ObjectivePlasma cancer antigen (CA)-125 is a tumour marker recently shown to be associated with systolic heart failure and new-onset atrial fibrillation (AF) after myocardial infarction. However, no reports have described the relationship between CA-125 and new-onset AF in healthy postmenopausal women. The aim of the present study was to evaluate the relationship between CA-125 and new-onset AF in postmenopausal women.MethodsBetween 2005 and 2015, 2086 women, including 1012 postmenopausal women, visited our hospital for annual health check-ups. We excluded patients with systolic dysfunction, chronic inflammatory disease, chronic obstructive pulmonary disease, histories of AF or neoplastic diseases. A total of 746 postmenopausal women underwent thorough physical examinations, including those for biomarkers such as brain natriuretic peptide, high-sensitivity C-reactive protein (hs-CRP) and CA-125.ResultsDuring the 10-year observation period, AF was documented in 31 participants (4.2%). The mean age of participants developing AF (75±6 years) was higher than that of those without AF (68±8 years). Participants developing AF showed significantly higher CA-125 (11.4±6.3 U/mL) and hs-CRP (0.10±0.11 mg/dL) levels than did those without AF (7.7±3.2 U/mL, p<0.01; 0.07±0.08 mg/dL, p<0.05). Cox regression analyses revealed ageing (HR 1.3; 95% CI 1.08 to 1.57; p<0.01) and plasma CA-125 levels (HR 1.29; 95% CI 1.10 to 1.51; p=0.02) as independent predictors of AF.ConclusionsHigh CA-125 levels might be associated with new-onset AF in healthy postmenopausal women.

To evaluate the effect of granulocyte/colony-stimulating factor (G-CSF) on the onset of the adult respiratory distress syndrome (ARDS), we investigated whether the incidence of ARDS due to pulmonary infection differed between the G-CSF group which received chemotherapy with G-CSF and historical controls without G-CSF. We evaluated 132 patients with hematological malignancy in complete remission without any main organ dysfunction who had been treated between April 1983 and December 1997. We compared the incidence of ARDS due to pulmonary infection between those who received G-CSF and those who did not. There was no remarkable difference in the number of patients, gender, age, or distribution of primary diseases between the two groups. The intensity of chemotherapy was not considered to significantly differ between the two groups, though the chemotherapy regimens administered differed slightly. In the G-CSF group, the duration of neutropenia was significantly shorter and the frequency of documented infection was significantly decreased. We could not find any relationship between ARDS due to pulmonary infection and any anticancer agent or antibiotics. There was no relationship between the kind of G-CSF and the incidence of ARDS due to pulmonary infection (per chemotherapy session; p > 0.10, per case; p > 0.30, χ² test). The incidence of ARDS due to pulmonary infection per chemotherapy session was 4.21%, and showed a higher tendency in the G-CSF group (p < 0.100, χ² test). The incidence of ARDS due to pulmonary infection per case was 25.4% and was significantly higher in the G-CSF group (p < 0.025, χ² test). The incidence of ARDS due to pulmonary infection was higher in the G-CSF group than in the controls, suggesting that G-CSF promotes the development of ARDS due to pulmonary infection.

A 55-year-old woman came to our hospital because of cutaneous sclerosis of the limbs in September 1996, and was diagnosed with scleroderma based on a skin biopsy. In August 1997, the cutaneous sclerosis became progressive (hemoglobin level, 4.3 g/dl; platelet count, 7 × 10⁹/l). The laboratory results were positive for the direct Coombs test, bone marrow aspiration showed a dry tap, and the bone marrow biopsy showed marked fatty marrow. Indium-111 bone marrow scintigraphy showed a markedly decreasing uptake. These findings indicated bone marrow hypoplasia associated with hemolytic anemia. After prednisolone therapy (60 mg) was initiated, the direct Coombs test became negative but the blood cell count did not increase. Then, 300 mg of cyclosporin was initiated and anemia and thrombocytopenia improved. The cyclosporin dosage was gradually decreased and the patient’s hematological condition was good, although the cutaneous sclerosis changed only a little. This is a rare and interesting case of a patient with scleroderma associated with bone marrow insufficiency and hemolysis who responded well to cyclosporin.

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