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Biomedical subjects

I Nordback

Publications and source records attributed to I Nordback.

At least 91 records · Page 5Linked to original sources
PubMed1987

Lactoferrin in acute necrotizing pancreatitis.

Lactoferrin, as measured in the pancreatic juice, has been thought to be of diagnostic value in chronic pancreatitis, but due to the hazards in cannulation of the pancreatic duct in the acute phase of pancreatitis the behavior of lactoferrin has remained obscure. In this study, lactoferrin levels were studied in pancreas tissue specimens obtained in ablative surgery for acute necrotizing pancreatitis (ANP) and in serum samples. A higher pancreatic lactoferrin content was found in ANP than in normal pancreas. Lactoferrin seemed not to leak from a necrotic pancreas in any considerable amounts into the circulation, as no differences were found in serum lactoferrin concentrations between ANP and controls. It remains an open question whether the lactoferrin increase is only an unspecific reaction in inflammation or is something specific for pancreatitis.

Acute Disease↗
PubMed1987

Postprandial hyperglycemia after different carbohydrates in patients with total gastrectomy.

Eating related difficulties and symptoms and postprandial serum glucose levels were studied in 11 patients (44 to 70 years old) five to 48 months after total gastrectomy and Roux-en-Y reconstruction for carcinoma of the stomach with no signs of metastasis or residual tumor. Three tests were used. The first contained 150 milliliters of 50 per cent glucose alone, the second had 150 milliliters of 50 per cent glucose with 5 grams of guar gum (viscose dietary fiber) and the third was a vegetable meal containing 75 grams of glucose. All of the patients with total gastrectomy had eating related symptoms, such as dumping and difficulties with the large volume of a meal. They had to eat small meals and the most usually experienced postprandial symptoms were abdominal pain, nausea and faintness. The postprandial serum glucose level was highest after drinking glucose alone and the lowest after eating the vegetable meal (as the highest 9.4 +/- 2.0 and 6.2 +/- 1.6 millimole per liter, respectively, 50 minutes postprandially, p less than 0.01). Hyperglycemia was associated with nausea, sweating, faintness, reduction of blood pressure and increase of pulse rate. The large volume of the vegetable meal produced difficulties (dysphagia and abdominal distension) in eating for everyone except one patient. Guar gum eaten with glucose reduced the postprandial hyperglycemia near to the level found after the vegetable meal. Also, the symptoms experienced after glucose with guar gum reduced from that after glucose alone, five patients became symptomless. Four of these five patients have supplemented guar gum regularly for several months into their daily meals with the result of reduction of the postprandial subjective symptoms. The dose has been adjusted individually from 2 to 7 grams of guar gum three times daily. Loose stools and diarrhea may occur at the beginning. These are avoided by a gradual increase of the dose during an adaptation period of two weeks. Sometimes glucose with guar gum may result in hypoglycemia with prolonged symptoms after immediate hyperglycemia. It is concluded that guar gum gives a possibility to avoid the symptoms related to a large volume of a meal and to reduce those produced by a high glucose content of a meal in patients after total gastrectomy. Guar gum also works in practical prolonged use when the dose is estimated from postprandial symptoms.

Adult↗
PubMed1986

Clinical pathology of acute necrotising pancreatitis.

Seventy nine pancreatic specimens were obtained from patients treated with pancreatic resection for acute necrotising pancreatitis. The necrotising process had started in the periphery of the gland, so that eight of seventy nine cases contained peripancreatic (mainly fat) necrosis only without any parenchymal necrosis. Peripheral parenchymal necrosis was characterised by a severe inflammatory reaction, with multinucleated leucocytes and microabscess. In the deep parts of the pancreas coagulation necrosis was found. Vascular changes (thrombosis, vessel necrosis) correlated with postoperative haemorrhagic complications, but they did not seem to have any important role in the necrotising process. The vascular changes seemed to be a secondary phenomenon. In clinical practice the most important aspects in reporting the histology of acute necrotising pancreatitis are the extent of parenchymal necrosis, because the surgeon may overestimate its extent, and the existence of vascular changes, because of the correlation with postoperative recovery.

Acute Disease↗
PubMed1986

Complications after pancreatic resection for acute necrotizing pancreatitis.

