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Biomedical subjects

J Forsström

Publications and source records attributed to J Forsström.

At least 37 records · Page 2Linked to original sources
PubMed1985

Serum cysteine proteinase inhibitors with special reference to kidney failure.

Serum levels of proteins reactive in radioimmunoassay with an antiserum prepared in rabbits against purified human spleen neutral cysteine proteinase inhibitor (NCPI) was determined in 70 healthy controls and from 80 patients suffering from suspected or proven kidney failure. The values varied from less than 0.2 mg/l in normal sera to levels over 2 mg/l in some patient sera. Serum level of NCPI was found to roughly correlate with serum creatinine values. However, there were sera with high NCPI levels which did not have increased serum creatinine values. In sera with high NCPI levels subjected to double radial immunodiffusion two precipitin lines, one completely and the other partially identical to NCPI were registered. After fractionating of serum proteins with gel chromatography on Sephadex G 100, two protein peaks of immunological similarity to purified NCPI were found: one low molecular weight (MW around 12,000) and one high molecular weight (MW around 100,000). The low molecular weight NCPI-like material appeared to inhibit human cathepsin B and papain and is thus free serum NCPI. alpha-Cysteine proteinase inhibitor did not increase with serum creatinine as did NCPI.

Blood Proteins↗
PubMed1982

Influenza vaccination in patients with chronic renal failure.

27 patients with chronic renal failure (CRF), 12 of whom were on maintenance hemodialysis, and 40 healthy control individuals were immunized with a split-type influenza vaccine containing A/Victoria/75 (H3N2), A/USSR/77 (H1N1), B/Hong Kong/73 antigens; 2 doses were given 4 weeks apart. Antibody responses were determined by the single radial hemolysis (SRH) technique. After immunization a significant rise (increase in SRH greater than or equal to 2 mm) was measured to A/Victoria in 11 (73%) azotemic and in 11 (92%) hemodialyzed patients and in 35 (88%) controls. To B/Hong Kong a significant antibody rise was observed in 10 (67%) azotemic, in 11 (92%) hemodialyzed and in 27 (68%) control individuals. The mean prevaccination and postvaccination antibody titers in patients with CRF, either azotemic or hemodialyzed, were significantly lower than in healthy control individuals to both A/Victoria and B/Hong Kong antigens (p less than 0.001). On the other hand the mean antibody rises after vaccination were of the same magnitude in all groups. The patients on maintenance hemodialysis had lower prevaccination antibody titers but the postvaccination mean titers were slightly higher than in the azotemic patients. No adverse reactions to the vaccination or deterioration of the renal function were observed; thus we recommend an annual vaccination of patients with CRF.

Adolescent↗
PubMed1979

Plasma lipids on chronic uraemic and transplantation patients.

We studied the concentrations of total cholesterol, HDL-cholesterol and triglyceride in the plasma in renal (n = 48) patients. In undialyzed uraemic patients (mean serum creatinine value 439 mumol/l) the plasma cholesterol level was somewhat higher (6.47 mmol/l) than in the control (n = 27) group (5.67 mmol/l). HCL-cholesterol was lower (1.02 mmol/l vs 1.49 mmol/l) and the triglycerides higher (2.07 mmol/l vs 1.07 mmol/l) than in the control group. In dialyzed patients the cholesterol level (5.88 mmol/l) was lower but the triglyceride level higher (2.58 mmol/l) than in undialyzed patients. Renal transplantation corrected the lipid variables to a certain degree (plasma cholesterol 5.55 mmol/l, plasma HDL-cholesterol 1.27 mmol/1 plasma triglycerides 1.15 mmol/l) but HDL-cholesterol remained still somewhat lower than in the control group. No "critical level" of renal function at which the changes of lipoprotein metabolism arise, could be demonstrated, and it seems that e.g. HDL-cholesterol is low already when the diagnosis of renal insufficiency is made.

Adolescent↗
PubMed1978

Does transient blocking of axonal conduction occur in uraemic neuropathy?

In uraemic and other patients with neuropathies, motor unit spike intervals were analysed using a special computer program to detect prolonged intervals of twice the normal duration, so-called "double intervals." These may have different causes--trigger failure, double discharge, or a transient fall in the firing rate of coactive motor units. There was not sufficient evidence that transient conduction blockings will occur in the main axon in uraemic neuropathies.

Axons↗
PubMed1977

Statistical variation of nerve conduction velocity. An analysis in normal subjects and uraemic patients.

