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A case report of simultaneous presentation of chronic neutrophilic leukemia and multiple myeloma (IgG kappa) in a 71-year-old male is described. The patient showed mature neutrophilic leukocytosis, hepatosplenomegaly, high neutrophil alkaline phosphatase score, hyperuricemia, neutrophils with toxic granulation and Döhle bodies, absence of Philadelphia chromosome and of the bcr-abl fusion gene. Moreover, a monoclonal IgG kappa paraproteinemia (36.93 g l(-1)) was detected. Bence-Jones proteinuria was 3.84 g l(-1). The bone marrow was grossly hypercellular with marked myeloid hyperplasia and aggregates of plasma cells. The patient died of severe bronchopneumonia after the transformation of chronic neutrophilic leukemia to acute myelomonocytic leukemia, 1.5 years following diagnosis.

Primary pure red cell aplasia (PRCA) was diagnosed in two male patients, 65 and 69 years old respectively. In both, surface markers of peripheral blood nuclear cells revealed the presence of TCR alphabeta+ phenotype. Clonality of T cells was confirmed by the polymerase chain reaction in both patients, in whom, prednisone at a dose of 1 mg/kg/day improved the anemia and lower doses caused its renewal, resulting in the reappearance of the patient's transfusion requirement. On the other hand, the anemia seems to have been treated permanently (second case) with horse antithymocyte globulin (ATG) (20 mg/kg/day 1 to 8 +) since his hemoglobin was about 15 g/dl at the time of writing. In the first patient, the hemoglobin level was 10.5 g/dl one month after the administration of ATG (15 mg/kg/d 1 to 5 +), but unfortunately, the patient died because of a massive gastrointestinal bleeding on the fortieth day following this treatment. We, therefore, suggest that, patients with acquired primary PRCA should be screened to detect the presence of a T-cell clone and recommend that, treatment should start earlier with ATG, if the PRCA is due to a T-cell clonal disorder.

For the diagnosis of bone metastasis in breast cancer patients during systemic treatment serum tumor markers, including carbohydrate antigens 15-3 (CA 15-3) and 19-9 (CA 19-9), cancer antigen 125 (CA 125), alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), beta-2 microglobulin (BMG), ferritin, and tissue polypeptide antigen (determined by the M3 monoclonal antibody, TPS) were measured in 22 patients with known bone metastases and in 30 patients without documented metastases. The most useful single marker was CA 15-3. By stepwise discriminant analysis, it was found that 90% of the patients could be diagnosed truly by using the markers CA 15-3, BMG and ferritin. It is concluded that monitoring with combinations of tumor markers at regular intervals increases the diagnostic efficiency.

Haptoglobin and transferrin types were examined in Eti-Turks. The Hp1 frequency was 0.26. With the exception of two individuals with transferrin D, only the transferrin C was observed. The gene frequencies were in the range of most of the Asiatic populations including Turks.

A series of 14 patients with Wilson's disease were evaluated in order to determine the characteristic bone changes found in this metabolic disorder. The following radiologic and clinical findings deserve to be summarized: (1) Osteoarticular pains as first manifestations of Wilson's disease were found in six patients. (2) In all but 2 of our patients, minor or moderate or even severe bone abnormalities characteristic for Wilson's disease were observed. (3) There were three groups of sibs. Among these sibs, the lesions were not only similar in type but were also acquired approximately at the same time, showing the influence of the different genes responsible for this metabolic disorder.

The serum concentrations of neuraminic acid, CEA, gamma-Gt, 5-nucleotidase, haptoglobin, and alkaline phosphatase were determined before therapy and three and six months after the initiation of therapy in 42 patients with small cell bronchial carcinomas. Before therapy, a significantly increased serum concentration as compared to normal values was found for neuraminic acid in 97% of patients (43/44), for CEA in 54.7% (23/42), for gamma-Gt in 19% (8/42), for 5-nucleotidase in 11.9% (5/42), for haptoglobin in 36.3% (14/44), and for alkaline phosphatase in 9.5% of all patients (4/42). Three and six months later, these laboratory investigations did not give any valuable hint with respect to therapy results, with the exception of neuraminic acid (p less than 0.05). Prior to therapy, the concentrations of neuraminic acid were considerably increased in patients (mean = 3.16 +/- 0.47 mumol/ml) with regard to normal values (mean = 1.90 +/- 0.14 mumol/ml). Within the total group of 42 patients suffering from small cell bronchial carcinomas, there was no significant difference between the serum concentrations of neuraminic acid of eleven patients with localized tumors (mean = 3.12 +/- 0.53) and those of 31 advanced tumor patients (mean = 3.16 +/- 0.45) (p less than 0.05). During the six months' treatment period, the concentration of neuraminic acid was valuable as clinical parameter in 36 patients, i.e. 85% of all cases (0.001 less than p less than 0.01). It was shown that the serum concentration of neuraminic acid indicated a regression of the disease in 23 patients (p less than 0.001), a progression in 8 patients (0.02 less than p less than 0.05), and a regression with subsequent progression of the tumor in 5 patients (0.001 less than p less than 0.01).