The risks of pancreatic resection for acute necrotizing pancreatitis were evaluated in 37 patients, all with greater than or equal to 3 positive Ranson signs, most with extensive peripancreatic fat necrosis and almost half with extensive parenchymal necrosis. The mortality (43%), though comparable with most other reports, was higher than in the authors' earlier experience. The reason was not clear. Postoperative bleeding from the surgical field was the most common problem, being responsible for half of the deaths. Septicaemia due to abscess or fistulation occurred in eight patients and was fatal in five. Pulmonary and renal complications were common, but caused only three deaths. Time from onset of symptoms to operation did not influence complications or age-matched mortality. With increasing extent of resection, lung complications diminished, but not other complications or mortality. All patients older than 60 died. Resection thus should be avoided for the elderly, and its role in younger cases remains far from clear. The postoperative complications and insignificantly lower death rate than after other treatments have diminished the former enthusiasm for resection in acute necrotizing pancreatitis.

Acute Disease↗
PubMed1985

Determination of necrosis in necrotizing pancreatitis.

The diagnosis of necrosis and its extent in acute necrotizing pancreatitis is one main problem in establishing criteria for possible pancreatectomy. With this in mind a clinicopathological analysis was carried out on 54 patients who had undergone pancreatic resection for acute necrotizing pancreatitis. The macroscopic appearance of the gland correlated poorly with its histology. Parenchymal necrosis varied from 0 to 100 per cent of the resected specimen though all the glands were considered totally or subtotally necrotic. In the clinicobiochemical status no criteria were found determining the extent of necrosis. Obesity, hypotension, hypocalcaemia and elevated serum creatinine in severely ill patients (as determined by Ranson criteria) strongly supported extensive peripancreatic and septal necrosis; however, 38 per cent of patients developed necrosis without those stigmata. While waiting for new methods to determine necrosis we prefer conservative treatment. In contrast to our previous tactics we think that resection should be limited to extreme cases in order to avoid resection of glands with limited necrosis and thus mainly reversible parenchymal damage.

Acute Disease↗
PubMed1985

Clinicobiochemical factors in predicting gallstones in necrotizing pancreatitis.

Sixty-one patients with acute necrotizing pancreatitis were studied for age, sex, ASAT, ALAT, alkaline phosphatase, bilirubin and amylase 48 hours after admission, these factors having recently been found to be significant in predicting this gallstone-associated disease. Age, ASAT, ALAT and alkaline phosphatase were found to be significant. However, 38 per cent of the patients with pancreatitis and gallstones remained unidentified with these criteria only. Thus, more intensive methods of investigation should be used whenever gallstone-associated pancreatitis is suspected. Increased hepatic chemistry could seldom be explained by the necrotizing form of pancreatitis if there was no biliary tract cause.

Acute Disease↗
PubMed1985

Migration of Kirschner pin from clavicle into ascending aorta.

Kirschner pins are widely used for fixation of bone, with few and very rarely serious complications. A case is described in which a Kirschner pin migrated in 10 days from the sternal end of the left clavicle into the lumen of the ascending aorta. The exact location of the pin remained unknown until right thoracotomy, during which X-ray examination revealed the unexpected situation. The pin was simply extracted by pushing it through the vessel wall. The patient recovered uneventfully. The complication could have been prevented by bending the outer part of the pins. The possible route of migration is discussed.

Adult↗
PubMed1985

Secondary appendicitis--a sign of some other intra-abdominal inflammation.

An operation was performed on a 37-year-old man with symptoms of acute appendicitis. A severely inflamed appendix was removed. Histology, however, showed an atypical picture of inflammation: the outer layers of the appendix were severely inflamed but the epithelium was intact. Re-laparotomy revealed an abscess around a perforated Meckel's diverticulum, with no evidence of complications at the site of appendicectomy. It appeared that the appendix had become inflamed directly from the primarily inflamed Meckel's diverticulum. The case shows that a careful exploration of the neighbouring organs as well as the dissection of the specimen by the surgeon himself is indicated during laparotomy despite detection of appendicitis. To distinguish the situation described here from classical appendicitis we suggest the term secondary appendicitis to define the direct invasion of inflammation to the appendix from an adjacent organ.

Acute Disease↗
PubMed1984

Side incidence of inguinal hernias.

