Tumor diagnosis preceding Alzheimer's disease onset: is there a link between cancer and Alzheimer's disease?

Studies reporting an inverse association between Alzheimer's disease (AD) and cancer are scant. Available data are mostly based on ancillary findings of mortality data or obtained from studies evaluating frequency of neoplasms in AD patients independently if they occurred before or after AD. Moreover, some studies estimated frequencies of neoplasms in demented individuals, who were not necessarily AD patients. We estimated frequency of tumors preceding the onset of AD in AD patients and compared it to that of age- and gender-matched AD-free individuals. Occurrence of tumors preceding AD onset was assessed through a semi-structured questionnaire. Tumors were categorized as benign, malignant, or of uncertain classification and as endocrine-related or not. Odds ratios (OR), used as measure of the association between the two diseases, were adjusted for tumor categories and known risk factors for AD and tumors. We included 126 AD patients and 252 matched controls. Tumor frequency before AD onset was 18.2% among cases and 24.2% among controls. There was a suggestive trend of an overall inverse association between the two diseases (adjusted OR 0.6; 95% CI 0.4-1.1; p = 0.11). Risk for neoplasms was significantly reduced only for women (adjusted OR, 0.5; 95% CI 0.3-0.9; p = 0.03) and for endocrine related tumors (adjusted OR, 0.5; 95% CI 0.2-1; p = 0.04). Our study confirms the inverse association reported in previous epidemiological studies. Though our findings might be explained by processes playing an opposite role in tumors development and neurodegeneration, they are also suggestive for a possible role of estrogen.     

A family history of Parkinson's disease and its effect on other PD risk factors.

Parkinson's disease (PD) is likely a result of both inherited and exogenous factors. In a study of 144 PD cases and 464 controls, we used PD family history as a surrogate for inherited PD susceptibility. Cases were more likely to report a first- or second-degree relative with PD: 16.0 vs. 4.3%; odds ratio (OR) = 4. 2; 95% confidence interval (CI) = 2.3-7.6. A PD family history was a greater risk factor for PD in subjects under age 70 (OR = 8.8; 95% CI = 3.4-22.8) compared with those over 70 (OR = 2.8; 95% CI = 1.3-6. 1) and in men (OR = 8.1; 95% CI = 3.4-19.2) compared with women (OR = 2.6; 95% CI = 1.1-6.0). We also tested whether a PD family history modified the effects of other PD risk factors. In subjects with a PD family history, occupational exposure to copper, lead or iron increased the risk for PD (OR = 3.0; 95% CI = 0.7-13.3), but this was not the case for those without a family history (OR = 1.1; 95% CI = 0.7-1.6). Ever smoking cigarettes was inversely associated with PD in those without a PD family history (OR = 0.6; 95% CI = 0.4-0.9), but was positively associated with PD in those with a PD family history (OR = 1.7; 95% CI = 0.5-5.9). In summary, our results suggest that a PD family history, and perhaps, therefore, an inherited susceptibility, confers a greater risk for PD in men and individuals under 70 years of age and may modify the effects of environmental risk factors for PD.     

Do risk factors for Alzheimer's disease predict dementia in Parkinson's disease? An exploratory study

The extent to which concomitant Alzheimer's disease (AD) is etiologically related to the development of dementia in Parkinson's disease (PD) remains controversial. We explored the association of four risk factors associated with AD, including head injury, smoking, hypertension, and diabetes mellitus, with incident dementia in PD. A cohort of 180 nondemented PD patients from the Washington Heights community in northern Manhattan, New York, completed a risk factor questionnaire at baseline and was followed annually with neurological and neuropsychological evaluations. The association of baseline variables with incident dementia was analyzed by using Cox proportional hazards models. All analyses controlled for age at baseline, gender, years of education, duration of PD, and total Unified Parkinson's Disease Rating Scale (UPDRS) motor score at baseline. Of 180 patients (mean age, 71.0 +/- 10.3 years), 52 (29%) became demented during a mean follow-up period of 3.6 +/- 2.2 years. Head injury risk ratio ([RR] 0.9; 95% confidence interval [CI], 0.4-2.2; P = 0.9), hypertension (RR, 0.7; 95% CI, 0.4-1.4, P = 0.3), and diabetes mellitus (RR, 0.8; 95% CI, 0.3-2.3; P = 0.7) were not significantly associated with incident dementia in the Cox models. Patients who reported having ever smoked were at increased risk for the development of dementia compared with nonsmokers (RR, 2.0; 95% CI, 1.0-3.9; P = 0.05). Current smoking was significantly associated with incident dementia (RR, 4.5; 95% CI, 1.2-16.4; P = 0.02), whereas past smoking approached significance (RR, 1.9; 95% CI, 0.9-3.7; P = 0.07). Although an inverse association between smoking and PD has been reported in several studies, our study showed a positive association between smoking and dementia in the setting of PD. The association of smoking with incident dementia in PD deserves further study.     

