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Biomedical subjects

U Kiistala

Publications and source records attributed to U Kiistala.

At least 37 records · Page 2Linked to original sources
PubMed1991

Lactate dehydrogenase, creatine kinase, and their isoenzymes in pleural effusions.

Lactate dehydrogenase (LD; EC 1.1.1.27) and creatine kinase (CK; EC 2.7.3.2) are widely distributed cytoplasmic enzymes. LD has five and CK has three isoenzymes distributed in different proportions in various tissues. The amounts of LD and CK and the distribution of isoenzymes in different body fluids are not thoroughly characterized. We have measured the total LD and CK concentrations and their isoenzyme distribution in pleural aspirates and in serum from 22 patients with benign conditions and from 14 patients with malignant effusions. In malignant pleural fluid, the mean total LD was 662 U/L; in benign conditions, it was nearly 5840 U/L with large variations (91-43 400 U/L) according to clinical diagnosis, the highest values being reached in inflammatory lesions. The mean total CK concentration in pleural fluid was close to the serum value in both groups of patients, as was the pleural CK isoenzyme distribution. The LD isoenzyme distribution in pleural effusions differed from that in serum in both groups, with LD-4 and -5 being the main isoenzymes in their pleural fluid specimens (greater than 42% of total LD). The total LD concentration correlated somewhat (r = 0.57) with the total pleural protein content. In conclusion, the pleural LD isoenzyme distribution, both in benign and malignant conditions, differs from that in serum, having shifted towards more anaerobic and embryonic isoenzymes (LD-4 and -5). Moreover, the greater the concentration of pleural total LD, the greater the proportion of LD-4 and -5. These data suggest that visceral or parietal pleural cells are rich in LD isoenzymes 4 and 5.

Adolescent↗
PubMed1989

Epidermis is the origin of high creatine kinase levels in skin blister fluid.

Creatine kinase (CK) isoenzyme, CK-BB, known as the brain fraction, is not normally present in serum but predominates in several normal and malignant tissues and body fluids. We recently reported increased CK-BB levels in suction blister fluid. In the present study the cellular origin of the enzyme in skin was studied from homogenates of blister top epidermis and blister base dermis as well as from homogenates of split skin dermatome shavings and isolated keratinocytes. The CK-BB in human skin was derived almost exclusively from the epidermis. Enzyme determinations from various spontaneous bullae suggest that all types of skin blisters initially contain high CK-BB levels.

Biopsy↗
PubMed1988

The BB-isoenzyme is a major component of creatine kinase in skin blister fluid.

We measured levels of creatine kinase and its three isoenzymes in serum and blister fluid from 16 healthy volunteers. The BB-isoenzyme was found to be the predominant form in blister fluid while only the MM isoenzyme was found in serum. The levels of BB-isoenzyme in blister fluid decreased as the blisters aged. The source of BB-isoenzyme in blister fluid is most probably the damaged epidermis.

Adult↗
PubMed1987

Baseline water loss and sweat gland response in acne patients during treatment with isotretinoin.

Eleven acne patients were treated with isotretinoin for 3-7 months. The water barrier function and the response of sweat glands to dilute methacholine injections were examined on upper back skin at onset and at several visits during therapy. Bilaterally located test sites representing healthy skin or skin sites which were least affected by acne lesions were selected for the study. The same sites were used at each visit for assessing the parameters. Although skin dryness was a common finding on the face and arms, no significant changes in baseline water loss (BWL) rates were found on the back skin during isotretinoin treatment. Instead there was a significant increase in the sweat gland responsiveness to methacholine during isotretinoin treatment as measured by the evaporimetric technique. Furthermore, in four out of five patients the numbers of active sweat glands, counted in plastic imprints from the stimulated test sites, showed a similar increase during therapy when compared to pretreatment values.

Acne Vulgaris↗
PubMed1986

Proteolytic enzymes in blister fluids from patients with dermatitis herpetiformis.

