Nasal inflammation and chronic ear disease in Australian Aboriginal children

Objective : Chronic middle ear disease is common in Aboriginal children, and may be linked to nasal inflammation and Eustachian tube dysfunction. The pattern of nasal inflammation is unknown. The study reported here was performed to define the role of allergy and infection in causing nasal inflammation in Aboriginal children with chronic middle ear disease.
Methodology : Thirty-one Aboriginal children aged between 3 and 7 years underwent clinical assessment, audiometry and allergy skin tests. Nasal swabs for bacterial culture and cytology were performed during the winter and again in spring to identify any seasonal variation. A randomized trial of nasal beclomethasone for 8 weeks was conducted in children with abnormal tympanometry to identify the effect of therapy upon nasal cytology.
Results : Twenty-six of the 31 children had abnormal tympanograms. Average hearing levels were reduced in nine children. Pathogenic organisms were isolated from most children: Streptococcus pneumoniae (82%), Haemophilus influenzae (79%), Moraxella catarrhalis (39%) and Staphylococcus aureus (29%). Eight of the 31 children (26%) were atopic. Nasal cytology disclosed a marked neutrophil infiltrate (80% of cells) during the winter, which fell significantly in spring to 52% of cells. Only two subjects had nasal eosinophilia of >10%. There was no effect of beclomethasone on nasal cytology.
Conclusions : Chronic ear disease in Aboriginal children is associated with nasal inflammation, neutrophil infiltration and the presence of bacteria. These features suggest respiratory infection as the main cause of chronic nasal inflammation in Aboriginal children with middle ear disease. There is a seasonal variation in the severity of the nasal infiltrate, consistent with increased infections during winter. Despite a high prevalence of atopy, allergic nasal disease was uncommon.     

Review article: nitroimidazole resistance in Helicobacter pylori

The efficacy of a nitroimidazole-containing regimen for the treatment of Helicobacter pylori infection is decreased by nitroimidazole resistance. Nitroimidazoles are meta- bolized by H. pylori by several nitro-reductases of which an oxygen-insensitive NADPH nitroreductase encoded by the rdxA gene is the most important. Null mutations in this gene are associated with resistance.
Susceptibility testing to nitroimidazoles may give variable results. This is not only related to the slow growth under specific conditions, but also to variability in the activity of the other nitroreductases and the ability to deactivate toxic metabolites of an NI and to repair DNA damage. Moreover, co-infections with resistant and susceptible bacteria are frequently found. The presence of nitroimidazole resistance is related to the previous use of this drug. The prevalence of resistance is rising and nowadays 10–50% of the isolates are resistant.
Resistance reduces the efficacy of a treatment regimen to a variable degree. This is related to efficacy of the other components of the regimen and the treatment duration. Whether a nitroimidazole is still effective in resistant strains remains unresolved.
When nitroimidazole resistance is present, a nitro-imidazole-containing regimen should be avoided or a regimen with other highly effective components should be used.     

The Nobel Prize in Physiology or Medicine for 2005 for the discovery of the stomach bacterium Helicobacter pylori

This year, the Nobel Prize in Physiology or Medicine was awarded to the Australian doctors Marshall and Warren for their discovery and further identification of the stomach bacterium Helicobacter pylori. Thanks to their confidence in their own observations, we are now able to cure people with peptic-ulcer disease and low-grade gastric lymphoma and are potentially able to prevent gastric cancer.     

Feasibility, safety, and efficacy of percutaneous transhepatic injection of beta-cell grafts

PURPOSE: To evaluate the safety, feasibility, and clinical efficacy of percutaneous transhepatic injection of beta-cell grafts in patients with type 1 diabetes mellitus. MATERIALS AND METHODS: Between December 2001 and November 2003, 15 patients with C-peptide-negative type 1 diabetes underwent 31 percutaneous injections for intraportal implantation of beta-cell grafts. Grafts consisted of cultured beta-cell preparations as previously described. In 13 cases, the transplant procedure was done under sedation, whereas in 18 cases, general anesthesia was given. In all procedures, percutaneous access to the right portal vein occurred under ultrasound (US) guidance with use of a microbore puncture needle. The subsequent catheterization of the main portal vein was performed under fluoroscopic and angiographic control with use of a microbore delivery catheter and guide wire. Clinical, biochemical, and radiologic evaluation was performed before and after the procedure. RESULTS: In all cases, it was possible to access the portal vein (median number of needle passes, 1; range, 1-6). The volume of cultured beta-cell grafts injected for each transplantation averaged 0.58 mL (range, 0.26-1.60 mL) and the mean recorded procedure time (from puncture to catheter withdrawal) was 19 minutes (range, 10-80 min). Three patients presented with transient abdominal pain immediately after the procedure; postprocedural duplex US of the liver revealed a patent portal vein and end branches in all cases and a minor perihepatic fluid collection in another three patients. From the end of week 1 to week 3, a mean 3.8-fold increase in liver aminotransferase levels was measured in all recipients after the first implantation session. A similar increase was seen in only one patient after a second transplantation session. At 6 months after transplantation, 13 of 15 patients (86%) had a functioning graft with plasma C-peptide levels greater than 0.5 ng/mL. CONCLUSIONS: The combined US, fluoroscopic, and angiographic monitoring of percutaneous transhepatic injection with use of a microbore delivery catheter is a safe and reproducible radiologic procedure for transplantation of beta-cell grafts in diabetic patients. Increased posttransplantation C-peptide levels, which demonstrate acceptable graft function, can be obtained.     