Ten-year follow-up of Parkinson's disease patients randomized to initial therapy with ropinirole or levodopa.

In a 5-year, double-blind study, subjects with Parkinson's disease (PD) who were randomized to initial treatment with ropinirole had a significantly lower incidence of dyskinesia compared with subjects randomized to levodopa, although Unified Parkinson's Disease Rating Scale (UPDRS) motor scores were significantly more improved in the levodopa group. Subjects who completed the original study were eligible to participate in a long-term extension study conducted according to an open, naturalistic design and were evaluated approximately every 6 months until they had been followed for a total of 10 years. Comparing subjects randomized to initial treatment with ropinirole (n = 42) and levodopa (n = 27), the incidence of dyskinesia was significantly lower in the ropinirole group (adjusted odds ratio [OR] = 0.3; 95% confidence interval [CI]: 0.1, 1.0; P = 0.046) and the median time to dyskinesia was significantly longer (adjusted hazard ratio = 0.4; 95% CI: 0.2, 0.8; P = 0.007). The incidence of at least moderate wearing off ("off" time >/=26% of the awake day) was also significantly lower in the ropinirole group (adjusted OR = 0.3; 95% CI: 0.09, 0.03; P = 0.03). There were no significant differences in change in UPDRS activities of daily living or motor scores, or scores for the 39-item PD questionnaire, Clinical Global Impression, or the Epworth Sleepiness Scale. Early treatment decisions for individual patients depend largely on the anticipated risk of side effects and long-term complications. Both ropinirole and levodopa are viable treatment options in early PD.     

Haemostatic genetic variants,ABO blood group and bleeding risk during oral anticoagulant treatment after cerebral ischaemia of arterial origin

Oral anticoagulant treatment for secondary prevention after cerebral ischaemia of presumed arterial origin is associated with a higher bleeding rate than cardioembolic stroke. This discrepancy is only partly explained by known bleeding risk factors. Haemostatic genetic variants and AB0 blood group may be involved.We performed a nested casecontrol study in patients with cerebral ischaemia of presumed arterial origin on anticoagulant treatment (International Normalized Ratio between 3.0-4.5). All 34 cases with non-fatal haemorrhage (10 intracranial and 24 extracranial) and 68 control patients on anticoagulant treatment without such a bleeding were selected from the SPIRIT study. AB0 blood group and 11 haemostatic genetic variants were investigated.The Thr312Ala variant of the alpha fibrinogen gene was associated with a decreased bleeding risk (odds ratio (OR) 0.3 for Ala/Ala and Thr/Ala versus Thr/Thr genotype; 95% CI 0.1-0.8). Factor V Leiden was associated with an increased bleeding risk (OR 11.6; 95% CI 1.3-103). The APOE2 allele (OR 0.5; 95% CI 0.2-1.7) and the Tyr204Phe variant in the factor XIII subunit A (OR 2.1; 0.9-5) had nonsignificant relationships with bleeding risk. AB0 blood group and 7 other genetic variants in coagulation factors II and XIII, vitamin K epoxide reductase complex, beta fibrinogen and apolipoprotein E were not related with the risk of haemorrhage.The Ala312Thr variant in the alpha fibrinogen gene is associated with a decreased and factor V Leiden with an increased bleeding risk in patients on anticoagulant treatment after cerebral ischaemia of presumed arterial origin.     

