Antihypertensive Adherence Trajectories among Older Adults in the First Year after Initiation of Therapy

BACKGROUND Adherence to antihypertensives is suboptimal, but previous methods of quantifying adherence fail to account for varying patterns of use over time. We sought to improve classification of antihypertensive adherence using group-based trajectory models, and to determine whether individual factors predict adherence trajectories. METHODS We identified older adults initiating antihypertensive therapy during 2008-2011 using a 20% sample of Medicare (federal health insurance available to US residents over the age of 65) beneficiaries enrolled in parts A (inpatient services), B (outpatient services), and D (prescription medication). We developed monthly adherence indicators using prescription fill dates and days supply data in the 12 months following initiation. Adherence was defined as having at least 80% of days covered. Logistic models were used to identify trajectory groups. Bayesian information criterion and trajectory group size were used to select the optimal trajectory model. We compared the distribution of covariates across trajectory groups using multivariable logistic regression. RESULTS During 2008-2011, 282,520 Medicare beneficiaries initiated antihypertensive therapy (mean age 75 years, 60% women, 84% White). Six trajectories were identified ranging from perfect adherence (12-month adherence of 0.97, 40% of beneficiaries) to immediate stopping (12-month adherence of 0.10, 18% of beneficiaries). The strongest predictors of nonadherence were initiation with a single antihypertensive class (adjusted odds ratio = 2.08 (95% confidence interval: 2.00-2.13)), Hispanic (2.93 (2.75-3.11)) or Black race/ethnicity (2.04 (1.95-2.13)), and no prior history of hypertension (2.04 (2.00-2.08)) (Area under the receiving operating characteristic curve: 0.53). CONCLUSIONS There is substantial variation in antihypertensive adherence among older adults. Certain patient characteristics are likely determinants of antihypertensive adherence trajectories

Intoxicação em suínos pela ingestão de sementes de Aeschynomene indica (Leg.Papilionoideae) Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds

Relata-se um surto espontâneo de intoxicação em suínos pela ingestão de sementes de Aeschynomene indica e a reprodução da doença nessa espécie animal. O surto espontâneo ocorreu numa propriedade de criação de suínos localizada na região central do Rio Grande do Sul. Nessa propriedade havia 100 suínos (20 matrizes e 80 suínos jovens de várias categorias). Os suínos eram alimentados com uma ração feita na propriedade pela mistura de 50% farelo de milho, 25% de farelo de soja, 5% de um suplemento vitamínico-mineral de origem comercial e 20% quirera de arroz contaminada por 40% de sementes de A. indica. Embora aparentemente todos os suínos tenham recebido a mesma ração, apenas os suínos de 45 dias de idade foram afetados; as taxas de morbidade, mortalidade e letalidade foram respectivamente 25%-40%, 8,5%-20% e 25%-66%. Os sinais clínicos apareceram cerca de 24 horas após o início da administração da ração contendo sementes de A. indica e incluíam vários graus de incoordenação no andar, quedas, decúbito esternal com membros pélvicos posicionados afastados entre si, decúbito lateral e morte. Não foi possível determinar quantos suínos se recuperaram e quanto tempo levou a recuperação. Um suíno foi submetido à eutanásia e necropsiado na propriedade. A doença foi reproduzida em 5 suínos jovens (A-E) alimentados com uma ração contendo 10% (Suíno A), 15% (Suíno B) e 20% (Suínos C-E) de sementes de A. indica e em um suíno mais velho (Suíno F) que recebeu uma ração com 16,5% de sementes de A. indica. Os sinais clínicos foram semelhantes aos observados nos suínos do surto espontâneo. Os Suínos A, B e F foram submetidos à eutanásia e os Suínos C-E morreram de uma doença aguda respectivamente 16, 21 e 24 horas após o início do experimento. Os achados de necropsia incluíam acentuada hiperemia das leptomeninges em todos os suínos, grandes quantidades de sementes de A. indica no estômago e avermelhamento transmural da parede do intestino e conteúdo intestinal sanguinolento nos Suínos C-E. Um hematoma foi observado no pulmão do Suíno C. Os achados histopatológicos no encéfalo dos suínos alimentados com as maiores concentrações (20%) de sementes de A. indica (C-E) consistiram em áreas focais e simétricas de congestão, edema, hemorragia e tumefação do endotélio vascular em diversos núcleos e no córtex telencefálico. Nos Suínos A e B, que receberam menores concentrações das sementes de A. indica, e no Suíno F, caso espontâneo da doença, as alterações histológicas no encéfalo consistiam de áreas bem definidas de malacia focal simétrica; nessas áreas a neurópila normal era obliterada por numerosos macrófagos espumosos dispostos em estreita aposição, astrocitose e capilares com endotélios tumefeitos. Os focos de malacia focal simétrica em suínos intoxicados com sementes de A. indica afetavam os núcleos cerebelares e vestibulares, a substância negra, o putâmen e os núcleos mesencefálicos, oculomotor e núcleo vermelho. Esses dados indicam que a ingestão de sementes de A. indica é responsável por essa condição neurológica, que a doença pode ser fatal e que parece afetar igualmente suínos jovens e adultos. O desenlace clínico e as alterações patológicas são dependentes da dose e as lesões encefálicas progridem de danos vasculares a edema vasogênico, hemorragia e malacia.<br>A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia