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PubMed2006

Epidemiology of non-dialysis-requiring chronic kidney disease and cardiovascular disease.

PURPOSE OF REVIEW: To review recent literature about the relationship between non-dialysis-requiring chronic kidney disease and cardiovascular disease as well as possible explanatory factors. RECENT FINDINGS: Reduced estimated glomerular filtration rate below 60 ml/min/1.73 m independently predicts the risk of death and cardiovascular events in persons with or without known cardiovascular disease as well as those undergoing coronary or peripheral arterial revascularization. This risk is not linearly associated with level of kidney function. Chronic kidney disease is associated with a larger burden of traditional vascular risk factors but is also linked to abnormalities in a variety of nontraditional pathways such as dysregulation of mineral metabolism and arterial calcification, vessel stiffness and endothelial dysfunction, insulin resistance, inflammation, malnutrition, and anemia, among others. Other novel kidney-specific proteins (e.g. renalase) may play direct mediating roles. The relative contribution of these factors to excess cardiovascular disease in chronic kidney disease remains unclear. SUMMARY: Recent evidence demonstrates the importance of non-dialysis-requiring chronic kidney disease as a potent predictor of cardiovascular disease and its complications. Randomized trials should be performed to determine whether modification of traditional and nontraditional risk factors can reduce incident cardiovascular disease as well as which interventions can optimize treatment outcomes in persons with chronic kidney disease and cardiovascular disease.

Cardiovascular Diseases↗

PubMed1994

Complex genetic disease: can genetic strategies in Alzheimer's disease and new genetic mechanisms be applied to epilepsy?

Strategies used in molecular genetics have changed modern neurology. The gene or genes responsible for several major neurologic diseases have now been identified using "reverse" or positional genetics. Unexpected new genetic mechanisms have been discovered in human neurologic diseases, including (a) identical mutations of the prion protein gene in Creutzfeldt-Jakob disease and fatal familial insomnia with the phenotypic expression directed by an accompanying polymorphism; (b) stable duplications of chromosome 17 in Charcot-Marie-Tooth disease (type 1A) that involve many genes, only one of which appears to cause neuropathy; and (c) highly variable, dynamic mutations in myotonic dystrophy, fragile X syndrome, and Kennedy's syndrome that modulate variable expressivity in multiple tissues. There is growing recognition that neurologic diseases are often complex genetic diseases with multifactorial rather than simple modes of inheritance. For example, genetic association/linkage strategies have interacted with biochemistry and immunopathology studies to produce new insights into the disease mechanism of late-onset Alzheimer's disease. The role of apolipoprotein E in late-onset Alzheimer's disease is an example of how new analytical techniques of genetic disease can be applied to dissect multiple genes. Similar research strategies are suggested for the study of epilepsy as a complex disease.

Alleles↗

PubMed2004

Is inflammatory bowel disease an independent and disease specific risk factor for thromboembolism?

BACKGROUND: Patients with inflammatory bowel disease (IBD) are thought to be at increased risk of venous thromboembolism (TE). However, the extent of this risk is not known. Furthermore, it is not known if this risk is specific for IBD or if it is shared by other chronic inflammatory diseases or other chronic bowel diseases. AIMS: To compare the risk of TE in patients with IBD, rheumatoid arthritis, and coeliac disease with matched control subjects. PATIENTS AND METHODS: Study subjects answered a questionnaire assessing the history of TE, any cases of which had to be confirmed radiologically. A total of 618 patients with IBD, 243 with rheumatoid arthritis, 207 with coeliac disease, and 707 control subjects were consecutively included. All three patient groups were compared with control subjects matched to the respective group by age and sex. RESULTS: Thirty eight IBD patients (6.2%) had suffered TE. This was significantly higher compared with the matched control population with only 10 cases reported (1.6%) (p<0.001; odds ratio (OR) 3.6 (95% confidence interval (CI) 1.7-7.8)). Five patients with rheumatoid arthritis (2.1%) had suffered TE compared with six subjects (2.5%) in the control population matched to patients with rheumatoid arthritis (NS; OR 0.7 (95% CI 0.2-2.9)). TE had occurred in two patients with coeliac disease (1%) compared with four subjects (1.9%) in the control population matched to the coeliac disease group (NS; OR 0.4 (95% CI 0.1-2.5)). In 60% of TE cases in the IBD group, at least one IBD specific factor (active disease, stenosis, fistula, abscess) was present at the time TE occurred. CONCLUSIONS: IBD is a risk factor for TE. It seems that TE is a specific feature of IBD as neither rheumatoid arthritis, another chronic inflammatory disease, nor coeliac disease, another chronic bowel disease, had an increased risk of TE.