Psychostimulant treatment and risk for substance abuse among young adults with a history of attention-deficit/hyperactivity disorder: a population-based, birth cohort study

OBJECTIVE: The aim of this study was to evaluate the association between stimulant treatment and the risk for substance abuse among young adults with a childhood diagnosis of attention- deficit/hyperactivity disorder (ADHD). METHODS: Subjects included 295 research-identified ADHD incidence cases treated with psychostimulant medication and 84 ADHD cases not treated with psychostimulants. These subjects are from a 1976-1982 population-based birth cohort, retrospectively, followed from birth until emigration, death, or last follow-up (mean = 17.2 years of follow-up). Medical and school records were reviewed for documented substance abuse and psychostimulant treatment. The association was evaluated using logistic regression models. RESULTS: Socioeconomic characteristics at birth, and comorbidities, were similar between treated and untreated ADHD cases. Sixty (20.3%) of treated ADHD cases had documented substance abuse compared to 23 (27.4%) of cases not treated (OR = 0.7; 95% CI = 0.4-1.2). Among treated ADHD boys, 21.8% had substance abuse compared to 36.4% not-treated ADHD boys (OR = 0.5; 95% CI = 0.3-0.9). Among treated ADHD girls, 15.2% had substance abuse compared to 10.3% not-treated ADHD girls (OR = 1.5; 95% CI = 0.4-6.1). CONCLUSION: While these results cannot demonstrate cause and effect, our findings indicate that psychostimulant treatment of childhood ADHD is associated with reduced risk for later substance abuse among boys with ADHD.     

Familial and environmental risk factors in Parkinson's disease: a case-control study in north-east Italy

BACKGROUND AND OBJECTIVE: The aetiology of Parkinson's disease remains unknown, although both genetic susceptibility and environmental factors are considered putative contributors to its origin. We performed a case-control study to investigate the association of familial and environmental risk factors with Parkinson's disease (PD). METHODS: We studied 136 patients with neurologist confirmed PD and 272 age- and sex-matched controls, affected by neurological diseases not related to PD. The risk of developing idiopathic PD associated with the following familial and environmental factors: positive family history of PD, positive family history of essential tremor (ET), age of mother at subject's birth, rural birth, rural living, well water use, farming as an occupation, exposure to pesticides, head tremor, exposure to general anaesthesia and to ionizing radiations, food restriction, concentration camp imprisonment and smoking has been assessed by using univariate and multivariate statistical techniques. RESULTS: In the conditional multiple logistic regression analysis, positive family history of PD (OR 41.7, 95% CI 12.2-142.5, P < 0.0001), positive family history of ET (OR 10.8, 95% CI 2.6-43.7, P < 0.0001), age of mother at subject's birth (OR 2.6, 95% CI 1.4-3.7, P=0.0013), exposure to general anaesthesia (OR 2.2, 95% CI 1.3-3.8, P=0.0024), farming as an occupation (OR 7.7, 95% CI 1.4-44.1, P=0.0212) and well water use (OR 2.0, 95% CI 1.1-3.6, P=0.0308) exhibited a significant positive association with PD, whereas smoking showed a trend toward an inverse relationship with PD (OR 0.7, 95% CI 0.4-1.1, P < 0.06). CONCLUSIONS: We conclude that both familial and environmental factors may contribute to PD aetiology.     

A case-control study on cigarette,alcohol, and coffee consumption preceding Parkinson's disease

OBJECTIVE: To investigate the association between cigarette smoking, alcohol drinking, coffee consumption and Parkinson's disease (PD). METHODS: We selected subjects affected by idiopathic PD, with a Mini-Mental State Examination of > or =24, and controls matched 1 to 1 with cases by age (+/- 2 years) and sex. Controls were randomly selected from the resident list of the same municipality of residence of the cases. We assessed cigarette smoking, alcohol drinking, and coffee consumption preceding the onset of PD or the corresponding time for controls using a structured questionnaire, which also evaluated the duration and dose of exposure. Using conditional logistic regression analysis, we calculated adjusted OR and 95% CI. RESULTS: We interviewed 150 PD patients and 150 matched controls. Cigarette smoking (ever vs. never smokers OR = 0.66, 95% CI = 0.41-1.05, p = 0.08) did not show a statistically significant association with PD. We observed an inverse association between alcohol drinking (ever vs. never OR = 0.61, 95% CI = 0.39-0.97, p = 0.037) and coffee consumption (ever vs. never OR = 0.16, 95% CI 0.05-0.46, p = 0.0001) and PD. These associations remained significant after adjustment for other covariates: OR for ever vs. never alcohol consumption was 0.62 (95% CI = 0.43-0.89, p = 0.009) and that for coffee drinking 0.19 (95% CI = 0.07-0.52, p = 0.001). Heavy coffee consumption confirmed the inverse association between coffee and PD (more than 81 cup/year vs. none: OR = 0.20, 95% CI = 0.08-0.47, p < or = 0.0001). CONCLUSIONS: Consistent with previous studies, our results suggest an inverse association between coffee drinking, alcohol consumption and PD. The multiple inverse association observed may indicate a complex interaction between genetic and environmental factors.     

