Prevalence of early stages of chronic kidney disease in healthy army personnel

Introduction: Chronic kidney disease (CKD) is associated with significant morbidity and mortality. Screening and detection of early stages of CKD can help institute interventions that may delay the progression of the disease. One aim was to study the prevalence of early stages of CKD in the Army.Methods: A cross-sectional study ofArmy Personnel in an Army cantt in Central India was carried out. All participants filled a structured questionnaire and anthropometric data was collected. Investigative profile included routine urine exam, semi-quantitative microalbuminuria (MAU), serum creatinine, lipid profile and fasting blood glucose. Glomerular Filteration rate (eGFR) was calculated using the Modification of Diet in Renal Diseases (MDRD) study equation.Result: A total of 1920 subjects were examined with 731 (38.07%) from Arms and 1189 (6I.93%) from Services. 348 were excluded and of the remaining 1572 subjects, 141 (8.97%) had MAU and 157 (9.99%) had deranged Albumin Creatinine Ratio (ACR). Mean eGFR by MDRD equation was 102 ± 25.84 ml/min/1.73m². Early CKD was seen in 150 (9.54%) with 84 (5.34%) in stage I CKD, 55 (3.5%) in stage II and 11 (0.7%) in stage III. Multiple logistic regression showed BMI > 23, the presence of DM and HTN were independent risk factors for CKD.Conclusion: 9.54 % of healthy army personnel were found to have early stages of CKD. Institution of screening programs can result in early detection of CKD.     

Characterization of antibody and selection of alternative drug therapy in hydrochlorothiazide-induced immune hemolytic anemia

The authors report the clinical and laboratory findings of a patient who had severe immune hemolytic anemia due to hydrochlorothiazide (HCTZ). In this case, the HCTZ antibody reacted not only with other thiazide and thiazide-like drugs, but also with a chemically unrelated diuretic, ethacrynic acid. These results indicate that HCTZ antibody activity is not restricted solely to the thiazides and imply that therapy with any of the reactive drugs would be contraindicated for this patient. The serologic screening for drug reactivity may be useful for selecting alternative therapy for patients with drug-induced immune hemolytic anemia.     

Protein C, an antithrombotic protein, is reduced in hospitalized patients with intravascular coagulation

Activated protein C is a potent anticoagulant and profibrinolytic enzyme that can be derived from the vitamin-K-dependent serine protease zymogen, protein C, by the action of thrombin. Protein C antigen concentration was determined in plasmas from normals (n = 40) and from 38 patients with intravascular coagulation as evidenced by positive FDP (greater than micrograms/ml). Plasma protein C was 4 micrograms/ml in normals and was significantly depressed (less than 2 SD below the mean of normals) in 19 of the 38 patients. Of 15 patients with suspected intravascular coagulation but normal FDP, protein C was decreased in 5 individuals; 3 of these 5 patients had liver disease. Based on these results, we suggest that extensive activation of the coagulation system in vivo causes a significant consumption of protein C, presumably due to its activation by thrombin and subsequent clearance.     

Treatment of refractory adult lymphoblastic leukemia (ALL) with 4'(9- acridinylamino) methanesulfon-M-anisidide (AMSA)

Twenty-four adults with ALL were treated with AMSA alone or in combination. Twenty-two were treated at time of relapse and two patients after failing primary induction therapy. All had been treated with anthracyclines prior to receiving AMSA. Of the 22 patients with ALL in relapse, 4 achieved a complete remission. Two of these patients have relapsed while receiving maintenance chemotherapy; one died 1 mo after achieving remission due to the occurrence of cholycystitis in the setting of pancytopenia and one patient underwent bone marrow transplantation and is in remission at 8 mo after the second remission. Both patients who failed primary induction therapy remain in remission at 11 and 36 mo, respectively. The use of AMSA should be considered for patients with ALL who fail primary induction as well as those whose leukemia becomes resistant to conventional agents.     

A new variant of type II von Willebrand disease with aberrant multimeric structure of plasma but not platelet von Willebrand factor (type IIF)

A patient with a lifelong bleeding disorder was diagnosed as having Type II von Willebrand disease. The larger multimers of von Willebrand factor were absent from her plasma but present in platelets. A high- resolution electrophoretic technique was used to study the complex structure of individual von Willebrand factor multimers. In normal plasma, each multimer could be resolved into five bands: a more intense central one and four less intense, two moving faster and two slower than the central band. In normal platelets, each multimer could also be resolved into five bands. The central one had a mobility similar to that in plasma, whereas the four satellite bands had a mobility that differed from that of the corresponding plasma bands. In the patient, platelet von Willebrand factor antigen content and ristocetin cofactor activity were normal, and von Willebrand factor showed the same structure of individual multimers as seen in normal platelets. On the other hand, plasma von Willebrand factor antigen and ristocetin cofactor activity were decreased, and the structure of individual von Willebrand factor multimers was different from that of normal plasma and similar to that seen in normal and patient's platelets. After infusion of 1-deamino-8-D-arginine vasopressin, the largest von Willebrand factor multimers, as well as new satellite bands with a mobility similar to those in normal plasma, appeared in the patient plasma, and the levels of von Willebrand factor antigen and ristocetin cofactor activity became normal. Yet no relevant change in the prolonged bleeding time was observed. This new variant of von Willebrand disease, therefore, is characterized by the presence of a dysfunctional von Willebrand factor molecule that exhibits unique structural abnormalities in plasma but appears to be normal in platelets. The designation of Type IIF is proposed for this type of von Willebrand disease in accordance with the terminology that has been previously used.     