Adult↗

PubMed1984

Respiratory manifestations of systemic disease. 3. Neurologic, skeletal, dermatologic, gynecologic, and gonadal diseases and disorders of pregnancy.

Many nonpulmonary diseases may present with respiratory manifestations or may involve the lungs later in the disease course. The mechanisms by which such involvement occurs are almost as diverse as the diseases themselves and include the following. Hematogenous spread of disease is one of the most common mechanisms of lung involvement, for example, lung involvement by metastatic malignant disease. Cytotoxic factors from another anatomic location may be deposited in the alveolar basement membranes and cause pulmonary damage, for example, pulmonary hemorrhage associated with Goodpasture's syndrome. The pulmonary vasculature may prominently manifest generalized disease, as frequently occurs in Wegener's granulomatosis. Toxins accumulated as a result of disease in another organ system may damage the alveolar capillaries and result in pulmonary edema, as can occur in patients with severe azotemia due to renal failure. Depletion of lung surfactant as a consequence of disease in another organ system may produce alveolar collapse and respiratory failure; a disease that can have this effect is acute pancreatitis. The lungs may be the first organs to exhibit, through unknown mechanisms, underlying systemic diseases such as the collagenoses. Humoral factors released in another anatomic site may cause pulmonary problems; for example, bronchospasm may develop in patients with carcinoid of the intestine as a result of serotonin released by the tumor. Injury to another organ system can produce lung damage by complex mechanisms; an excellent example is the occasional development of neurogenic pulmonary edema in patients with trauma to the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Diseases↗

PubMed2004

Clinical features of patients with Kawasaki disease whose parents had the same disease.

OBJECTIVE: To observe the clinical characteristics of patients with Kawasaki disease whose parent also had the same disorder. DESIGN: Cross-sectional study using the data from nationwide surveys of Kawasaki disease in Japan. SETTING: All hospitals with a bed capacity of 100 or more and pediatric departments in Japan. PATIENTS: All patients described on the 16th and 17th surveys covering the 4-year period from January 1, 1999, through December 31, 2002. MAIN OUTCOME MEASURES: We compared clinical details, including sibling case, recurrence, diagnosis, administration of intravenous immunoglobulin, and coronary abnormalities, between patients whose parents had Kawasaki disease and patients with no parental history of Kawasaki disease. We also observed age at onset and sex of affected parent-offspring pairs with Kawasaki disease confirmed by using the data of previous nationwide surveys. RESULTS: The odds for having sibling cases were significantly increased among patients whose parents also had Kawasaki disease (odds ratio, 6.94; 95% confidence interval, 2.77-17.38). Patients with parental Kawasaki disease were more likely to experience recurrent Kawasaki disease, receive additional administration of intravenous immunoglobulin, and experience coronary abnormalities at 1 month after onset. Among confirmed parent-offspring pairs with Kawasaki disease, the mean age at onset of offspring was younger than that of their parents (25.6 vs 41.8 months), despite the lack of statistical significance. CONCLUSIONS: Some cases of Kawasaki disease show familial susceptibility to the disorder. Family history, especially parental history of Kawasaki disease, may be an indicator of disease severity.

Child↗

PubMed2005

Efficacy of famotidine and omeprazole in healing symptoms of non-erosive gastro-oesophageal reflux disease: randomized-controlled study of gastro-oesophageal reflux disease.

BACKGROUND: The epidemiology and pathophysiology of non-erosive gastro-oesophageal reflux disease differs from erosive gastro-oesophageal reflux disease. There is a possibility that non-erosive gastro-oesophageal reflux disease treatment requires a different regimen/approach but it is not yet acknowledged. AIM: To investigate the efficacy of famotidine and omeprazole in the treatment of gastro-oesophageal reflux disease, especially non-erosive gastro-oesophageal reflux disease. PATIENTS AND METHODS: A randomized, open-label trial was conducted. Fifty-four gastro-oesophageal reflux disease patients were assigned to treatment with famotidine at a dosage of 20 mg twice daily; or omeprazole, 20 mg once daily, for a period of 8 weeks. The Short Form-36 Health Survey and Gastrointestinal Symptom Rating Scale administered at baseline and after 8 weeks of treatment as well as a symptom questionnaire were conducted daily. RESULTS: Short Form-36 revealed that gastro-oesophageal reflux disease has severe impact on health-related quality of life. Thirty-nine subjects (77%) were endoscopically diagnosed as non-erosive gastro-oesophageal reflux disease. The mean Gastrointestinal Symptom Rating Scale abdominal pain, and indigestion score of non-erosive gastro-oesophageal reflux disease significantly improved in famotidine-treated patients (P < 0.05), but not in the omeprazole. There was no significant change regarding improved heartburn symptoms of non-erosive gastro-oesophageal reflux disease between treatments in the daytime or night-time. CONCLUSION: Famotidine and omeprazole were both effective in improving symptoms of gastro-oesophageal reflux disease, particularly non-erosive gastro-oesophageal reflux disease.