The maximal nerve conduction velocity (NCV) of 6 sensory nerves (N. radialis, suralis and peronaeus superficialis, bilaterally) was determined in 88 normals and 59 uraemic patients. When the effect upon nerve conduction velocity of age and temperature was removed through partial correlations, it became possible to verify the negative correlation between the height of the patient and NCV. This explained as much as 35% of the remaining variance in males. There were also other significant differences in the nerve functions between the sexes. A set of "statistical corrections" (grouping of NCV's according to the subject's sex, computing of the average NCV's of an individual, and height-, age- and temperature normalization of single or mean NCV values) substantially decreased the variability of NCV. At the same time, the sensitivity of NCV measurement in the early diagnosis of nerve dysfunction caused by uraemia was increased. It is suggested that the results of NCV measurements should not only be reported as rough, absolute data, but also as normative values, taking into account the known physiological determinants.

Age Factors↗
PubMed1977

Transient changes of sensory nerve functions in uraemia.

The neurophysiological parameters (conduction velocity, amplitude and rise time of the compound action potential) of two sensory nerves of the lower limb (N. suralis and peronaeus superficialis) were determined bilaterally in five patients. Measurements were carried out at least twice in each subject during a time of great metabolic change. Two patients were recovering from acute renal failure (a single haemodialysis had to be performed on one of them) and three were under chronic maintenance haemodialysis. In the case of the haemodialysis patients, measurements were performed on two successive days, before and after one haemodialysis session. All the neurophysiological parameters showed significant improvement in successive measurements. In one patient the follow-up after acute renal failure revealed a delayed deterioration of the nerve functions, but after one year the values were normal. From the results it seems probable that an acute metabolic disturbance may cause transient inhibition of nerve functions without morphological changes in the nerve fibres.

Action Potentials↗
PubMed1977

Yersinia enterocolitica infection complicated by glomerulonephritis.

A case of mild glomerulonephritis in a 24-year-old man with clinical and immunohistological findings associated with Yersinia enterocolitica serotype 3 infection is described. The role of IgA in the pathogenesis of glomerulonephritis associated with mucosal infection is briefly discussed. Although attempts to demonstrate Y. enterocolitica 3 antigen in the biopsy specimen were unsuccessful, the glomerular deposits of immunoglobulins and complement suggest immune pathogenesis.

Adult↗
PubMed1976

The protein binding of diazepam and N-demethyldiazepam in patients with poor renal function.

The plasma protein binding of diazepam and of its main metabolite, N-demethyldiazepam, was measured in patients with renal disease and in healthy volunteers by ultracentrifugation. The total and non-protein bound concentrations of diazepam and N-demethyldiazepam, and the concentration of unconjugated oxazepam in the plasma were determined by gas chromatography after an oral 10 mg dose of diazepam. In the volunteers 98% of diazepam and N-demethyldiazepam were bound to the plasma proteins. In patients with renal disease the corresponding values were 92% and 95%, respectively. In the patients with renal disease no correlation could be found between the percent protein binding of diazepam or N-demethyldiazepam in the plasma and the serum creatinine concentration. Considerable variations in diazepam concentrations at 1 and 24 hours and in N-demethyldiazepam concentrations at 24 hours were found in the patients with renal disease. In contrast to the volunteers, 5 patients out of 28 with renal disease had measurable amounts of unconjugated oxazepam in the plasma. The deficient ability of the plasma proteins of patients with renal disease to bind diazepam may increase its clinical effect.

Adolescent↗
PubMed1976

Acute renal failure subsequent to the administration of rifampicin. A follow-up study of cases reported earlier.

A clinical presentation is made of a 2-3 year follow-up of six cases of acute renal failure that have been reported earlier. The patients had developed transient renal failure after the intermittent administration of rifampicin. The stage of olig-anuria lasted for 1-3 weeks, and five of the patients were treated by hemodialysis. Two of the patients died due to unrelated causes during the follow-up period. The four patients re-examined were clinically cured. Pathologic findings by light microscopy and immunofluorescence at biopsy were scarce. Nothing abnormal was seen by electron microscopy in two of the cases studied. Renal function was normal. In three cases the excretion at 131I-hippuran renography was slightly slowed. Although in the acute stage the renal lesions histologically appeared toxic, evidence suggestive of an immunological mechanism cannot be excluded.

Acute Kidney Injury↗
PubMed1975

Serum levels and half-life of sotalol in chronic renal failure.

The elimination of sotalol was studied in 25 patients with chronic renal failure. All patients were given a single 160 mg dose of sotalol orally and their sotalol serum levels were determined after 4, 6, 8, 10 and 12 hours. The elmination of sotalol was distinctly slower as the serum creatinine concentration rose. The half-lives, calculated graphically, were in lenear ratio to the serum creatinine values (r = 0,91; p less than 0.001). In accordance with the results, it is probable that sotalol accumulates in chronic renal insufficiency. Since beta-blockers may impair renal function, even in therapeutic concentrations, the dosage of sotalol, in particular, must be reduced in patient with kidney disease.

Administration, Oral↗