thrombosis and embolism. However, fracture and dislodgement of the catheter with subsequent embolization is an unexpected complication. Endovascular treatment is a promising method to remove intravascular foreign bodies. We herein report a case of a 58-year-old woman undergoing prolonged hemodialysis who required central venous catheter removal because of mechanical fracture of the tunneled cuffed catheter and its migration in the internal jugular vein. An urgent chest X-ray showed that the two free ends of the fractured tunneled cuffed catheter were located in the right atrium and right internal jugular vein. Phlebotomy of the internal jugular vein was successfully performed to retrieve the fractured tunneled cuffed catheter and the associated thrombi. In this case, phlebotomy for retrieval of the embolized catheter fragment extending into the right atrium was a safe alternative to an endovascular technique of catheter fragment retrieval. Phlebotomy preserved the integrity of the catheter fragment and its associated thrombus and was both cost-effective and safe.     

Anterior cruciate ligament injury about 20 years post‐treatment: A kinematic analysis of one‐leg hop

Reduced dynamic knee stability, often evaluated with one‐leg hops (OLHs), is reported after anterior cruciate ligament (ACL) injury. This may lead to long‐standing altered movement patterns, which are less investigated. 3D kinematics during OLH were explored in 70 persons 23 ± 2 years after ACL injury; 33 were treated with physiotherapy in combination with ACL reconstruction (ACL_R) and 37 with physiotherapy alone (ACL_PT). Comparisons were made to 33 matched controls. We analyzed (a) maximal knee joint angles and range of motion (flexion, abduction, rotation); (b) medio‐lateral position of the center of mass (COM) in relation to knee and ankle joint centers, during take‐off and landing phases. Unlike controls, ACL‐injured displayed leg asymmetries: less knee flexion and less internal rotation at take‐off and landing and more lateral COM related to knee and ankle joint of the injured leg at landing. Compared to controls, ACL_R had larger external rotation of the injured leg at landing. ACL_PT showed less knee flexion and larger external rotation at take‐off and landing, and larger knee abduction at Landing. COM was more medial in relation to the knee at take‐off and less laterally placed relative to the ankle at landing. ACL injury results in long‐term kinematic alterations during OLH, which are less evident for ACL_R.