Comparison of clinical and biologic features of Kingella kingae and Staphylococcus aureus arthritis at initial evaluation

We conducted a retrospective study comparing the presenting clinical and biologic features of 64 children who had septic arthritis caused by Kingella kingae with 26 children who had septic arthritis caused by Staphylococcus aureus. Children with K. kingae septic arthritis were significantly younger than those with S. aureus septic arthritis. Otherwise, there were no significant differences between the 2 groups with respect to fever, location, white blood cell count, synovial fluid cell count, C-reactive protein, or serum fibrinogen. However, the clinical course was significantly better for children with septic arthritis caused by K. kingae as evidenced by shorter hospitalization and fewer adverse events. Presumptive antibiotic therapy for septic arthritis in young infants should take into account both of these pathogens, even in case of mild presentation.     

Idiopathic juvenile osteoporosis: a new observation]

Idiopathic juvenile osteoporosis is a rare form of bone demineralization which occurs during childhood. The mechanism of disease remains unknown. We report a new case which illustrates the main difficulties of diagnosis and treatment. CASE REPORT: A 7 year old girl was admitted because of painful disability of her lower limbs. Diagnosis was based on radiological signs, total bone density and bone histologic pattern. Plasma levels of calcium, phosphorus, alkaline phosphatases, 25-OH D3 and parathormone were within the normal range value. Other diseases associated with bone demineralization, such as enteric malabsorption, endocrine or tumoral diseases, were excluded. Recovery occurred after some months of treatment with calcium, vitamin D and rehabilitation, but we could not establish a clear causal relationship. CONCLUSION: The relative role of increased bone resorption or defective osteoblast function remain to be discussed. Recovery often occurs with or without treatment, but sequelae can lead to disability.     

Detection of Hpdel among Thais, a deleted allele of the haptoglobin gene that causes congenital haptoglobin deficiency

BACKGROUND: Congenital haptoglobin deficiency is a risk factor for anaphylactic nonhemolytic transfusion reactions in Japan. The deleted allele of the haptoglobin gene, Hp(del), which causes congenital haptoglobin deficiency, has also been observed in other Northeast Asian populations, such as Korean and Chinese persons. It has not been reported in several African and European-African populations, however, or investigated in other countries. STUDY DESIGN AND METHODS: To investigate the distribution of congenital haptoglobin deficiency in Southeast Asian countries, blood samples collected from 200 randomly selected healthy Thai volunteers were analyzed for serum haptoglobin and the haptoglobin gene. Plasma haptoglobin concentration was measured to identify haptoglobin deficiency. Haptoglobin phenotyping was performed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by Western blotting. The presence of the Hp(del) allele was determined with genomic DNA by an Hp(del)-specific polymerase chain reaction (PCR) method. RESULTS: There were no haptoglobin-deficient subjects detected among the 200 Thais. Their haptoglobin phenotypes were as follows: Hp 1-1 in 10, Hp 2-1 in 81, and Hp 2-2 in 109. Six individuals heterozygous for Hp(del) were detected. The frequency of the Hp(del) allele was calculated to be 0.015. The prevalence of haptoglobin deficiency caused by Hp(del) homozygosity was estimated to be approximately 1 in 4000. CONCLUSION: Congenital haptoglobin deficiency caused by Hp(del) homozygosity is presumed to be present in Thailand as a risk factor for anaphylactic transfusion reactions with a frequency similar to that in Japan. The causative deleted allele of the haptoglobin gene, Hp(del), is distributed among Southeast Asian populations as well as among Northeast Asian populations.     

Subclavian-vertebral artery bifurcation stenting using drug-eluting stents: a report of two cases using different techniques

Endovascular treatment of vertebral artery stenosis and subclavian artery stenosis are low-risk procedures, but there are few reports of the best approach for subclavian-vertebral artery stenoses where there is an ostial stenosis of a vertebral artery that arises from a stenosed segment of the subclavian artery. This is a report of two cases with subclavian-vertebral artery stenosis that were treated with two different techniques. One-year follow up demonstrated widely patent stents. Also, to our knowledge, this is the first report of the use of the crush-stenting technique using drug-eluting stents in subclavian-vertebral artery bifurcation lesions.     

Cocaine-induced renal infarction: report of a case and review of the literature

Background

Cocaine abuse has been known to have detrimental effects on the cardiovascular system. Its toxicity has been associated with myocardial ischemia, cerebrovascular accidents and mesenteric ischemia. The pathophysiology of cocaine-related renal injury is multifactorial and involves renal hemodynamic changes, alterations in glomerular matrix synthesis, degradation and oxidative stress, and possibly induction of renal atherogenesis. Renal infarction as a result of cocaine exposure, however, is rarely reported in the literature.

Case presentation

A 48 year-old male presented with a four-day history of severe right flank pain following cocaine use. On presentation, he was tachycardic, febrile and had severe right costovertebral angle tenderness. He had significant proteinuria, leukocytosis and elevated serum creatinine and lactate dehydrogenase. Radiographic imaging studies as well as other screening tests for thromboembolic events, hypercoagulability states, collagen vascular diseases and lipid disorders were suggestive of Cocaine-Induced Renal Infarction (CIRI) by exclusion.