Analysis of Variance↗

PubMed1991

Adult Still's disease: manifestations, disease course, and outcome in 62 patients.

Clinical and laboratory manifestations, disease course, outcome, and HLA associations were studied in an inception cohort of 62 subjects with adult Still's disease (ASD) from 5 Canadian universities. Twenty-eight patients (45%) were female and the median age at disease onset was 24 years. In general, the clinical features observed in our patients were identical to those in other published series. However, significantly higher frequencies of sore throat (92%), weight loss (76%), lymphadenopathy (74%), pleuritis (53%), pneumonitis (27%), and abdominal pain (48%) were noted in our patients compared to those in a recent literature review. Liver involvement with hepatomegaly (44%) or abnormal liver function tests (LFTs) (76%) was common and was responsible for the 2 deaths attributed to Still's disease in our series. Severe liver failure always occurred in conjunction with aspirin or NSAID therapy. Therefore, whether or not aspirin or other NSAIDs are used, we recommend close monitoring of LFTs in patients with ASD, especially early in the disease course. Laboratory manifestations were similar to those already reported. Leukocytosis (greater than or equal to 15,000/mm3) was present in 50 patients (81%), a normochromic, normocytic anemia (hemoglobin less than or equal to 10 g/dl) in 42 (68%), and an elevated ESR in all. The mean follow-up of the 62 patients was 70 months (range, 2-163). Twenty-one patients (34%) had a self-limited disease course, 15 (24%) an intermittent course, and 22 (36%) a chronic disease course. Four patients (6%) died, and 2 of these deaths were attributed to Still's disease. For those patients who experienced a recurrence of ASD, the flares were usually of shorter duration and milder in severity than the initial episode. No initiating factor for disease exacerbation was identified in our patients. Although 22 of 62 patients (36%) had a chronic disease course, 52 (90%) were in ARA Functional Class I, and only 4 and 2 patients were in ARA Functional Class II and III, respectively. Patients with Still's disease had higher scores than the controls on the Pain (P less than 0.01) and Physical Disability (P less than 0.05) subscales of Arthritis Impact Measurement Scales health status questionnaire. Joint radiographs performed at the follow-up evaluation disclosed typical carpometacarpal and intercarpal involvement in 16 of 39 patients. In our series, HLA-B17, B18, B35, and DR2 were significantly associated with ASD. Three significant predictors of an unfavorable outcome, either a chronic disease course or a longer time to clinical remission, were identified.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed2006

10-year follow-up of subclinical cardiovascular disease and risk of coronary heart disease in the Cardiovascular Health Study.

BACKGROUND: The incidence of coronary heart disease (CHD) is very high among individuals 65 years or older. METHODS: We evaluated the relationships between measurements of subclinical disease at baseline (1989-1990) and at the third-year follow-up examination (1992-1993) and subsequent incidence of cardiovascular disease and total mortality as of June 2001. Approximately 61% of the participants without clinical cardiovascular disease at baseline had subclinical disease based on our previously described criteria from the Cardiovascular Health Study. RESULTS: The incidence of CHD was substantially increased for participants with subclinical disease compared with those who had no subclinical disease: 30.5 per 1000 person-years with and 16.3 per 1000 person-years without for white individuals, and 31.2 per 1000 person-years with and 12.5 per 1000 person-years without for black individuals. The risk persisted over the entire follow-up period. Incidence rates were higher for men than for women with or without subclinical disease, but there was little difference in rates for black individuals and white individuals. CONCLUSIONS: In multivariable models, subclinical disease at baseline remained a significant predictor of CHD in both men and women; the hazard ratios (95% confidence intervals) of their relative risks were 1.64 (1.30-2.06) and 1.49 (1.21-1.84), respectively. The presence of subclinical disease substantially increased the risk of subsequent CHD for participants with hypertension, diabetes mellitus, or elevated C-reactive protein. In summary, subclinical disease is very prevalent among older individuals, is independently associated with risk of CHD even over a 10-year follow-up period, and substantially increases the risk of CHD among participants with hypertension or diabetes mellitus.