Cancer incidence among people with intellectual disability

The aim of the present study was to address the unresolved question of the risk of neoplasms among people with intellectual disability (ID). A total of 2173 individuals with ID from a large, representative, nation‐wide population study conducted in Finland in 1962 were followed‐up for cancer incidence between 1967 and 1997. Standardized incidence ratios (SIRs) were defined as ratios of observed to expected numbers of cancer cases. Expected rates were based on national incidence rates. The observed number of cancers in the cohort (173) was close to what was expected [SIR = 0.9, 95% confidence interval (95% CI) = 0.8–1.0]. There was a significantly reduced risk of cancers of the prostate (SIR = 0.2, 95% CI = 0.0–0.5), urinary tract (SIR = 0.3, 95% CI = 0.1–0.7) and lung (SIR = 0.6, 95% CI = 0.4–1.0). The risk was increased in cancers of the gallbladder (SIR = 2.8, 95% CI = 1.1–5.8) and thyroid gland (SIR = 2.1, 95% CI = 1.0–4.8). The risks of lung and gallbladder cancer were lowest and highest, respectively, in those subjects with profound and severe ID, a group who also had significantly elevated SIRs for brain cancer (SIR = 3.46, 95% CI = 1.5–14.4) and testicular cancer (SIR = 9.9, 95% CI = 1.2–35.6). The incidence of cancer among people with ID was comparable with the general population, despite their low prevalence of smoking and apparently decreased diagnostic screening activity. Nevertheless, a few types of cancer carry a higher risk in the population with ID, possibly because of conditions typical among this group, such as gallstones or oesophageal reflux.     

Prevalence of headache in patients with Parkinson’s disease and its association with the side of motor symptom onset

We compared the lifetime prevalence and the prevalence of headache during the previous year in patients with Parkinson’s disease (PD) and control subjects. We also investigated the association between the side of PD symptom onset and the side of the headache. We interviewed 98 consecutive patients with an established diagnosis of PD between December 2010 and January 2012. The control group consisted of the 98 oldest sex-matched individuals from the nationwide Brazilian headache database. PD patients showed a significantly lower prevalence (40.8 %) of headache in the previous year than controls (69.4 %) (adjusted OR 0.5, CI 95 % 0.2–0.9, p = 0.03). PD patients also showed a lower prevalence of headache throughout life (74.5 %) than controls (93.9 %) (adjusted OR 0.2, CI 95 % 0.1–0.6, p = 0.01). Considering only patients who presented headache during the previous year, PD patients showed a higher association with occurrence of migraine than tension-type headache compared with controls (adjusted OR 3.3, CI 95 % 1.2–8.9, p = 0.02). The headache side was ipsilateral to the side of PD onset in 21 patients (84 %), with a concordance of 85.7 % on the left side and 81.8 % on the right side (p < 0.01). The prevalence of primary headache was significantly lower in patients with PD than controls. The predominant side of headache was ipsilateral to the side of initial motor signs of PD.     

Cancer risk in association with Parkinson disease: A population-based study

PurposeData from large population-based studies on the association between Parkinson disease (PD) and the risk of developing cancer are scarce. We compared the risk of developing incident cancer between patients with or without PD.MethodsWe conducted a population-based follow-up study and a nested case-control analysis using data from the UK-based General Practice Research Database. We included PD patients aged ≥40 years with a first PD diagnosis between 1994 and 2005, and a matched comparison group free of PD. We assessed cancer incidence rates and relative risk estimates (odds ratios [ORs] with 95% confidence intervals [CI]).ResultsThe risk of developing cancer overall was lower in PD patients as compared to patients without PD (crude incidence rate ratio 0.77, 95% CI 0.64–0.92). In the nested case-control analysis (adj. OR for all cancers 0.72, 95% CI 0.59–0.87) the risk reduction was strongest for smoking-related cancers (adj. OR 0.47, 95% CI 0.31–0.72). The adjusted OR for hematological malignancies was 0.32 (95% CI 0.14–0.74). Due to small numbers, ORs for other cancer entities did not reach statistical significance.ConclusionsWith the exception of melanoma, PD patients were less likely to develop cancer than individuals without PD in this large observational study.     

