Acquired isolated factor X deficiency associated with systemic amyloidosis. Case report and review of literature.

The demonstration of acquired isolated factor X deficiency and of a biclonal homogeneous lambda and kappa light polypeptide chain proteinuria in a patient of 49 years having an obscure hepatomegaly gave clinical evidence for the rate, amyloidosis-associated factor X deficiency, which could be proven by postmortem examination. The mechanisms by which amyloid may affect factor X levels in this case may be preferentially binding to the amyloid fibrils of lambda light chain type.

[The influence on PHA-stimulation by inhibition of prostaglandin synthesis in vitro in patients with Hodgkin's disease (author's transl)].

Adherent mononuclear cells may have suppressor functions mediated by prostaglandins (PG). In the present study we tested a large number of normal donors and patients with Hodgkin's disease (HD) using PHA and the prostaglandin inhibitor indomethacin (IM). Stimulation of mononuclear cells from 24 healthy volunteers with PHA led to a mean response of 27 833 cpm; addition of IM caused a 32% increase of 3H-thymidine incorporation.

A micro-method for PHA-induced stimulation of human lymphocytes. II. communication: effect of splenectomy on the inhibitory activity of serum in patients with Hodgkin's disease.

Lymphocytes of 19 unselected patients with Hodgkin's disease were stimulated with PHA in vitro using a microculture system. The sera of these donors were simultaneously tested for their ability to support PHA-induced stimulation of normal lymphocytes as compared to sera drawn from healthy volumteers. Wheras DNA synthesis in Hodgkin's disease using normal sera was almost uniformly decreased, transformation of normal lymphocytes was suppressed in 9 of 11 sera from patients with Hodgkin's disease without splenectomy, but only in 1 of 8 sera from patients tested after removal of the spleen.

[Attempted murder with phenprocoumon (marcumar)(author's transl)].

The first known case of attempted murder by means of a coumarine-containing drug, administered by a nurse to her husband, is reported. Small doses of phenprocoumon were regularly added to his food or drinks. He was admitted to hospital with a severe haemorrhagic diathesis which, at first, was thought to be a familial haemorrhagic disease, his mother having died of recurrent hypoprothrombinaemia a few years earlier, the cause of her bleeding trouble never having been established.

[Contribution to the aetiology of "reversible hepatic dysfunction" (Stauffer's syndrome) associated with renal tumours].

Biochemical changes, especially isolated rise in alkaline phosphatase and increased thromboplastin time, which have been described as "reversible hepatic dysfunction" (Stauffer's syndrome) were found in a 47-year-old patient with hypernephroma and hepatomegaly without liver metastases at post-mortem examination. The alkaline phosphatase could not be distinguished from the placental isoenzyme (Regan's enzyme). Increased thromboplastin time was due to circulating fibrinogen degradation products.