Aged↗

PubMed2004

Association of Crohn's disease and latent celiac disease: a case report and review of the literature.

BACKGROUND: Crohn's disease is a chronic inflammatory disease of the intestine potentially affecting all parts of the intestine with predilection sites in the terminal ileum and proximal colon. Its prevalence in Western Europe is 20-40/100,000 with equal affection of both sexes and familiar accumulation. Histopathologically, it is characterized by a discontinuous, segmental manifestation and implication of all intestinal layers. Celiac disease, on the other hand, is defined by histologically proven villous atrophy associated with hyperplasia of crypts, lymphocytic infiltration and clinical improvement after a gluten-free diet. CASE REPORT: We report the case of a 52-year-old man presenting with long-term diarrhea and loss of weight associated with Crohn's disease. After interventional therapy for an unstable coronary artery syndrome and medical therapy for hyperthyroidism, the diarrhea stopped only after maintaining a gluten-free diet. A latent form of celiac disease (clinical symptoms, improvement after gluten-free diet, detection of anti-gliadin IgA antibodies, negative histology) was diagnosed. CONCLUSION: To our knowledge, this is the first report on the association of Crohn's disease and the latent form of celiac disease in the same patient. Whereas in most cases, Crohn's disease develops secondary to a pre-existing celiac disease, in our patient, latent celiac disease was diagnosed years after the onset of and therapy for Crohn's disease.

Celiac Disease↗

PubMed1997

IgA nephropathy and thin basement membrane disease in association with Crohn disease.

There have been a wide variety of reported renal parenchymal diseases associated with inflammatory bowel disease, ranging from interstitial nephritis to amyloidosis to immune complex glomerulonephritis. Two pediatric cases of renal parenchymal pathology in association with Crohn disease are presented. The first is an 11-year-old child who presented with recurrent bouts of gross hematuria, biopsy-proven IgA nephropathy, and later developed Crohn disease 4 years after the initial presentation. Her renal function is normal with persistent isolated microscopic hematuria. The second case is that of a 9-year-old male who presented with the classic gastrointestinal manifestations of Crohn disease, later developed hematuria and proteinuria, and was found on a renal biopsy to have thin basement membrane disease. There have been several reported cases of IgA nephropathy associated with inflammatory bowel disease; but to our knowledge, this is the first case of thin basement membrane disease occurring in conjunction with Crohn disease. Discussion focuses on the relationship of IgA nephropathy with inflammatory bowel disease with additional comments on thin basement membrane disease.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1980

Von Hippel-Lindau disease simulating polycystic kidney disease.

Polycystic kidney disease and the renal manifestations of von Hippel-Lindau disease have much in common. Making the distinction between these two diseases is important. There is a strong association of renal cell carcinoma with von Hippel-Lindau disease, whereas renal cell carcinoma is rare in polycystic kidney disease. Furthermore, the many extrarenal manifestations of von Hippel-Lindau disease are serious and can be fatal while those of polycystic kidney disease are generally benign. Early diagnosis of the lesions of von Hippel-Lindau disease could lead to effective surgical treatment and prevent death. A case of von Hippel-Lindau disease is presented which was incorrectly diagnosed as polycystic kidney disease for sixteen years. The case is instructive in that the possibility of making the correct diagnosis prior to the patient's terminal illness was only through careful assessment of the family. The case is also remarkable in that the patient suffered from progressive renal failure requiring hemodialysis, which has not been associated previously with von Hippel-Lindau disease.

Adult↗

PubMed1998

Influence of risk factors on peripheral and cerebrovascular disease in men with coronary artery disease, low high-density lipoprotein cholesterol levels, and desirable low-density lipoprotein cholesterol levels. HIT Investigators. Department of Veterans Affairs HDL Intervention Trial.