The UCHL1 S18Y polymorphism and Parkinson's disease in a Japanese population

UCHL1 plays an important role in the ubiquitin-proteasome system and is a biologically plausible candidate gene for Parkinson's disease (PD). However, results from genetic association studies of the UCHL1 S18Y polymorphism have been equivocal. Meta-analyses indicate that the polymorphism's risk effect might be restricted to Asian populations and early-onset disease. To further explore the role of UCHL1 in PD, we genotyped S18Y in 605 PD patients and 1620 controls of Japanese ancestry. We did not find evidence of an association in the overall sample (SY vs. SS: adjusted OR=1.11, P=0.37; YY vs. SS: adjusted OR=1.01, P=0.94). In the early-onset stratum, however, we observed a trend toward a reduction in risk for those with the Y allele (SY vs. SS, adjusted OR, 0.75; 95% CI, 0.47-1.20; YY vs. SS, OR, 0.64; 95% CI, 0.36-1.14; trend test, P=0.12). These results indicate that, if involved in PD, the S18Y variant is not a major determinant of risk and its effect might be restricted to early-onset disease.     

Which dietary and lifestyle behaviours may be important in the aetiology (and prevention) of stroke?

Prevention of stroke requires optimal control of causal risk factors. However, only three-quarters of all strokes can be attributable to known causal risk factors. We aimed to identify novel risk factors for acute stroke in 48 patients with acute (<1 week) stroke admitted to Royal Perth Hospital Stroke Unit and 47 controls matched for age and sex from the northeast Perth metropolitan area. Patients and controls were interviewed, and had physical measurements and blood taken. Multiple odds ratios (OR) for risk factors, with 95% confidence intervals (CI), were calculated by unconditional multiple logistic regression. Mediterranean diet (OR: 0.1; 95% CI, 0.02-0.4), increased waist-to-hip ratio (OR 4.0, 95% CI, 1.5-11), physical activity during leisure time (OR 0.2; 95% CI, 0.1-0.9), periodontal disease (OR 6.4; 95% CI, 1.5-27), and acute febrile illness (OR 14; 95% CI, 1.5-127) were associated significantly and independently with ischaemic stroke. These preliminary data suggest that certain dietary and lifestyle behaviours may play as important a role in the aetiology (and prevention) of stroke as other conventional causal risk factors for stroke. However, these associations need confirmation from larger randomised trials given the small sample size of the current study.     

Intelligence and other predisposing factors in exposure to trauma and posttraumatic stress disorder: a follow-up study at age 17 years

CONTEXT: Prospective data on standardized measures of early predispositions would allow a strong test of hypotheses about suspected risk factors of posttraumatic stress disorder (PTSD) and exposure to traumatic events. OBJECTIVE: To prospectively examine the extent to which intelligence, anxiety disorders, and conduct problems in childhood influence the risk for PTSD and for exposure to traumatic events. DESIGN: A longitudinal study of a randomly selected sample assessed at age 6 years and followed up to age 17 years. SETTING: Samples were randomly selected from the 1983-1985 newborn discharge lists of 2 major hospitals in southeast Michigan (N=823). PARTICIPANTS: Cohort members with follow-up data at age 17 years (n=713; 86.6% of the initial sample). MAIN OUTCOME MEASURES: Cumulative exposure up to age 17 years of qualifying traumatic events; DSM-IV PTSD among participants who have experienced 1 or more traumatic events. RESULTS: Youth with teacher ratings of externalizing problems above the normal range at age 6 years were at increased risk for exposure to assaultive violence (adjusted odds ratio, 2.6; 95% confidence interval, 1.4-4.9). Youth aged 6 years with an IQ greater than 115 had decreased risk for exposure to traumatic events (adjusted odds ratio for assaultive violence, 0.3; 95% confidence interval, 0.2-0.7); a decreased risk for nonassaultive trauma (adjusted odds ratio, 0.6; 95% confidence interval, 0.3-0.9); and a decreased conditional risk for PTSD (adjusted odds ratio, 0.2; 95% confidence interval, 0.1-0.9). The conditional risk for PTSD was increased for youth with anxiety disorders and teacher ratings of externalizing problems above the normal range at 6 years of age. CONCLUSIONS: The results of this prospective community study highlight the role of intelligence in avoidance of exposure to traumatic experiences and their PTSD effects. They underscore the need for investigating cognitive processes in persons' responses to traumatic experiences and the involvement of general intelligence in these processes.     

