Immune thrombocytopenia in lymphoproliferative diseases.

We have studied the thrombocytopenia of lymphoproliferative disorders using a measurement of membrane-bound IgG by an antiglobulin consumption assay. Nine patients with chronic lymphocytic leukemia (CLL) and thrombocytopenia had increased membrane-bound IgG. Two patients with non-Hodgkins lymphoma and 1 patient with Hodgkins disease also had thrombocytopenia and increased membrane-bound IgG. Five of the patients with CLL had positive direct antiglobulin (Coombs) tests on red cells; of these, 3 patients had hemolytic anemia. In eight of the 9 patients with CLL, thrombocytopenia, and increased platelet-bound-IgG, the platelet count increased with the administration of prednisone or an alkylating agent, with splenectomy, or with a combination of these.

Platelet-bound complement (C3) in immune thrombocytopenia.

The fixation of complement to the circulating platelet in immune thrombocytopenia was detected by measurement of one of the complement components, C3, on the surface of platelets from patients with idiopathic thrombocytopenic purpura (ITP) and systemic lupus erythematosus (SLE) using the anti-C3 consumption assay. The surface IgG was determined simultaneously using the previously described anti-IgG consumption assay. Washed platelets from normal controls had 3.5 fg (10(-15) g) of C3, or about 11,000 molecules, per platelet, an amount comparable to the IgG (4.1 FG, or 15,000 molecules, per platelet). For most patients with ITP both C3 and IgG were increased on the platelet surface, although for 5 of 16 patients only IgG was increased. Two patients with SLE and thrombocytopenia had an increase in both C3 and Ig, six patients with SLE who were not thrombocytopenic had normal amounts of membrane-bound C3 and IgG. In 5 patients, 3 with ITP and 2 with collagen vascular disease, both surface immunoproteins decreased with successful treatment of the thrombocytopenia.

Pulmonary mucormycosis: another cure.

Pulmonary mucormycosis in an ill patient with poorly controlled chronic lymphocytic leukemia was diagnosed with open lung biopsy without excision. He improved on medical management and became ambulatory. At autopsy one year later, no residual mucormycosis was present. Better control of leukemia and more specific antimicrobial therapy are discussed as potentially important factors in patient management.

Gastric operations and glucose homeostasis. II. glucagon and secretin.

Alimentary hyperglycemia in patients who have undergone gastric operations may be due, in part, to altered intestinal signals for glucose disposition. We measured glucose, immunoreactive insulin (IRI) pancreatic glucagon (IRG), and glucagon-like immunoreactivity (GLI) after oral glucose in patients with prior antrectomy or vagotomy and pyloroplasty and in normal individuals. All subjects had normal assimilation coefficients for intravenous glucose, which suggests that the responsiveness of the pancreatic beta-cells had not been altered by the surgical procedures. The early hyperglycemic response to oral glucose and the associated elevation of plasma GLI were much greater and the IRI levels slightly higher in both experimental groups in comparison to normal subjects. A decrease in the level of IRG, albeit not statistically significant, was noted in all groups after the ingestion of glucose. In gastrectomy patients, secretin infusion during repeated oral glucose tolerance tests partially corrected the hyperglycemia and lowered plasma GLI and IRI levels. The responses of the vagotomy and pyloroplasty patients and of the normal subjects were not altered by secretin infusion. We conclude that the intolerance or oral glucose after gastric surgery may be related to elevated GLI levels, and that the beneficial effect of secretin may be due to its ability to decrease these levels.

Meningeal mycosis fungoides: clinical and cellular characteristics.

A patient with mycosis fungoides developed meningeal disease while his skin disease was in remission with systemic chemotherapy. His central nervous system involvement with mycosis fungoides was controlled with intrathecal methotrexate for 7 months. The proliferating cells recovered from the spinal fluid showed similarities to the Sézary cell by light and electron microscopy. Surface receptor sutudies suggested that these cells were lymphoid cells of thymic derivation. Although mycosis fungoides has been shown to spread to the central nervous system in autopsied cases, reports of clinical neurologic disease are rare, and in only one earlier report have malignant cells have been found in the spinal fluid. Thus, as in other lymphoproliferative disorders, prompt consideration of meningeal involvement in a patient exhibiting neurologic symptoms while in peripheral remission may allow earlier treatment of this complication.