Age-Related Differences in Non-Persistence with Statin Treatment in Patients after a Transient Ischaemic Attack.

BACKGROUND AND OBJECTIVE: Non-persistence with secondary preventive measures, including medications such as statins, adversely affects the prospects of successful outcomes. This study was aimed at evaluating non-persistence with statin therapy in cohorts of young and elderly patients after a transient ischaemic attack (TIA) and identifying patient-associated characteristics that influence the risk for non-persistence. METHODS: The study cohorts included 797 adult patients who were initiated on statin therapy following a TIA diagnosis between 1 January 2010 and 31 December 2010. Patients were followed up for 3 years and those with a treatment gap of at least a 6-month period were considered 'non-persistent'. In order to identify any age-related differences, all analyses were conducted in the entire study cohort (n = 797) as well as separately in the 'younger' (aged <65 years, n = 267) and the 'older' (aged ≥65 years, n = 530) patients. RESULTS: Non-persistence was significantly more common in younger patients compared to older patients (67.8% vs. 49.1%; p < 0.001). Factors that decreased the probability of non-persistence in younger and older patients included diabetes mellitus (hazard ratio [HR] = 0.72 and HR = 0.64, respectively) and hypercholesterolaemia (HR = 0.43 and HR = 0.62, respectively). Female gender (HR = 1.42) was associated with a higher and increasing number of medications taken (HR = 0.93), with lower probability for non-persistence in younger patients but not in the older patients. CONCLUSIONS: Our results indicate that certain patients with TIA require special counselling to improve persistence with statin therapy. These include younger patients, especially females and those not on polypharmacy, and both younger and older patients without diabetes mellitus or hypercholesterolaemia.

Non-persistence with antiplatelet therapy in elderly patients after a transient ischemic attack.

BACKGROUND: Antiplatelet therapy following a transient ischemic attack (TIA) constitutes an important secondary prevention measure. AIMS: The study was aimed at evaluating the development of non-persistence with antiplatelet therapy in elderly patients after a TIA and identifying patient-related characteristics associated with the probability of non-persistence during the follow-up period. METHODS: The study cohort (n = 854) was selected from the database of the largest health insurance provider of the Slovak Republic. It included patients aged ≥65 years, in whom antiplatelet medication was initiated following a TIA diagnosis during the period between 1 January 2010 and 31 December 2010. Each patient was followed for a period of 3 years from the date of the first antiplatelet medication prescription associated with TIA diagnosis. Patients in whom there was a treatment gap of at least 6 months without antiplatelet medication prescription were defined as "non-persistent". The factors predicting non-persistence were identified in the Cox proportional hazards model. RESULTS: At the end of the follow-up period, 345 (40.4%) patients were non-persistent with antiplatelet medication. Protective factors decreasing a patient´s likelihood of becoming non-persistent were age ≥75 years [hazard ratio (HR) = 0.75], polypharmacy (concurrent use of ≥6 drugs) (HR = 0.79), arterial hypertension (HR = 0.68), diabetes mellitus (HR = 0.74), hypercholesterolemia (HR = 0.75), and antiplatelet medication switching during the follow-up period (HR = 0.73). CONCLUSIONS: It is concluded that following a TIA, elderly patients aged <75 years or those with normal serum cholesterol levels, without certain comorbid conditions and polypharmacy may benefit from special counselling to encourage persistence with secondary preventive medication.

Patient-related characteristics associated with non-persistence with statin therapy in elderly patients following an ischemic stroke.

PURPOSE: This study was aimed at evaluating the extent of non-persistence with statin therapy in elderly patients after an ischemic stroke and identifying patient-related characteristics that are risk factors for non-persistence. METHODS: The evaluable study cohort (n = 2748) was derived from the database of the largest health insurance provider in the Slovak Republic. Patients aged ≥65 years who were initiated on statin therapy following the diagnosis of an ischemic stroke during one full year (1 January 2010 to 31 December 2010) constituted this cohort. Each patient was followed for a period of 3 years from the date of the first statin prescription. Patients with a continuous treatment gap of 6 months without statin prescription were designated as non-persistent. The Cox proportional hazard model was applied to determine patient-associated characteristics that influenced the likelihood of non-persistence. RESULTS: During the 3-year follow-up period, 39.7% of patients in the study cohort became non-persistent. Factors associated with decreased probability of a patient becoming non-persistent were age ≥75 years (hazard ratio (HR) 0.75), polypharmacy (concurrent use of ≥6 drugs) (HR 0.79), diabetes mellitus (HR 0.80), dementia (HR 0.81) and hypercholesterolemia (HR 0.50). On the other hand, the presence of anxiety disorders (HR 1.33) predicted an increased likelihood of a patient being non-persistent. CONCLUSIONS: Our findings suggest that patients aged ≥75 years or those with the presence of diabetes mellitus, dementia, hypercholesterolemia or polypharmacy were likely to be persistent with statin therapy, whereas those with anxiety disorders may need greater assistance with persistence of statin therapy. Copyright © 2016 John Wiley & Sons, Ltd.