Corticosteroid use and risk of aneurysmal subarachnoid haemorrhage

OBJECTIVES: Corticosteroids can induce hypertension and inhibit collagen synthesis in the blood vessel wall. Deficiencies in collagen have been found in intracranial aneurysms. Therefore use of corticosteroids could be a risk factor for intracranial aneurysms and aneurysmal subarachnoid haemorrhage (SAH). We investigated the relationship between the systemic use of corticosteroids in the past and the occurrence of aneurysmal SAH. METHODS: We compared the systemic use of corticosteroids (oral or intravenous) in the past between a consecutive series of 1158 patients with aneurysmal SAH and a control group consisting of 1019 patients diagnosed with a primary central nervous system (CNS) tumour. We discriminated between definite use of corticosteroids defined as use mentioned in the medical record and possible use defined as note in the medical record of a disease that may be treated with corticosteroids. We calculated odds ratios (OR) with corresponding 95% confidence intervals (CI) and adjusted for age and sex by means of logistic regression analyses. RESULTS: Twenty (1.7%, 95% CI 1.1-2.7) of the SAH patients and eight (0.8%, 95% CI 0.3-1.5) of the controls had used systemic corticosteroids (OR: 2.22; 95% CI 0.97-5.05; p-value 0.058; adjusted OR 2.23; 95 % CI 0.97-5.15; p-value 0.059). For definite plus possible use the OR was 1.67 (95% CI 1.09-2.54; p-value 0.016) and the adjusted OR 1.52 (95% CI 0.99-2.33; p-value 0.055). CONCLUSIONS: Patients with aneurysmal SAH more often have used systemic corticosteroids in the past than controls. This may suggest that the use of corticosteroids is a risk factor for aneurysmal SAH.     

Prevalence of Congenital Hydrocephalus in California, 1991-2000

In a population-based retrospective cohort of 5,353,022 California births from 1991 to 2000, 3,152 newborns were diagnosed with congenital hydrocephalus during the birth hospitalization. We compared demographic and clinical characteristics of infants with and without congenital hydrocephalus, and examined in-hospital fatality rates. The prevalence of congenital hydrocephalus was 5.9 per 10,000. During the study period, there was a decline in congenital hydrocephalus due to spina bifida (1.4 to 0.9 per 10,000), and an increase in congenital hydrocephalus due to obstructive hydrocephalus (0.5 to 1.0 per 10,000). Independent risk factors for congenital hydrocephalus were birth weight <1,500 g (odds ratio [OR] 51.6, 95% confidence interval [CI] 47.7-55.8) and birth weight 1,500-2,000 g (OR 14.1, 95% CI 12.4-16) compared to birth weight greater than 2,000 g, low socioeconomic status (OR 1.5, 95% CI 1.4-1.6), and male sex (OR 1.2, 95% CI 1.1-1.3). Asians had a decreased risk for congenital hydrocephalus (OR 0.7, 95% CI 0.6-0.8) when compared to whites. Thirteen percent of affected neonates died before hospital discharge.     

Factor XIII Val34Leu is a genetic factor involved in the etiology of venous thrombosis.

A mutation in the factor XIII gene (FXIII Val34Leu) gene was recently reported to confer protection against myocardial infarction, but its relationship with venous thrombosis is unknown. In addition, a mutation in the 5'-untranslated region of the FXII gene (46 C->T) was identified which is associated with low plasma levels of the protein. Its prevalence in patients with venous thrombosis is also unknown. We investigated the frequency of the FXIII Val34Leu and FXII 46 C->T mutations in 189 patients with deep venous thrombosis and in 187 age-, gender- and race-matched controls. FXIII Val34Leu was detected in 38.6% of the patients and in 41.2% of the controls. Interestingly, homozygosity for the FXIII mutation was found in 1.6% of the patients and in 9.6% of the controls, yielding an odds ratio (OR) for venous thrombosis of 0.16 (95% CI: 0.05-0.5). The OR for heterozygotes was 1.1 (95% CI: 0.7-1.7). The FXII 46 C->T mutation was detected in 46.0% of the patients and in 48.6% of the controls. The OR for heterozygotes was 0.9 (95% CI: 0.6-1.4) and for homozygotes the OR was 0.8 (95% CI: 0.3-1.9). Our data indicate that the FXII 46 C->T mutation is unlikely to be a major risk factor for venous thrombotic disease. In contrast, the homozygous state for FXIII Val34Leu is a strong protective factor against venous thrombosis, which emerges as a novel genetic factor involved in the aetiology of thrombophilia.     

