No abstract

A patient with chronic idiopathic thrombocytopenic purpura (ITP), a 28-year-old group A, Rh-positive woman, also had hemolytic anemia. At that time, her red cells typed as group A, but the serum typed as group O. This typing followed intravenous high-dose immune globulin therapy, (400 mg/kg for 5 successive days) and was attributable to A antibody of the IgG type, composed of IgG1, IgG2, IgG3, and IgG4, in the immune globulin preparation, which had been given for treatment of ITP. All lots of commercial human plasma preparation products (heat-treated human plasma protein, albumin, factor VIII or IX products, and immune globulin) examined were found to contain A and/or B antibodies of the IgM or IgG type, with titers of 1 to 1024. Twelve of the 20 lots of immune globulin contained RBC antibodies of the IgG type. Subclass IgG1 was found in all 12 of these lots, and all four subclasses, including IgG3, were detected in 8 lots. All 8 showed antibody titers higher than 64.

Summary. A 24‐year‐old male was admitted to Kansai Medical University Hospital, complaining of fever, skin exanthema, jaundice, brown urine and lymphadenopathy. The patient was diagnosed as having haemolytic anaemia caused by a cold agglutinin following rubella infection. The cold agglutinin of the patient reacted strongly with group OI red blood cells (RBC), Oi cord RBC, Oi adult RBC and neuraminidase‐treated RBC, and much weaker with protease (papain, ficin, bromelin)‐treated RBC; it was identified as anti‐Pra. Cold agglutinins of anti‐Pra specificity following rubella infection in adults have rarely been reported.

To investigate both the incidence and the dosage used to treat gastrointestinal (GI) symptoms associated with enteric-coated sulfasalazine (Azulfidine EN, AZL) in patients with rheumatoid arthritis (RA), we studied the clinical history of 153 RA patients, and any available data on GI symptoms that might have been associated with AZL. GI symptoms appeared in 64 (42.5%) of the 153 cases. There were 19 events of nausea, vomiting, or dyspepsia, 14 events each of epigastric discomfort and reduction or loss of appetite, 10 events of epigastric, stomach, or abdominal pain, 9 events of heartburn, 8 events of mouth ulcer, 3 events each of loss of taste and abdominal bloating or borborygmus, 2 events each of diarrhea or loose stools, hematemesis or melanemia, and gastric or esophageal ulcer, and 1 event of stomatitis. These results indicate that GI symptoms associated with AZL are usually mild and treatment can continue, with almost all cases responding to a reduction in dose or drug cessation. In some cases, a histamine receptor-2 blocker or proton pump inhibitor is also required.

The addition of sera from patients with collagen diseases, particularly those with vascular complications, to the supernatant of cultured vascular endothelial cells (EC) in vitro significantly increased the surface and intracellular amounts of von Willebrand factor antigen (vWF:Ag) compared with results obtained with sera from normal healthy subjects. Peak levels of vWF:Ag occurred after 24 h of in vitro culture. Moreover, the amounts of vWF:Ag secreted into the EC supernatant with patient serum added were significantly higher than the amounts secreted into EC supernatant with control serum added, even after 48 h of in vitro culture. Levels of large and intermediate multimers (LIM) of von Willebrand factor (vWF) increased in EC supernatant exposed to serum from patients with collagen diseases as compared with levels in supernatant exposed to serum from normal controls, whereas no significant differences were detected overall between adding the plasma of patients and of normal subjects. In addition, C-reactive protein (CRP) induced a time- and dose-related release of vWF:Ag from EC, while glucocorticoid did not effect the release of vWF:Ag from EC. These results suggest that the sera of patients with collagen diseases, particularly those with vascular complications, stimulate the production and release of LIM of vWF from EC.