Conclusion

In a patient with a history of cocaine abuse presenting with fevers and flank pain suggestive of urinary tract infection or nephrolithiasis, cocaine-induced renal infarction must be considered in the differential diagnosis. In this article, we discuss the prior reported cases of CIRI and thoroughly review the literature available on this disorder. This is important for several reasons. First, it will allow us to discuss and elaborate on the mechanism of renal injury caused by cocaine. In addition, this review will demonstrate the importance of considering the diagnosis of CIRI in a patient with documented cocaine use and an atypical presentation of acute renal injury. Finally, we will emphasize the need for a consensus on optimal treatment of this disease, for which therapy is not yet standardized.     

Differences in Substrate Specificities for Cysteine Proteinases Used in Blood Group Serology, and the Use of Bromelain in a Two-Phase Inhibitor Technique

Because substrate specificities differ between proteolytic enzymes and because knowledge of the optimal enzyme activity levels is necessary in order to standardize procedures used in antibody screening, a study was made of the best common assay method for the routinely employed enzymes bromelain, papain and ficin. Casein degradation was found better suited to this purpose than azoalbumin. With standardization achieved, a useful two-phase bromelain inhibitor technique was devised using bromelain at 20 casein units of activity. This method improved upon the one-stage bromelain technique in terms of sensitivity, freedom from false positive reactions and it compared well with the two-phase papain inhibitor technique.     

Effects of smoking in patients treated with cardiac resynchronization therapy

Smoking is associated with increased morbidity and mortality in cardiac patients. However, data on the prognostic impact of smoking in heart failure (HF) patients on cardiac resynchronization therapy with defibrillator (CRT-D) are absent. We investigated the effects of smoking on all-cause mortality and on a composite endpoint (all-cause death/appropriate device therapy), appropriate and inappropriate device therapy, in 649 patients with HF who underwent CRT-D between January 2003 and October 2011 in 6 Centers (4 in Italy and 2 in USA). 68 patients were current smokers, 396 previous-smokers (patients who had smoked in the past but who had quit before the CRT-D implant), and 185 had never smoked. The risk of each endpoint by smoking status was evaluated with both Kaplan–Meier and Cox proportional-hazard analysis. After adjusting for age, left ventricular ejection fraction, QRS width and ischemic etiology, both current and previous smoking were independent predictors of all-cause death [HR = 5.07 (95 % CI 2.68–9.58), p < 0.001 and HR = 2.43 (95 % CI 1.38–4.29), p = 0.002, respectively) and of composite endpoint [HR = 1.63 (1.04–2.56); p = 0.033 and HR = 1.46 (1.04–2.04) p = 0.027]. In addition, current smokers had a significantly higher rate of inappropriate device therapy compared to never smokers [HR = 21.74 (4.53–104.25), p = 0.005]. Our study indicates that in patients with HF who received a CRT-D device, current and previous smoking increase the event rate per person-time of death and of appropriate and inappropriate ICD therapy more than other known negative prognostic factors such as age, left ventricular dysfunction, prolonged QRS duration and ischemic etiology.     

Comparison of anti-rheumatic effects of local RNAi-based therapy in collagen induced arthritis rats using various cytokine genes as molecular targets

RNA interference (RNAi) provides a powerful means of sequence-specific gene silencing. Several studies show that RNAi may provide promising strategies to treat human diseases by suppressing disease responsible genes in vivo. In locomotor diseases, the progression of collagen-induced arthritis (CIA) is suppressed by tumor necrosis factor-α (TNF-α)-specific small interfering RNA (siRNA) delivered into the joint. The aim of this study, is to compare the effects of intraarticularly administered siRNAs targeting TNF-α, interleukin-1β (IL-1β), interleukin-6 (IL-6) and receptor activator of NF-κB ligand (RANKL) on CIA in rats. We confirmed that the silencing effects of siRNA duplexes specific for rat TNF-α, IL-1β, IL-6 and RANKL in vitro. Each siRNA was also delivered into the knee joint of CIA rats by the in vivo electroporation method 7, 10, 13 and 16 days after immunization with collagen. Local delivery of TNF-α or IL-1β-specific siRNA ameliorated CIA in rats effectively at the gross morphological, radiographical and histological evaluations. Our results suggested that TNF-α and IL-1β were the cytokines to be targeted in the joint for the treatment of rheumatoid arthritis. The in vivo siRNA transfection method may be useful for selection of target molecules to be silenced for treatment of joint diseases.     

Hsp70 prevents nitric oxide–induced apoptosis in articular chondrocytes

Objective

To deliver and overexpress the hsp70 gene in cultured chondrocytes to investigate its effect on nitric oxide (NO)–induced apoptosis of chondrocytes.

Methods

Primary chondrocyte cultures were established from rabbit joints. The cells were transduced with an empty adenovirus vector (Ax1w) or an adenovirus vector harboring the hsp70 E‐tag fusion gene (AxSHEwt). Apoptosis was induced by sodium nitroprusside (SNP) dihydrate, which generates NO, or by staurosporine, which is a proapoptotic agent dependent upon Bax or Bak protein. Cell viability and apoptosis induction were estimated by lactate dehydrogenase (LDH) assay, Hoechst 33342 staining, or the TUNEL method. To study Hsp70, cytochrome c, and caspase 3, Western blot analyses were performed.

Results

The AxSHEwt‐transduced cells escaped apoptosis, as revealed by the LDH assay, Hoechst 33342 staining, and the TUNEL method. A massive amount of the tagged Hsp70 was demonstrated in the AxSHEwt‐transduced chondrocytes but not in control cells. Hsp70 did not affect the cytosolic cytochrome c level, but appeared to have obstructed the activation of caspase 3.

Conclusion

Experimentally overexpressed Hsp70 almost completely inhibited NO‐ or staurosporine‐induced apoptosis in primary chondrocytes.