Proteolytic enzymes may be involved in blister formation in dermatitis herpetiformis (DH). We have examined collagenase, gelatinase and elastase-like enzyme activities in fluids collected from spontaneous blisters and from suction blisters raised on developing DH-lesions induced by application of potassium iodide. Control suction blisters were raised on unaffected DH-skin and on healthy volunteers. High enzyme activities were found in spontaneous blisters, and suction blister fluids obtained from developing lesions showed increased levels of gelatinase and elastase-like enzymes. Inhibitor studies revealed that a part of the elastase-like enzyme activity might be derived from inflammatory cells. Gel filtration chromatography disclosed two separate elastase-like enzymes which, as they had high molecular weights, could be either enzyme-inhibitor complexes or aggregates.

Blister↗
PubMed1986

Characterization of elastase-like enzymes in various blistering diseases.

Blister fluid samples were collected from suction induced control blisters and from spontaneous blisters from various blistering diseases for the measurement of elastase-like enzyme activities using synthetic succinyl-L-(alanyl)3-paranitroanilide (SAPNA) and alanyl paranitroanilide (ala-PNA) as the substrates. The blister fluids derived from bullous pemphigoid, pyoderma or epidermolysis bullosa dystroficans lesions contained higher levels of elastase-like enzyme activities than burn blisters or fresh suction blisters. The gel filtration studies using Sepharose CL-4B chromatography revealed two major peaks of SAPNA hydrolysing enzyme activity in burn blister and in bullous pemphigoid blister. The first peak eluted in void volume, and the second peak had an apparent molecular weight of 2.5 X 10(5) daltons. The results indicate that various proteinases are present in blisters fluids and that they may participate in the blister formation by degrading structural components of the basement membrane zone and the dermis.

Aniline Compounds↗
PubMed1984

Suction blister device with regulation of temperature: demonstration of histamine release and temperature change in cold urticaria.

A suction blister device with a sensitive thermometer and with a temperature regulator was constructed. Utilizing this device, it was demonstrated that the cold challenge induces an increase in the skin temperature in cold urticaria patients during the cold challenge and a simultaneous release of histamine into the suction blisters. The skin temperature increases faster after the cold challenge period in cold urticaria patients than in normal control persons. This could be explained by vasodilatation and increased circulation in the skin, following the release of histamine in the cold urticaria reaction.

Cold Temperature↗
PubMed1984

Enhanced neutrophil migration in vivo HLA B27 positive subjects.

Chemotaxis of polymorphonuclear leucocytes in vivo was studied in patients with previous yersinia arthritis and in healthy subjects with or without HLA B27 by means of a skin chamber technique. Irrespective of previous arthritis the number of neutrophils in the chamber media was significantly higher in HLA B27 positive subjects than in those without HLA B27. The amounts of prostaglandins E2, F2 alpha, and 6-keto-F1 alpha in the chamber media correlated positively with the corresponding cell counts. The present results give credence to the view that the hyperreactive neutrophils and the vasodilatory prostaglandins produced by them can together trigger a vicious circle which results in increased inflammatory symptoms in patients with yersinia arthritis who have HLA B27 as compared with those who lack this antigen.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Local sweat stimulation with the skin prick technique.

Intracutaneous injections of cholinergic agonists are usually employed for induction of local sweating. The possibility to apply a less painful skin prick technique as a sweat test was examined. Pricks were made on the forearm skin of 25 young men by puncturing the skin through drops of methacholine (MCH) and control saline solutions with lancets having a point length of 1 mm. The drops were kept on skin for 10 min and were then wiped off. Using an evaporimeter the measurements of water loss (WL) were started 5 min later and continued at 5 min intervals. Sweat loss (SL) was calculated from the difference of rates of evaporative WL recorded at the MCH and saline pricks. Ten, 1, 0.1, and 0.01% solutions of MCH elicited the following average peak evaporative sweat losses: 107.1, 77.5, 32.4 and 5.4 g m-2h-1. Both the degree and duration of the sweat responses were dependent on concentration. The prick technique is well tolerated and may serve for comparative studies of local sweating.

