Essential cryofibrinogenaemia,leukocytoclastic vasculitis and chronic purpura

Abstract. Cryofibrinogenaemia refers to the presence of cold-precipitable proteins in plasma but not in serum. It is usually associated with malignancy, tromboembolic diseases or various inflammatory processes; rarely it may be essential. The most common clinical presentations of cryofibrinogenaemia are cold-intolerance, purpura, skin necrosis and ulcers. We describe a middle-aged woman with essential cryofibrinogenaemia, leukocytoclastic vasculitis, and chronic purpura for over 25 years with several exacerbations. In patients with otherwise unexplained purpura or skin necrosis, determination of plasma cryofibrinogen should be considered.     

THE DISAPPEARANCE OF HCG AND RETURN OF PITUITARY FUNCTION AFTER ABORTION

Plasma concentrations of HCG/LH and FSH were monitored after a first trimester abortion in eighteen healthy female volunteers three times weekly until the onset of first menstruation. Plasma concentrations of the HCG were measured with a specific RIA for the beta subunit (beta-sub-HCG) from the samples of six of these subjects. The elimination of HCG during the first 12 days was studied from plasma concentrations measured by the radioimmunoassay of LH. The experimental data were well explained by a mathematical model consisting of three exponentially decreasing components. The half-lives of the two more slowly decreasing components were 27 and 168 h. The estimate of the complete disappearance of HCG was 37.7 days, when the specific (beta-sub-HCG) assay was used. Recovery of pituitary function occurred within 4--9 days after abortion, as judged by increased plasma FSH concentrations. In fourteen of eighteen subjects a midcycle LH peak was observed which occurred between 16 and 29 days after abortion. Plasma oestradiol concentrations increased 2--16 days after the rise in plasma FSH. Considerable amounts of HCG still circulated in the blood but the preovulatory peak of oestradiol never began before HCG/LH concentrations had decreased to below the range of the mid-cycle LH peak.     

A case repot of Merkel cell carcinoma on chronic lymphocytic leukemia: differential diagnosis of coexisting lymphadenopathy and indications for early aggressive treatment

Background  

Chronic lymphocytic leukemia (CLL) is a monoclonal disorder, characterized by a progressive proliferation of functionally incompetent B lymphocytes. There is increased evidence of association between CLL and skin cancers, including the uncommon Merkel cell carcinoma (MCC).     

PERINATAL CAMPYLOBACTER FETUS SS JEJUNI ENTERITIS

ABSTRACT. Vesikari, T., Huttunen, L. and Mäki, R. (Department of Clinical Sciences, University of Tampere; Department of Paediatrics, Central Hospital of Päijät-Häme, and Department of Microbiology, Tampere Central Hospital, Finland). Perinatal Campylobacter fetus ss jejuni enteritis. Acta Paediatr Scand, 70:261, 1980. –A 2-day-old breast-fed male infant developed mucoid and bloody diarrhoea, and Campylobacter fetus ss jejuni was isolated from the stools but not from the blood. The probable source of transmission was his mother in whom symptoms of Campylobacter jejuni - associated illness began one day earlier. Both showed IgM, IgG and IgA antibody responses to autologous and reciprocal strains of Campylobacter jejuni as studied by ELISA.     

Effect of induced hypotension on serum concentrations of atropine after intramuscular administration

The serum concentrations of atropine after a single intramuscular injection of 0.01 mg/kg were determined by radioimmunoassay in nine general surgical patients during and after a combination anaesthesia and compared with those of 13 neurosurgical patients operated on during induced hypotensive anaesthesia (sodium nitroprusside plus trimetaphan). Surprisingly, comparable serum levels were found in both patient groups. We conclude that this kind of induced hypotension cannot be used as a model of drug absorption in such clinical situations as cardiac failure, haemorrhage or anaphylactic drug reactions.     

Enhanced Predictive Power of Quantitative TWA during Routine Exercise Testing in the Finnish Cardiovascular Study

Introduction: We examined whether quantification of T-wave alternans (TWA) enhances this parameter's capacity to evaluate the risk for total and cardiovascular mortality and sudden cardiac death (SCD).
Methods and Results: The Finnish Cardiovascular Study (FINCAVAS) enrolled consecutive patients (n = 2,119; 1,342 men and 777 women) with a clinically indicated exercise test with bicycle ergometer. TWA (time domain-modified moving average method) was analyzed from precordial leads, and the results were grouped in increments of 10 μV. Hazard ratios (HR) for total and cardiovascular mortality and SCD were estimated for preexercise, routine exercise, and postexercise stages. Cox regression analysis was performed. During follow-up of 47.1 ± 12.9 months (mean ± standard deviation [SD]), 126 patients died: 62 were cardiovascular deaths, and 33 of these deaths were sudden. During preexercise, TWA ≥ 20 μV predicted the risk for total and cardiovascular mortality (maximum HR >4.4 at 60 μV, P < 0.02 for both). During exercise, HRs of total and cardiovascular mortality were significant when TWA measured ≥50 μV, with 90 μV TWA yielding maximum HRs for total and cardiovascular death of 3.1 (P = 0.03) and 6.4 (P = 0.002), respectively. During postexercise, TWA ≥60 μV indicated risk for total and cardiovascular mortality, with maximum HR of 3.4 at 70 μV (P = 0.01) for cardiovascular mortality. SCD was strongly predicted by TWA levels ≥60 μV during exercise, with maximum HR of 4.6 at 60 μV (P = 0.002), but was not predicted during pre- or postexercise.
Conclusion: Quantification of TWA enhances its capacity for determination of the risk for total and cardiovascular mortality and SCD in low-risk populations. Its prognostic power is superior during exercise compared to preexercise or postexercise.     