Long-term effect of rituximab in a case with late-onset Rasmussen´s encephalitis with anti-ganglioside IgGQ1b and anti-GAD antibodies positivity. Case Report.

Rasmussen's encephalitis is a rare autoimmune encephalitis usually involving one brain hemisphere, presenting with refractory epileptic seizures, and neurological and cognitive decline. Only 10% of cases start later in adolescence/adulthood. The only effective treatment for refractory seizures in childhood is hemispherectomy. For late-onset cases with mild neurological deficit the hemispherectomy is usually postponed because of its severe consequences. Immunotherapy shows some temporal effect for seizure control and slowing the brain atrophy, mainly in late onset Rasmussen's encephalitis. We report a patient with late onset Rasmussen´s encephalitis with anti-ganglioside IgGQ1b and anti-GAD antibodies positivity, who failed immunotherapy with cytostatics, immunoglobulins and steroids. Anti-ganglioside IgGQ1b antibodies are typically associated with a Miller-Fisher variant of Guillain-Barre syndrome and Bickerstaff's brainstem encephalitis. The association with Rasmussen´s encephalitis was not described before. Patient´s neurological deficit was mild and hemispherectomy was refused. The treatment with rituximab, an anti-CD20+ monoclonal antibody, led to 36-month control of seizures without any signs of progression of neurological deficit and MRI brain atrophy. Although the treatment is associated with long term B-cells depletion, patient doesn´t suffer from any clinically relevant infection. The biological treatment with monoclonal antibodies might be the way to stabilize patients with Rasmussen´s encephalitis, mainly late-onset, to prevent them from harmful and devastating hemispherectomy.

Factors Influencing Non-Persistence with Antiplatelet Medications in Elderly Patients After Ischaemic Stroke.

OBJECTIVES: This study investigated the extent of, and patient-related characteristics for, non-persistence with antiplatelet therapy during follow-up in elderly patients after their first ischaemic non-cardioembolic stroke. METHODS: A database of the largest health insurance provider in the Slovak Republic was used to assemble the study cohort of 4319 patients (56.8% were women) aged ≥65 years in whom antiplatelet therapy was initiated following a hospital-based diagnosis of stroke during the period 1 January 2010 to 31 December 2010. Patients were followed for 3 years from the date on which the first prescription of antiplatelet medication was recorded. Patients with a 6-month treatment gap without antiplatelet medication prescription were designated as non-persistent, and the Cox proportional hazards model was used to identify predictors of non-persistence. RESULTS: At the end of the 3-year follow-up period, 1184 (27.4%) patients were considered non-persistent with antiplatelet medication. In 1244 (28.8%) patients, a switch in the use of a particular antiplatelet drug was registered during this follow-up period. Female sex (hazard ratio [HR] 1.25) was associated with increased risk of non-persistence. In contrast, factors associated with lower probability of non-persistence were age ≥75 years (HR 0.72), switch in antiplatelet medication use (HR 0.76), diabetes mellitus (HR 0.81), dementia (HR 0.69) and epilepsy (HR 0.69). CONCLUSIONS: Our results suggest that women, patients aged <75 years, and patients without certain comorbid conditions may need improved assistance in secondary prevention management after an ischaemic stroke.

Attenuated neuroendocrine response to hypoglycemic stress in patients with panic disorder.