Adolescent↗
PubMed1983

Neutrophil function and HLA-B27.

The pathogenesis of HLA-B27 linked diseases, including reactive enteroarthritides, is not known. Differences in immune response, cross-reaction between microbial antigens and host cell structures, attachment of microbial components on the host cell surfaces with subsequent autoimmune reaction, and inflammatory responsiveness of the host may be involved. In this contribution we present evidence to show that HLA-B27 positive subjects may be prone to an exaggerated inflammatory response, as compared with HLA-B27 negative subjects.

Arthritis, Infectious↗
PubMed1983

Demonstration of collagenase and elastase activities in the blister fluids from bullous skin diseases. Comparison between dermatitis herpetiformis and bullous pemphigoid.

We have investigated potential mechanisms for blister formation by assaying proteolytic enzymes in the blister fluids of patients with various bullous diseases. Blister fluids were obtained from patients with dermatitis herpetiformis (DH), bullous pemphigoid (BP), chronic bullous disease of childhood (CBDC), and pemphigus vulgaris (PV). The cells were recovered by centrifugation, and the supernatants as well as the cell pellets were assayed first for collagenase activity using [3H]proline-labeled type I collagen as substrate. Collagenase activity could be detected in most cases with DH, BP, and CBDC, while no activity was found in 2 cases of PV or in 5 control blister fluids obtained from suction blisters induced in healthy control subjects. Elastase activity was assayed in the same blister fluids by using a synthetic substrate succinyl-(L-alanyl)3-paranitroanilide or soluble [14C]valine-labeled tropoelastin. High levels of elastase activity were present in all DH patients, while lower, but clearly detectable, levels were found in BP, CBDC, and PV. The enzyme activity in BP was inhibited by Na2EDTA, but not by phenylmethylsulfonyl fluoride (PMSF), and Ca2+ stimulated the activity, suggesting that the enzyme in BP was a metalloproteinase. In cell-free supernatants of the DH blister fluids, the elastase activity was markedly decreased by PMSF, indicating that most of the enzyme activity was due to a serine protease. The cells recovered from DH blister fluids also contained high levels of elastase activity which could be inhibited by PMSF but not by Na2EDTA. Thus, in DH, the elastase activity is probably derived from polymorphonuclear leukocytes abundantly present in the lesions. The results indicate that active proteases are present in the blister fluids of skin diseases, and they may play a mechanistic role in the blister formation by degrading connective tissue components of the dermis and the dermal-epidermal junction.

Adult↗
PubMed1983

A local potent glucocorticosteroid decreases the induction of galactosylhydroxylysyl glucosyltransferase in suction blisters but has no effect on basement membrane structures.

The effects of local glucocorticosteroid treatment on collagen biosynthesis and basement membrane components were studied in suction blisters in human abdominal skin. Pretreatment with clobetasol-17-propionate, applied three times a day for 4 days, did not affect the activity of galactosylhydroxylysyl glucosyltransferase (GGT) in fresh blisters but post-blistering treatment for 3 days with the steroid markedly inhibited the increase of this enzyme activity during the initial phases of re-epithelialization. The GGT activity was over 50% lower in steroid-treated blisters compared with control values. Protein concentrations and blister fluid volumes were also significantly decreased in healing 3-day blisters after steroid treatment. These results suggest that local glucocorticosteroid decreases either the synthesis of GGT or its release from the tissue into the blister fluid. The treatment did not affect the blister histology nor the early process of re-epithelialization. Immunohistochemically, type IV and V collagens and laminin of the basement membrane zone were similarly located in blisters of steroid-treated and placebo-treated skin, suggesting that local glucocorticosteroid does not affect the integrity of the basement membrane.

Adult↗