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A Bartel

Publications and source records attributed to A Bartel.

At least 19 recordsLinked to original sources

[Fatal pulmonary embolism after endoscopic embolization of downhill esophageal varix].

HISTORY AND CLINICAL FINDINGS: A 79-year-old man was admitted with a history of recent haematemesis and tarry stools. 4 years before he had undergone a subtotal thyroidectomy for hyperthyroidism. INVESTIGATIONS: He was anaemic (haemoglobin 7.2 g/dl, haematocrit 23%). At the transition between the upper and middle third of the oesophagus gastroscopy revealed a bleeding oesophageal varix. TREATMENT AND COURSE: The bleeding varix was sclerosed with polidocanol. 3 erythrocyte concentrates were administered. Massive bleeding 2 days later was controlled with intravaricose injection of cyanoacrylate (Histoacryl). The patient died 6 weeks later from progressive cardiovascular failure. Autopsy revealed the cause of death as right heart failure with extensive foreign-body pulmonary emboli identified as thrombotic material containing polymerized cyanoacrylate found in the previously injected oesophageal varix. Also discovered was a retrosternal goitre which had compressed the brachiocephalic vein. Cause of the "washing-out" of the cyanoacrylate embolus from the varix into the systemic circulation was an oesophago-varicose collateral circulation in a cranio-caudal direction; this had been formed by the pressure of the retrosternal goitre on the brachiocephalic vein. CONCLUSION: Cyanoacrylate injection into a varix above the lower third of the oesophagus should only be done under strict indication. A similar risk as that described in this case potentially exists in the treatment of acute bleeding from a portosystemic varicose circulation.

Aged

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California

[Alpha interferon in the therapy of hairy cell leukemia. Results of 3 prospective multicenter studies in West Germany].

Within 19 months of recruitment 51 centers enrolled 84 patients in our prospective multicenter trial for low-dose IFN alpha-2c for HCL (1.2 x 10 IU/m x 28 days s.c.- or lower). Induction therapy of 84 days was followed by maintenance with 2 weekly doses. Patients who reached stage Jansen I or A were then randomized to 2 arms either to receive further IFN or to stop treatment. Reinduction was reinstituted whenever any patient lost Jansen stage A or I. Only 3 patients failed. But enrollment was discontinued when it became apparent that fatalities in splenectomized (SX) patients due to septicemia outnumbered deaths given in the literature. Low-dose IFN administered daily might compromise host defense. Our next study aimed at improving the safety of IFN for SX patients. Pulsatile IFN on 7 consecutive days within a 28-day period was given to all SX patients. A randomization of non-SX patients either to receive daily or pulsatile IFN should provide proof of the efficiency. The intermissions ought to be as suitable for in-vitro investigations as for observations concerning the capacity of IFN to produce 'induction of inducers'. Pulsatile treatment has so far been safe in 13 splenectomized patients. Central diagnostic procedures remained the same during both studies. It seems important to us to use an intermittent schedule for the injection of IFN in SX patients and to restrict splenectomy to selected patients.

Aged

Coffee consumption and mortality. Total mortality, stroke mortality, and coronary heart disease mortality.

Total mortality showed no association with coffee usage in the four race-sex groups of Evans County, Georgia. Deaths of coronary heart disease (CHD) in white men and women and black men showed no statistically significant difference between high and low coffee consumers. In an area that has been designated as the "Stroke Belt," neither CHD nor cerebrovascular death rates seem related to coffee-drinking habits. However, to refute or confirm the allegations of a detrimental influence of high coffee intake, larger samples are needed. Nevertheless, our finding that mortality from all causes is not increased in the high coffee-consuming group means that a finding of increased CHD mortality with high coffee consumption would have to be compensated by a protective lower rate for other causes of death.

Adult