Influence of common cardiac drugs on gastroesophageal reflux disease: multicenter questionnaire survey.

BACKGROUND: Although gastroesophageal reflux disease (GERD) causes noncardiac chest pain mimicking angina pectoris, systemic studies surveying the effects of common cardiac drugs on symptomatic GERD are rare. METHODS: To investigate the drugrelated GERD, this multicenter trial enrolled 201 consecutive cardiac outpatients (69.7 ± 10.5 y) after obtaining written informed consent. They were assessed using the Frequency Scale for Symptoms of GERD (F-scale) to screen for GERD with a cut-off value of 8.0. Clinical background was obtained from medical records. Gastric medicine was empirically administered at the discretion of the attending physician. F-scale score and incidence of GERD were analyzed individually in relation to background and prescription. RESULTS: The average F-scale score did not correlate with gender, age or underlying diseases. F-scale score was elevated significantly (p = 0.006) by administration of calcium channel blockers to the patients treated with gastric medicine, suggesting that calcium channel blockers exacerbate the possibly preexisting GERD. Incidence of GERD within 2 months after starting warfarin tended to be greater than that at other durations (p = 0.087). Patients showing a high score (≥ 8.0) suggestive of GERD showed a correlation with the combined administration of calcium channel blockers (OR = 3.19; 95% CI of 1.01 - 10.11; p = 0.049) and warfarin (OR = 3.05; 95% CI of 1.00 - 9.27; p = 0.049) in the best logistic model. CONCLUSION: Although larger cohort is required, this survey demonstrates that the combination of calcium channel blockers and warfarin is an independent risk factor for GERD.

[Severe left ventricular dysfunction in a patient with primary Sjögren's syndrome].

A 43-year-old woman was admitted to our hospital for evaluation of shortness of breath and palpitation on exertion. She had a 20-year history of dry mouth and a 10-year history of recurrent pneumonia. She had been diagnosed as having primary Sjögren's syndrome with interstitial pneumonia at 42 years of age. On admission, cardiac ultrasonography revealed reduced left ventricular systolic function. Complications that would elicit cardiac manifestations such as viral myocarditis, amyloidosis, sarcoidosis, and ischemic heart disease, were excluded. Oral corticosteroid therapy was effective for alleviating symptoms. In this patient, it appears that primary Sjögren's syndrome is involved in the reduced left ventricular systolic function.

Improvement of diabetic or obese patients' erythrocyte deformability by the program of the brain-oriented obesity control system (BOOCS).

Diabetes is characterized by absolute or relative insulin deficiency complicated with microangiopathy, whereas obesity stems from insulin resistance. A psychosomatic approach to obesity and diabetes has been highlighted, including the brain-oriented obesity control system (BOOCS). Impaired deformability of erythrocytes in obese or diabetic patients is closely linked to disturbed microcirculation, and improvement of abnormal erythrocyte rheology is a prerequisite for the prevention and treatment of microangiopathy. Therefore, erythrocyte filterability, whole cell deformability defined as flow rate of erythrocyte suspension relative to that of saline, was assessed by the nickel-mesh-filtration technique. Subjects included healthy controls (group A, n = 14), diabetic, non-obese participants (group B, n = 29), and non-diabetic, obese participants (group C, n = 32) in the 6-month BOOCS program, and most patients in groups B and C (86.9 %) completed this program. Baseline mean erythrocyte filterabilities were 89.4 ± 1.7 % in group A, 82.8 ± 5.2 % in group B, and 84.1 ± 5.6 % in group C, showing significant intergroup differences (p < 0.001). This program significantly improved (p < 0.001) the impaired erythrocyte filterability in groups B (87.9 ± 4.4 %) and C (88.5 ± 3.7 %). Declines in HbA1c (p = 0.387) and body mass index (p = 0.479) were not correlated to this improvement. These findings indicate that the mechanisms of BOOCS-induced improvement of diabetic or obese patients' erythrocyte deformability are multifactorial, and that the BOOCS program for these patients is a holistic, cost-effective, and highly compliant approach possibly ameliorating microcirculation.

Isoproterenol-induced creatine kinase leakage in Langendorff-perfused rat heart associated with significant myocardial edema.

Since the mechanism of creatine kinase (CK) leakage induced by beta-adrenoceptor activation remains unclear, we studied the effects of incremental application (10(-9) to 10(-4) M) of isoproterenol (ISP) on the CK efflux from Langendorff-perfused isolated rat hearts under aerobic conditions. Tissue water content was estimated after the perfusion experiment. ISP-induced dose-dependent CK leakage was noted in a sigmoidal fashion, which showed low temperature-dependency (Q10 of 2.41), sensitivity to cepharantine (10(-6) M) and propranolol (10(-7) to 10(-6) M) without any signs of demand ischemia or oxidant stress. CK liberation was not replicated at all by maneuvers activating cAMP-dependent protein kinase (A-kinase). Myocardial edema noted in the control ISP application was ameliorated by exposure to 10(-6) M propranolol or cepharantine (i.e., significant fall in tissue water content; p < 0.05). Histological study revealed nonspecific myocardial fiber swelling and separation without any myocyte necrosis for all the perfusion groups. These results suggest that ISP-induced CK leakage in this model is not mediated by beta-adrenoceptor stimulation, subsequent A-kinase activation or related demand ischemia, but is attributed most to the direct effects of ISP augmenting sarcolemmal CK and water permeability.

Lupus nephritis with adult T cell leukemia.

A 64-year-old Japanese male patient with lupus nephritis associated with adult T cell leukemia (ATL) is described. Percutaneous renal biopsy demonstrated findings consistent with membranous lupus nephritis. To our knowledge, this is the first case of lupus nephritis complicated by ATL, suggesting that human T cell leukemia virus type I may be correlated not only to outbreaks of ATL but also to lupus nephritis/systemic lupus erythematosus.