BACKGROUND/AIMS: There is a lack of information on the effects of metabolic stress exposure on hormone release in patients with panic disorder. The aim of this study was to test the hypothesis that neuroendocrine activation during hypoglycemic stress is altered in panic disorder patients compared to healthy subjects. METHODS: Hormone responses to an intravenous bolus of insulin (0.1 IU/kg) were evaluated in both fully remitted, medication-free panic disorder patients and healthy controls (n = 9/group). Blood samples for determination of cortisol, growth hormone, prolactin, adrenaline and noradrenaline concentrations were obtained at rest and over a 90-min period after insulin injection. RESULTS: In patients with panic disorder, basal prestress hormone levels were comparable to those in healthy subjects with the exception of plasma adrenaline, which was higher in panic disorder patients compared to controls. The degree of hypoglycemia induced by insulin administration was similar in patients and healthy subjects. Hypoglycemia-induced increases in growth hormone, prolactin and cortisol concentrations were significantly attenuated in panic disorder patients compared to healthy individuals. No differences between patients and controls were observed in adrenalin release induced by hypoglycemia. CONCLUSIONS: The present data demonstrate that somatotropic, lactotropic and corticotropic activation during hypoglycemic stress is blunted in patients with panic disorder. It is suggested that in contrast to the effects of relatively mild stress conditions used in other studies published in the literature, intensive stressors inducing a broad spectrum of hormonal changes fail to provoke an adequate neuroendocrine response in patients with panic disorder.

Sweat: a potential marker of clinical activity in panic disorder.

OBJECTIVE: Panic disorder (PD) is a paroxysmal neuropsychiatric disorder with unclear etiology and obscure pathophysiology. Despite the frequency of its occurrence, PD still has no reliable laboratory markers. The sweat is a neglected human secrete reacting immediately to various neurovegetative challenges including psychic imupulses. We hypothesized a possible dysfunction of sweat homeosthasis in PD. SUBJECTS AND METHODS: 10 patients with active PD, 9 patients with PD in remission and 11 age-matched controls participated in this study. All subjects underwent a single 8-min session in the dry-heat sauna. Sweat and venous blood have been collected immediately after the end of this session. Concentrations of lactate, glucose, creatinine, natrium, potassium, chlorine, calcium and magnesium have been quantitatively estimated in both liquids and compared statistically among three groups. RESULTS: We did not find any significant difference in blood parameters of the three above groups. However, the patients with active PD had significantly higher sweat levels of lactate, glucose, creatinine and magnesium than both the other groups which did not differ. Moreover, sweat concentrations of natrium, potassium and chlorine were significantly higher in active PD comparing to the group of PD patients in remission. CONCLUSIONS: The sweat of patients with active PD in comparison to PD in its clinical remission exhibits surprisingly distinctive changes of selected parameters after dry-heat sauna exposure. Increased concentrations of lactate, glucose and magnesium in the sweat are not contradictory with presupposed neurotransmitter-metabolic firing mechanisms in PD. These findings appear to be perspective biochemical markers in PD and its course.

Reduced plasma homocysteine levels in levodopa/entacapone treated Parkinson patients.

Hyperhomocysteinemia is not only a major risk factor for atherothrombotic disease, but is also strongly associated with an increased risk of dementia and cognitive impairment, both of which are common in the course of Parkinson's disease (PD). Previous work has found that levodopa increases plasma homocysteine concentrations. Animal studies have indicated that the catechol-O-methyltransferase (COMT) inhibitors can prevent levodopa-induced elevation of homocysteine concentrations by reducing the O-methylation of levodopa. The objective of our study was to assess the impact of entacapone, a COMT inhibitor, on plasma levels of homocysteine, serum folate, and vitamin B12 in levodopa-treated PD patients. Nineteen PD patients receiving only levodopa and 21 PD patients on a combination of levodopa and entacapone participated in the cross-sectional study. The control group consisted of 17 subjects on dopamine agonists. The mean plasma homocysteine concentration in the subjects on only levodopa was higher than that in the subjects on a combination of levodopa and entacapone (P=0.001) or in the control group (P=0.0001). Concentrations of serum vitamin B12 and serum folate were on average normal in all groups, but levodopa-treated subjects (with or without entacapone therapy) were more prone to have hypovitaminosis B12 (45%) than controls on dopamine agonists (6%). We suggest that the COMT inhibition may play a promising role in successfully controlling levodopa-induced hyperhomocysteinemia and in reducing the risk of pathologies probably linked to it. These preliminary findings and postulated hypotheses must now be confirmed in prospective studies.