von Willebrand disease "Vicenza" with larger-than-normal (supranormal) von Willebrand factor multimers

When normal volunteers or patients with type I von Willebrand disease (VWD) are given desmopressin (DDAVP), a set of larger-than-normal (supranormal) von Willebrand factor (VWF) multimers, similar to those present in VWF-containing cells such as platelets megakaryocytes and endothelial cells, appear transiently in postinfusion plasma. In two kindreds with mild lifelong bleeding symptoms transmitted as an autosomal dominant trait, all ten symptomatic members (but none of the five asymptomatic members) had a supranormal multimeric structure for plasma VWF, apparently identical to that seen for postdesmopressin normal plasma. Plasma factor VIII coagulant activity (VIII:C), VWF antigen (VWF:Ag), ristocetin-induced platelet agglutination, and ristocetin cofactor (RiCof) activity were low. Platelet VWF:Ag and RiCof levels (tested for three patients only) were normal. Bleeding times were normal or slightly prolonged. The patients' platelet multimeric structure was the same as that for normal platelets. After desmopressin infusion the plasma VWF multimeric structure remained supranormal as for preinfusion plasma, with VIII:C VWF:Ag and RiCof increasing markedly over baseline values and disappearing at a normal rate. Examination of the VWF subunit composition from three of these patients indicated that proteolytic processing of their VWF did not differ from normal. This study describes the first variant of VWD with a supranormal multimeric structure.     

NEONATAL OUTCOME IN MECONIUM STAINED DELIVERIES — A PROSPECTIVE STUDY

This prospective study analyzes the neonatal outcome in deliveries complicated by meconium stained amniotic fluid. In a study of 1000 live born deliveries, meconium staining of amniotic fluid was seen in 50 (5%) deliveries. Out of these, 20 newborns (40%) developed classical signs of meconium aspiration syndrome and were managed according to a predetermined protocol. Multiparity, term deliveries, use of sedatives in mother, intrauterine growth retardation and prolonged labour were some of the risk factors for development of meconium aspiration syndrome in newborns. This study highlights the need for review of management protocol in newborns after meconium staining of the amniotic fluid, including the use of prophylactic antibiotics.KEY WORDS: Amniotic fluid, Delivery, Meconium aspiration, Respiratory distress syndrome     

富碘中药海藻对甲状腺细胞凋亡及凋亡调控基因的影响

目的:通过观察富碘中药海藻对碘缺乏机体甲状腺滤泡上皮细胞凋亡,Fas,FasL,Bcl-2蛋白表达的影响,分析富碘中药过量对甲状腺损伤的机制。方法:实验于2006-03/09在辽宁中医药大学实验中心完成。①实验干预:选用健康鼠龄4周的Wistar大鼠150只。取120只喂低碘饲料建立缺碘大鼠模型,随机分为4组,每组30只:单纯高碘组喂含碘2000μg/L的双蒸水;模型组喂等体积双蒸水;常规剂量海藻组和3倍剂量海藻组分别灌胃海藻生药量13.5g/(kg·d)和40.5g/(kg·d)。以其余30只大鼠为正常对照组:正常饮食,每日灌服等体积双蒸水。②实验评估:分别在给药0,7,28d后取材。采用脱氧核糖核苷酸末端转移酶介导原位缺口末端标记确定甲状腺滤泡上皮细胞凋亡细胞数。采用免疫组化方法观察甲状腺滤泡上皮细胞Fas,FasL,bcl-2表达。结果:大鼠150只均进入结果分析。①凋亡细胞数:给药后7d,常规剂量海藻组和3倍剂量海藻组低于模型组,差异有非常显著性意义(P<0.01)。常规剂量海藻组和3倍剂量海藻组低于单纯高碘组,差异有显著性意义(P<0.05)。给药后28d,正常对照组甲状腺滤泡上皮细胞凋亡细胞数低于其他4组,差异有显著性或非常显著性意义(P<0.05～0.01)。常规剂量海藻组高于单纯高碘组,差异有显著性意义(P<0.05)。②Fas,FasL,Bcl-2蛋白表达:给药7d后,常规剂量海藻组和3倍剂量海藻组Fas蛋白的表达低于模型组,差异有显著性意义(P<0.05)。单纯高碘组和3倍剂量海藻组FasL表达低于模型组,差异有显著性意义(P<0.05)。常规剂量海藻组Bcl-2蛋白表达高于模型组,差异有显著性意义(P<0.05)。给药28d后,单纯高碘组和3倍剂量海藻组Fas蛋白的表达低于模型组,差异有显著性意义(P<0.05)。单纯高碘组、常规剂量海藻组和3倍剂量海藻组Bcl-2蛋白表达高于模型组,差异有显著性意义(P<0.05)。结论:富碘中药海藻给药28d可造成碘缺乏大鼠甲状腺细胞损伤,Fas,FasL,bcl-2可能参与诱导细胞凋亡。