Unconscious Confusion

Abstract Background Imprecise definitions of syncope and related conditions appear common in the medical literature. To investigate the scope of the problem we systematically searched for definitions in high-ranking medical journals. Methods Literature review of articles on syncope, neurocardiogenic syncope, neurally mediated syncope, orthostatic intolerance, and orthostatic hypotension with these keywords in the title, mainly published in the ten journals with the highest impact in the fields of cardiology, internal medicine, and neurology. Results Syncope, neurocardiogenic syncope, neurally mediated syncope, orthostatic intolerance, and orthostatic hypotension were defined in only 41%, 34%, 26%, 38%, and 48% of papers respectively. Definitions, when given, differed considerably among papers. Orthostatic hypotension was most frequently defined, with an increase in number and consistency of definitions after publication of a consensus in 1996. Conclusions Syncope and related conditions proved to be infrequently and inconsistently defined in current medical literature. The lack of consistent terminology is likely to harm medical education, research, and patient care. There is a strong need for a systematic terminology for syncope and related conditions.     

The immunoneuroendocrine axis in critical illness: beneficial adaptation or neuroendocrine exhaustion?

PURPOSE OF REVIEW: Over the last years, endocrinology has been incorporated in critical care medicine, and acknowledgment of the complex neuro-endocrine adaption of critical illness has led to new insights and major breakthroughs in clarifying pathophysiological mechanisms and the targeting of therapeutic strategies. This review focuses on the important role of the hypothalamic-pituitary-adrenal (HPA) axis during critical illness and the occurrence of neuroendocrine failure. RECENT FINDINGS: The distinction between acute (activated anterior pituitary function and inactivated peripheral anabolic pathways) and prolonged (reduced neuroendocrine stimulation) critical illness as different neuroendocrine paradigms has brought a new approach to the critically ill patient. The HPA adaptation in the prolonged phase is characterized by hypercortisolism induced by non-ACTH driven pathways as ACTH levels are low. In spite of the high-normal (total) cortisol levels, HPA insufficiency appears to be quite common. On the other hand, there is a marked depletion of corticosteroid-binding globulin (CBG) in the acute phase of critical illness, resulting in increased free and biologically active cortisol. There is a persistent marked depletion of dehydroeplandrosterone sulfate, possibly indicating adrenal exhaustion, while macrophage inhibitory factor is upregulated in sepsis, affecting and contraregulating the biological effects of glucocorticoids. SUMMARY: The endocrine system is highly interrelated with the immune and neural systems, the neuroimmunoendocrine axis is subject to clear biphasic changes in the acute and chronic phases of critical illness, most likely reflecting a beneficial adaptation. These neuroendocrine dynamics should be considered when assessing the neuroendocrine system, in particular the HPA axis.     

Association of early CT abnormalities, infarct size, and apparent diffusion coefficient reduction in acute ischemic stroke

BACKGROUND AND PURPOSE: Diffusion-weighted (DW) imaging is more sensitive for early ischemia than CT, and apparent diffusion coefficient (ADC) mapping permits quantification of the severity of cytotoxic edema. We examined the relationship between early CT findings, ischemic lesion volume on DW images, and edema subtype. METHODS: Patients in whom early signs of ischemia were detected on baseline CT scans were scored CT positive. Baseline DW lesion volumes were compared between the CT-positive and CT-negative patients. In CT-positive patients, we outlined the CT-positive part of the DW lesion and transferred these regions of interest to the corresponding DW sections. The ADC values of the outlined CT-positive areas were then compared with the ADC values of the CT-negative areas within patients. Lesions with significantly increased T2 hyperintensity were excluded to correct for the effect of early vasogenic edema on ADC measurements. RESULTS: Twenty-four patients with cerebral ischemia in whom both CT and DW imaging were performed within 8 hours of symptom onset were entered into the study. Patients with early CT signs of infarction (n = 12) had significantly larger DW lesion volumes than did patients without early CT abnormalities (mean volume, 62.8 versus 14.6 mL; P =. 002). In patients displaying early CT abnormalities, CT-positive regions of the DW lesion had lower relative ADC (rADC) values than did the CT-negative regions, when lesions with significant T2 hyperintensity were excluded (mean rADC, 0.65 versus 0.75; P =.037). CONCLUSION: These findings support the hypothesis that early CT signs of infarction indicate more extensive and severe cerebral ischemia, as reflected by lower ADC.