BACKGROUND: The Veterans Administration-HDL Intervention Trial is an ongoing, 20-center, randomized, double-blind, placebo-controlled study aiming to assess the effect of gemfibrozil-improved low high-density lipoprotein cholesterol levels on cardiovascular morbidity and mortality rates. METHODS AND RESULTS: Eligible patients were men with low high-density lipoprotein cholesterol levels and demonstrable coronary heart disease. A total of 2531 patients (average age 63.5 years) were randomly assigned in this study, with a mean high-density lipoprotein cholesterol level of 0.83 mmol/L (32 mg/dL) and low-density lipoprotein cholesterol level of 2.87 mmol/L (111 mg/dL). Baseline data provided the opportunity to assess the interaction of several coronary heart disease risk factors and comorbid vascular diseases. Of these patients, 206 had diabetes mellitus (DM) alone, 1021 had hypertension (HTN) alone, 421 had both DM and HTN, and 883 had neither ("others"). Considering the influence of these risk factors on comorbidities independent of smoking status, patients with DM alone had a 2-fold increase in the prevalence of peripheral vascular disease and a 1.5-fold increase in congestive heart failure. Patients with HTN had a significant increase in the prevalence of cerebrovascular disease, stroke, and congestive heart failure. Patients with HTN and DM had a significant increase in all comorbidities. Smoking resulted in substantial increase of both peripheral vascular disease and cerebrovascular disease. Compared with nonsmoking patients with no DM or HTN, patients with DM and HTN and smoking had a 3-fold increase in the prevalence of peripheral vascular disease and a 3.5-fold increase in cerebrovascular disease (P < .001). CONCLUSIONS: We conclude that DM is a strong correlate of peripheral vascular disease, hypertension of cerebrovascular disease, and that there is a strong additive effect between DM, HTN, and smoking on both.

Aged↗

PubMed2002

Inflammatory bowel disease: developing a short disease specific scale to measure health related quality of life.

AIM: To report on the preliminary development of a short scale, the Edinburgh inflammatory bowel disease questionnaire (EIBDQ) to measure disease specific aspects of inflammatory bowel disease (IBD) in terms of both physical impact and health related quality of life (HRQoL) consequences. METHODS: A survey of individuals with Crohn's disease (n=50), ulcerative colitis (n=50) and psoriatic arthritis (n=28) was carried out using the EIBDQ. The data were subject to factor analysis in order to investigate underlying dimension of the EIBDQ which were then analysed for internal consistency. Data for disease specific aspects of the EIBDQ were compared between IBD patients and psoriatic arthritis patients using contingency tables and the underlying dimension of the EIBDQ were correlated with measures of quality of life and psychological morbidity and a disease specific measure. RESULTS: There are three underlying dimensions to the EIBDQ: a disease specific factor, a bowel specific factor and an information factor. The disease specific factor and the bowel specific factor are internally consistent and correlate with other measures of disease activity, quality of life and psychological morbidity. The EIBDQ is able to discriminate between IBD and another inflammatory disease: psoriatic arthritis. CONCLUSION: The EIBDQ is a reliable and valid instrument for measuring disease specific aspects of IBD but further development is required.

Arthritis, Psoriatic↗

PubMed2002

Prospective surveillance of acute serious liver disease unrelated to infectious, obstructive, or metabolic diseases: epidemiological and clinical features, and exposure to drugs.

BACKGROUND/AIMS: Acute serious liver disease which is unrelated to infectious, obstructive, or metabolic disease is uncommon. Many drugs have been implicated. Data on its epidemiology are scarce. We performed a population-based prospective study of acute serious liver disease in Catalonia (Spain). METHODS: A collaborating hospital network was set up. All patients with acute serious liver disease and negative viral hepatitis serological markers, without an obvious cause of liver disease, were included. RESULTS: The incidence of acute serious liver disease was 7.4 per 10(6) inhabitants per year (95% CI; 6.0-8.8), which increased with age. The incidence of hepatocellular acute serious liver disease (3.84 per 10(6) per year) was greater than that of cholestatic and mixed patterns. The case-fatality ratio was 11.9% and mortality 0.8 per million person-years. The risk of death was similar among patients with hepatocellular and cholestatic patterns. Non-steroidal antiinflammatory drugs, analgesics, and antibacterials were the most frequently used drugs. CONCLUSIONS: Acute serious liver disease which is unrelated to infectious, obstructive, or metabolic disease is rare. Its incidence increases with age. The prognosis of cholestatic acute serious liver disease does not significantly differ from that of the hepatocellular pattern. Non-steroidal antiinflammatory drugs, analgesics, and antibacterials were the most common drugs likely to be responsible for acute liver disease.

Acute Disease↗

PubMed1999

Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease.

Huntington's disease is an autosomal-dominant progressive neurodegenerative disorder resulting in specific neuronal loss and dysfunction in the striatum and cortex. The disease is universally fatal, with a mean survival following onset of 15-20 years and, at present, there is no effective treatment. The mutation in patients with Huntington's disease is an expanded CAG/polyglutamine repeat in huntingtin, a protein of unknown function with a relative molecular mass of 350,000 (M(r) 350K). The length of the CAG/polyglutamine repeat is inversely correlated with the age of disease onset. The molecular pathways mediating the neuropathology of Huntington's disease are poorly understood. Transgenic mice expressing exon 1 of the human huntingtin gene with an expanded CAG/polyglutamine repeat develop a progressive syndrome with many of the characteristics of human Huntington's disease. Here we demonstrate evidence of caspase-1 activation in the brains of mice and humans with the disease. In this transgenic mouse model of Huntington's disease, expression of a dominant-negative caspase-1 mutant extends survival and delays the appearance of neuronal inclusions, neurotransmitter receptor alterations and onset of symptoms, indicating that caspase-1 is important in the pathogenesis of the disease. In addition, we demonstrate that intracerebroventricular administration of a caspase inhibitor delays disease progression and mortality in the mouse model of Huntington's disease.

Animals↗

PubMed1996

Handicap in Darier's disease and Hailey-Hailey disease.

One hundred and thirty-seven patients with Darier's disease and 66 patients with Hailey-Hailey disease completed the Dermatology Life Quality Index (DLQI). The average DLQI score for Darier's disease was 5.89 (19.6% of the maximum score), median = 4, quartiles: 1.9. The average DLQI score for Hailey-Hailey disease was 6.06 (20.2% of the maximum score), median = 5, quartiles: 2.9. The DLQI score did not correlate with the physician's assessment of clinical severity in both diseases, thus emphasizing the importance of remembering the potential for handicap even in patients with disease that seems to be mild. The domains of the questionnaire with the highest mean scores in both diseases were for questions relating to symptoms and feelings. Domains relating to personal relationships and work obtained low mean scores even in severe disease. It is encouraging that most patients with Darier's disease and Hailey-Hailey disease maintain good relationships at work and home and seem to be able to adapt to their skin disease.

Adolescent↗

PubMed2005

Analysis of Barmah Forest virus disease activity in Queensland, Australia, 1993-2003: identification of a large, isolated outbreak of disease.

Barmah Forest virus (BFV) disease is the second most common mosquito-borne disease in Australia. Although the majority of notifications are received from Queensland, little is known about the distribution of the disease within the state, or the important mosquito vectors and nonhuman vertebrate hosts. We conducted a retrospective statistical analysis of the notifications received from Queensland residents from 1993 to 2003 to establish long-term local incidence rates and to identify disease outbreaks. In total, 4,544 notifications were received over the 10-yr period. Disease reporting peaked in autumn, although the peak transmission season encompassed both summer and autumn. Long-term standardized incidence rates for summer/autumn and winter/spring varied across the state, showing positive spatial autocorrelation in both 6-mo periods. Although 15 instances of increased disease activity were identified, only one major disease outbreak affecting eight contiguous local government areas was detected in summer/autumn 2002/2003. This outbreak contained 297 cases, 115 more than would be expected over this period. The factors important to this outbreak are unknown and require further investigation. Although the incidence rates for BFV disease are lower than Ross River virus disease, the most reported mosquito-borne disease in Australia, several factors indicate that this virus should be considered an important public health risk in Queensland. These include consistent endemic transmission, apparent underreporting of the disease, and the potential for outbreaks in major population centers.

Alphavirus Infections↗

PubMedDate not supplied

Alexander disease: Alzheimer disease of the developing brain?

Alexander disease is a leukodystrophy-like neurodegenerative disease that typically presents in infancy or childhood. The disease is essentially a sporadic condition, and there is no known genetic predisposition or metabolic abnormality. The hallmark of the disease is the diffuse accumulation of Rosenthal fibers (RF) throughout the central nervous system. Although an etiological relationship of the RF to disease pathogenesis has been suspected since the initial description of Alexander disease, such a relationship has not been confirmed. We previously identified a number of oxidative post-translational modifications, including advanced glycation end products and lipid peroxidation adducts, in intimate association with the RF of Alexander disease. Such oxidative protein damage provides a mechanism, through protein crosslinking, for insolubility and accumulation of RF. Notably, these findings show a striking parallel with the biochemical features of age-related neurodegenerative diseases such as Alzheimer disease. Therefore, Alexander disease and Alzheimer disease likely share a common pathogenesis, namely oxidative injury as a potential primary process in the etiology and pathogenesis.

Alzheimer Disease↗