Personality disorders in somatization disorder patients: a controlled study in Spain

OBJECTIVE: The aim of this paper is to assess personality disorder (PD) comorbidity in somatization disorder (SD) patients compared with psychiatric controls in a Spanish sample. METHODS: This is a case-control study. Selection of 70 consecutive SD patients was made, and an age-, sex-, and ethnic-group-matched control group of 70 mood and/or anxiety disorder patients recruited in psychiatric outpatient clinics was selected. PDs were measured using the International Personality Disorder Examination, and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Axis I morbidity was measured by means of the Standardized Polyvalent Psychiatric Interview. RESULTS: PD comorbidity in SD patients was 62.9%, compared to 28.2% in controls [odds ratio (OR)=3.7; 95% confidence interval (95% CI)=1.8-7.6]. The highest ORs of PD in SD patients, compared with controls, were for paranoid (OR=9.2; 95% CI=1.9-43), obsessive-compulsive (OR=6.2; 95% CI=1.2-53.6), and histrionic (OR=3.6; 95% CI=0.9-13.9) PDs. CONCLUSIONS: This is a controlled study with the largest sample of SD patients. The prevalence of PD comorbidity is similar to that of a previously published controlled study but is different from those of the most frequent PD subtypes.     

Aneurysmal and clinical characteristics as risk factors for intracerebral haematoma from aneurysmal rupture

Intracerebral haematoma (ICH) occurs in one-third of patients with aneurysmal subarachnoid haemorrhage (SAH) and is associated with poor prognosis. Identification of risk factors for ICH from aneurysmal rupture may help in balancing risks of treatment of unruptured aneurysms. We assessed potential clinical and aneurysmal risk factors for ICH from aneurysmal rupture. In all 310 SAH patients admitted to our service between 2005 and 2007, we compared clinical risk factors (gender, age, smoking, hypertension, history of SAH and family history) of patients with and without an ICH. From the latest admitted, 50 patients with and 50 without ICH, we compared the location, shape and direction of blood flow of the aneurysms on CT-angiography. Relative risks (RRs) of ICH were 1.2 (95% confidence interval, CI):0.7–1.8) for males, 1.0 (95%CI:0.7–1.4) for age ≥55 year, 1.0 (95%CI:0.6–1.6) for smoking, 0.9 (95%CI:0.5–1.5) for hypertension, 0.6 (95%CI:0.1–3.8) for history of SAH and 0.5 (95%CI:0.2–1.3) for family history of SAH. RRs of ICH were 1.8 (95%CI:1.2–2.5) for MCA aneurysms, 0.5 (95%CI:0.3–1.0) for ICA aneurysms, 0.4 (95%CI:0.1–1.3) for posterior circulation aneurysms, and 0.7 (95%CI:0.3–1.3) for multilobed aneurysms. The RRs of other aneurysmal characteristics varied between 0.9 and 1.2. Patients with MCA aneurysms are at a higher risk of developing ICH. The other aneurysmal or clinical factors have no or only minor influence on the risk of ICH after rupture and are, therefore, not helpful in deciding on treatment of unruptured aneurysms.     

Diabetes preceding Parkinson's disease onset. A case–control study

ObjectiveTo assess the association between diabetes preceding Parkinson's disease (PD) and PD.MethodsPD individuals were matched to PD free individuals randomly selected from people in the same municipality as the cases. Occurrence of diabetes preceding PD onset among cases and controls was assessed through a structured questionnaire. Information regarding current and past medical treatment and other variables was also collected. We used univariate and multivariate logistic models to calculate crude and adjusted odds ratios (OR). Covariates are adjusted for included education, smoking habit, alcohol and coffee consumption.Results318 PD individuals (165 women, 153 men) and 318 matched controls were included in the study. PD patients had a mean age at interview of 66.7 years. Mean age at PD onset was 60.8 years and mean PD duration 5.9 years. We found an inverse association between PD and diabetes preceding PD onset in all groups stratified by gender, age at PD onset, body mass index (BMI), smoking habit, alcohol and coffee consumption. Multivariate analysis yielded the same findings after controlling for the variables (adjusted OR 0.4; 95% CI, 0.2–0.8).ConclusionsOur findings provide additional support for a potential link between diabetes and PD.