Fibronectin in synovial fluid and tissue in rheumatoid arthritis

Fibronectin is a glycoprotein found in body fluids, loose connective tissue matrix and in basement membranes. Fibronectin in rheumatoid arthritis synovial fluid was immunologically indistinguishable from the plasma form, as shown by double-diffusion analysis. Fibronectin isolated from rheumatoid synovial fluid by affinity chromatography on gelatin--Sepharose had a polypeptide pattern similar to that of plasma fibronectin in SDS--polyacrylamide gel electrophoresis. In fifty-one patients with rheumatoid arthritis and related diseases fibronectin concentrations is synovial fluid were 445 +/- 103 micrograms/ml (mean +/- SD) and within normal range, 335 +/- 52 micrograms/ml, in plasma. Immunofluorescence staining showed a prominent increase of fibronectin in the proliferating synovial connective tissue in rheumatoid arthritis as compared to normal synovial membrane. The results suggest an increased local production of fibronectin in rheumatoid synovial tissue.     

The Asn-291→Ser and Ser-477→Stop mutations of the lipoprotein lipase gene and their significance for lipid metabolism in patients with hypertriglyceridaemia

We examined 99 Finnish patients whose serum fasting triglycerides (TG) had exceeded 6.0 mmol L^?1, with special interest to their lipid, lipoprotein and post-heparin plasma lipase activities. The control group consisted of 75 healthy individuals. We also determined the frequency of the Asn-291→Ser and Ser-447→Stop mutations both in hypertriglyceridaemic (HTG) subjects and in control subjects. A total of 51 of the original 99 hypertriglyceridaemic patients still had TG > 6.0 mmol L^?1 when measured a second time. They are referred to as persistently hypertriglyceridaemic subjects (pHTG). The remaining 48 subjects had TG < 6.0 mmol L^?1 in the second measurement and are referred to as sporadically hypertriglyceridaemic subjects (sHTG). The allelic frequencies of the Ser-447→Stop mutation in the total HTG and sHTG groups were similar to the frequencies present in the control group, but lower in pHTG patients compared with the control group (0.049 vs. 0.153, χ² = 6.63, P < 0.05). The Asn-291→Ser mutation was more frequent in HTG group than in the control group (0.0606 vs. 0.013, χ² = 4.86, P < 0.05). This difference was due to the higher frequency of the minor allele of Asn-291→Ser in the cohort with persistent hypertriglyceridaemia compared with the control group (0.088 vs. 0.013, χ² = 8.00, P < 0.01 ). The highest frequency (0.114) of the minor allele of Asn-291→Ser was found in type 2 diabetic patients with persistent hypertriglyceridaemia. The carrier status of Asn-291→Ser or Ser-447→Stop did not predict either post-heparin plasma lipoprotein lipase (LPL) activities or lipid and lipoprotein levels in any of the groups studied. Our data suggest that overproduction of very low-density lipoproteins (VLDL) is a more important cause of hypertriglyceridaemia in the Finns than is the LPL deficiency.     

Roles of purines in synaptic modulation evoked by hypercapnia in isolated spinal cord of neonatal rat in vitro

Background and purpose

The purine compounds, adenosine 5′-triphosphate (ATP) and adenosine, are known to accumulate in the extracellular space and to elicit various cellular responses during hypoxia/ischemia, whereas the roles of purines during hypercapnia are poorly understood. In this study, we examined the effects of various drugs affecting purine turnover on the responses to hypercapnia in the spinal cord.

Experimental approach

Electrically evoked reflex potentials were measured in an in vitro preparation of the isolated spinal cord of the neonatal rat by extracellular recording. Extracellular adenosine concentrations were assayed by high performance liquid chromatography (HPLC) methods.

Key results

Hypercapnia (20% CO₂) depressed the reflex potentials, which were partially reversed by an adenosine A₁ receptor antagonist, 8-cyclopentyl theophylline, but not by a P2 receptor antagonist, pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid. Exogenous adenosine and ATP also depressed the reflex potentials via adenosine A₁ receptors. The hypercapnia-evoked depression was not reversed by inhibitors of gap junction hemichannels, anion channels, P2X₇ receptors or equilibrative nucleoside transporters, all of which might be involved in purine efflux pathways. The adenosine accumulation evoked by hypercapnia was not inhibited by tetrodotoxin, ethylene glycol-bis(β-amino ethyl ether) tetraacetic acid (EGTA) or an ecto-ATPase inhibitor, ARL 67156. Homocysteine thiolactone, used to trap intracellular adenosine, significantly reduced extracellular adenosine accumulation during hypercapnia.

Conclusions and implications:

These results suggest that hypercapnia released adenosine itself from intracellular sources, using pathways different from the conventional exocytotic mechanism, and that this adenosine depressed spinal synaptic transmission via adenosine A₁ receptors.