BackgroundAlthough histamine H2-blockers (H2B) and proton pump inhibitors (PPI) are used commonly to prevent gastrointestinal bleeding in acute stroke, they are implicated in the increased risk of pneumonia in other disease populations. In acute stroke, the presence of distinctive risk factors of pneumonia, including dysphagia and impaired consciousness, makes inclusive analysis vulnerable to confounding. Our aim was to assess whether acid-suppressive drugs increase pneumonia in acute stroke in a population controlled for confounding.MethodsWe analyzed acute stroke patients admitted to a tertiary care hospital. To minimize confounding, we only included subjects who could not feed orally during 14 days of hospitalization. Exposure was defined as H2B or PPI, given in days; the outcome was development of pneumonia within this period. The incidence was calculated from the total number of pneumonias divided by the sum of person-days at risk. We additionally performed multivariate Poisson regression and propensity score analyses, although the restriction largely eliminated the need for multivariate adjustment.ResultsA total of 132 pneumonias occurred in 3582 person-days. The incidence was 3.69%/person-day (95% confidence interval (CI); 3.03–4.37%/day). All subjects had dysphagia. Stroke severity and consciousness disturbances were well-balanced between the groups exposed to H2B, PPI, or none. The relative risk (RR) compared with the unexposed was 1.22 in H2B (95%CI; 0.83–1.81) and 2.07 in PPI (95% CI; 1.13–3.62). The RR of PPI compared with H2B was 1.69 (95%CI; 0.95–2.89). In multivariate regression analysis, the RRs of H2B and PPI were 1.24 (95% CI; 0.85–1.81) and 2.00 (95% CI; 1.12–3.57), respectively; in propensity score analyses they were 1.17 (95% CI; 0.89–1.54) and 2.13 (95% CI; 1.60–2.84).ConclusionsThe results of this study suggested that prophylactic acid-suppressive therapy with PPI may have to be avoided in acute stroke patients susceptible to pneumonia.

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Background: Adenomyosis is a common and benign uterine disease. Acute cerebral infarction (CI) associated with adenomyosis is rarely reported and difficult to treat. We experienced successful treatment for this disease. Case Description: A 50-year-old woman presented with a 2-day history of visual disturbance. Magnetic resonance imaging showed multiple tiny diffusion-weighted high-density spots on several lobes. No common risk factors for stroke were detected. Cancer antigen 125 level was 999 U/mL, along with massively expanded uterus and adnexa. Based on the diagnosis of benign adenomyosis, Xa inhibitor and GnRH agonists were administered for CI and adenomyosis, respectively. Acute CI recurred 7 days after admission. We suspected a relationship between infarction and adenomyosis and concluded hysterectomy as a proper treatment strategy based on the literature. Eighteen months after hysterectomy, no recurrence of CI without anti-thrombus medications has been detected. Conclusion: Hysterectomy is a radical therapy that is effective in preventing acute CI due to adenomyosis associated with ischemic symptoms.

BackgroundThyrotropin-producing pituitary tumor is relatively rare. In particular, concurrent cases associated with Graves’ disease are extremely rare and only nine cases have been reported so far. We describe a case of a thyrotropin-producing pituitary adenoma concomitant with Graves’ disease, which was successfully treated.Case presentationA 40-year-old Japanese woman presented with mild signs of hyperthyroidism. She had positive anti-thyroid-stimulating hormone receptor antibody, anti-thyroglobulin antibody, and anti-thyroid peroxidase antibody. Her levels of serum thyroid-stimulating hormone, which ranged from low to normal in the presence of high levels of serum free thyroid hormones, were considered to be close to a state of syndrome of inappropriate secretion of thyroid-stimulating hormone. Magnetic resonance imaging showed a macropituitary tumor. The coexistence of thyrotropin-producing pituitary adenoma and Graves’ disease was suspected. Initial therapy included anti-thyroid medication, which was immediately discontinued due to worsening symptoms. Subsequently, surgical therapy for the pituitary tumor was conducted, and her levels of free thyroid hormones, including the thyroid-stimulating hormone, became normal. On postoperative examination, her anti-thyroid-stimulating hormone receptor antibody levels decreased, and the anti-thyroglobulin antibody became negative. The coexistence of thyrotropin-producing pituitary adenoma and Graves’ disease is rarely reported. The diagnosis of this condition is complicated, and the appropriate treatment strategy has not been clearly established.ConclusionsThis case suggests that physicians should consider the coexistence of thyrotropin-producing pituitary adenoma with Graves’ disease in cases in which thyroid-stimulating hormone values range from low to normal in the presence of thyrotoxicosis, and the surgical treatment of thyrotropin-producing pituitary adenoma could be the first-line therapy in patients with both thyrotropin-producing pituitary adenoma and Graves’ disease.