Bone metabolism in patients with systemic lupus erythematosus. Effect of disease activity and glucocorticoid treatment.

The bone metabolism in patients with systemic lupus erythematosus (SLE) has previously been examined, but the results are conflicting. In the present study the bone mineral density (BMD) of the axial and the appendicular skeleton was examined by means of dual energy x-ray absorptiometry. The bone turnover was evaluated by means of biochemical markers in serum and urine in a prospective cohort consisting of 36 female and male SLE patients. Repeated measurements of BMD were performed for up to two years. The BMD was decreased in the hand and in the femoral neck but normal in the spine and in the distal forearm. A weak correlation was found between the BMD of the femoral neck and the total consumption of glucocorticoids. Apart from this finding the BMD was uninfluenced by treatment with glucocorticoids and cyclophosphamide. No significant changes of BMD were found during the follow-up period. The serum concentration of the carboxyterminal cross-linked telopeptide of type I collagen was increased in almost all patients, but no other biochemical markers of bone metabolism were abnormal.

Bone loss in rheumatoid arthritis. Influence of disease activity, duration of the disease, functional capacity, and corticosteroid treatment.

Axial and appendicular bone mass were studied in 95 patients with rheumatoid arthritis. The aims were to quantify bone mineral density (BMD) and to evaluate the importance of disease activity, duration of disease, functional capacity, and corticosteroid treatment for bone loss in patients with rheumatoid arthritis. The BMD in the lumbar spine (BMDSPINE) did not differ from age-matched healthy controls, but distal forearm BMD (BMDARM) and metacarpal BMD (BMDMCB) were significantly lower in the patients (p < 0.01 and p < 0.001, respectively). Neither BMDSPINE nor BMDMCB were related to the disease activity at the time of investigation. By contrast, BMDARM was decreased in patients with active disease. BMD in any of the three measured locations was not directly correlated to duration of the disease. However, the bone mass in the appendicular skeleton was already decreased within the first two years after the start of the disease. The overall functional capacity in terms of physical activity increased BMD in the axial skeleton. The local functional capacity in terms of grip strength was positively related to BMD in the appendicular skeleton. Patients with severe functional impairment had the lowest BMDARM. The decreased BMD in patients with rheumatoid arthritis seems primarily to be caused by an impaired physical activity which may be related to disease activity. Corticosteroids did not decrease BMD in neither the axial nor the appendicular skeleton. The antiinflammatory effect of steroids lead to clinical improvement, which may counteract the expected negative effect of these drugs on bone in rheumatoid arthritis.

[Primary antibiotic treatment of corneal ulcers in contact lens patients]. / Antibiotische Primärbehandlung von Hornhautulzera bei Kontaktlinsenträgern.

Two patient histories show that the therapy of contact lens corneal ulcers is complicated by bacterial resistance and mixed infection. To start an effective therapy against pseudomonas, gram-negative as well as gram-positive germs, a primary combination of tobramycin with fusidic acid seems to us as reasonable. Because of possible resistance to these antibiotics a smear should be taken from the ulcer and the contact lens case before therapy is begun and the clinical evolution must be controlled. In the choice of the antibiotics, the actual state of resistance and commercial availability was taken into account.

Specific aspects of depressed skull fractures in childhood.

From 1971 to 1982, 35 children with a depressed skull fracture (d.s.f.) were observed. Their data are used to trace specific aspects of aetiopathogenesis, characteristics, clinical picture, treatment and prognosis of d.s.f. in childhood and to propose guidelines for treatment and follow-ups. The most important causes were falls and road accidents. Celluloid ball fractures were observed mainly in infants and green-stick fractures in toddlers and schoolchildren, and the clinical diagnosis was possible in 70%. Skull defects following surgery did not change their size beyond the age of 1 year and should be covered as soon as possible. The outcome of mild d.s.f. is good, in d.s.f. with contusion the outcome depends on the severity of brain trauma, mental retardation and/or posttraumatic epilepsy being the most important sequels. The latter and mild types of d.s.f. with early seizures, dural tear or residual skull defects need further follow-up; EEG recordings are of some interest.

[Thrombosis in a probable double heterozygote young man from an asymptomatic family with protein C deficiency and protein C dysfunction]. / Thrombose bei einem wahrscheinlich doppelt-heterozygoten jungen Mann aus einer asymptomatischen Familie mit Protein-C-Mangel und Protein-C-Dysfunktion.

A family with combined quantitative and qualitative protein C deficiency is presented. The probably double heterozygote propositus with 7% residual amidolytic protein C activity had deep leg vein thrombosis at the age of seventeen. Other family members were asymptomatic.

[Constitutional dysfunction of heparin cofactor II with a tendency for venous thrombosis]. / Konstitutionelle Dysfunktion von Heparin-Kofaktor II mit venöser Thromboseneigung.

Simultaneous determination of heparin cofactor II (HC II) immunologically as antigen (HC II:Ag) and functionally as heparin cofactor (H-HC II) and as dermatan sulfate cofactor (DS-HC II) renders possible a distinction between quantitative and qualitative deficiencies. The usefulness of these methods is demonstrated in the light of a family with several heterozygotes of quantitative HC II deficiency and two unrelated heterozygote men with defective dermatan sulfate cofactor function (DS HC II) and normal HC II:Ag and H-HC II.

Heparin cofactor II: purification and antibody production.

Heparin cofactor II (HCII) was purified from plasma to homogeneity. The procedure includes adsorption with (A1)OH3, fractionation with polyethylene glycol 6000, chromatography on QAE-Sephadex A-50, on heparin-Sepharose 4B and on Sephadex G-150. QAE-Sephadex A-50 chromatography provides a good separation of HCII from antithrombin III (AT) and most contaminants having a heparin affinity similar to that of HCII. HCII is eluted at 0.28 M NaCl from the heparin-Sepharose column. After gel filtration on G-150, contaminating AT was removed by immunoadsorption. Purified HCII shows an apparent Mr of 66,500 daltons as analyzed on SDS-polyacrylamide gel and 62,100 daltons by ultracentrifugation. Antibodies to HCII were raised in rabbits. Former antisera mostly directed to a contaminating protein were used to remove it from the HCII preparation. Antibodies to HCII were made monospecific by immunoadsorption on HCII-free plasma linked to Sepharose 4B. Since many functional AT assays have neglected the presence of HCII in plasma, antibodies to HCII using as immunoadsorbent will provide a more specific test for AT.

Methodology and clinical significance of heparin cofactor II. Probable heparin cofactor II deficiency in a patient with cerebrovascular thrombosis.

HC II was functionally determined by thrombin inhibition in the presence of heparin in AT III-free plasma prepared by immunoadsorption on anti-AT III-Sepharose 4B column. HC II antigen concentration was assayed using specific antibodies to HC II. Simultaneously, AT III was measured. Plasma levels of HC II and AT III were determined in 110 patients with thrombotic tendency and two patients with obstetric complications and DIC. Highly significant correlations between activity and antigen prove the suitability of the methods. Reduced levels of HC II to about 50% with normal AT III values were repeatedly found in one patient with thrombotic tendency. The course of AT III and HC II during the process of DIC suggests that HC II may function as a thrombin inhibitor reserve when AT III becomes subnormally low.