The reason for the right side predominance of inguinal hernias was studied. The case histories of 469 patients who had undergone inguinal hernia operations were analysed. 116 of the hernias were bilateral whereas 207 were right and 146 left sided, the difference being significant at the level p less than 0.05. More right than left hernias were found in every subgroup studied (children, women, men; direct, indirect, older people; with suspected increased intra-abdominal pressure). Neither of the two hypotheses envisaged for this side difference could be confirmed. These were a structural side difference in the inguinal canals, and a neuromusculature damaging abdominal incision. It is postulated that a physiological asymmetricity of the body musculature could be an explanation rather than any anatomical reason.

Abdominal Muscles↗
PubMed1982

Characterization of progesterone-independent avidin production of chicken tissues in culture.

1. Primary cell cultures of chick oviduct, intestine, peritoneal membrane and lung, but not those of wing muscle or calcaneal tendon, produced avidin progesterone-independently through a 5-week culture. 2. Actinomycin D and cycloheximide, but not hydroxyurea, inhibited the avidin production. 3. The common feature of the cultures producing avidin was a fibroblast-like cell type. 4. Similarly, oviduct and lung, but not muscle or tendon, also produced avidin in hormone-free short-term organ cultures, where the avidin synthesis began during the first 8 h of culture. 5. Induction of the general protein synthesis does not explain the avidin production, since another egg-white protein, ovalbumin, was not induced by the culture procedure.

Animals↗
PubMed1982

Effects of glucocorticoids and disodium cromoglycate on avidin production in chick tissues.

The effects of anti-inflammatory glucocorticoids and a membrane stabilizer (disodium cromoglycate) on avidin induction were studied. Chicks were primed for 0, 3 or 7 days with diethylstilboestrol (DES; 0.5 mg/day per animal, s.c.). Actinomycin D (0.2 mg/kg, i.p.) stimulated avidin production in the oviduct, intestine, lung and wing muscle of both DES-primed and unprimed chicks. Prednisolone (5 mg/animal, i.m.) given 1 h before actinomycin D reduced the avidin amounts to control levels in the unprimed oviducts and in non-oviductal tissues. The signs of inflammation (ascites, oedema) in chicks receiving actinomycin D also disappeared with prednisolone premedication. Cortisol (50 mg/animal, i.m. or 1, 5 or 50 microgram/ml medium), prednisolone (5 mg/animal, i.m. or 0.5, 5, 10 or 50 microgram/ml medium) and dexamethasone (1 mg/animal, i.m. or 0.05 or 0.5 microgram/ml medium) stimulated avidin production in DES-primed oviducts in vivo and in vitro. Culture in vitro induced avidin production in lung and oviduct but not in wing muscle. This avidin production in culture was not inhibited by cortisol, prednisolone or disodium cromoglycate. It is concluded that actinomycin D induces avidin production through its inflammatory effect and that the induction can be prevented by anti-inflammatory glucocorticoids. It is proposed that the 'spontaneous' avidin production in culture is not the effect of trauma during tissue preparation but rather a new form of avidin induction.

Animals↗
PubMed1982

Massive hemothorax in a child after removal of subclavian vein catheter.

A case is described where a near-fatal hemothorax developed in a child (age 13 months) right after the removal of the subclavian vein catheter. The catheter was introduced a week earlier and it had functioned without disorder. The possible mechanism of the complication is discussed. Even though this kind of complication is very rare, we recommend that the patients, especially children, must be carefully watched also after removal of the subclavian vein catheter to find a possibly life-threatening complication immediately.

Catheterization↗
PubMed1981

Progesterone-independent avidin in chick oviduct fibroblast culture.

The production of avidin was studied in chick oviduct cell cultures derived from immature chicks or from chicks with 4, 8, or 14 days of estrogen priming in vivo. Cells were grown for 5--7 weeks, and the monolayers formed were composed of collagen-producing fibroblasts. In some cultures, epithelial cells were also found, but only in the original explants. Two-day avidin production of cultures was measured in the media weekly. Cultures produced avidin spontaneously, the amount being fairly stable during the 7-week culture period. No difference was found in avidin production or cell morphology when estrogen-containing medium was used. Cultures from 4- to 8-day-estrogen-primed chick oviducts produced the same amount of avidin as cultures from immature oviducts, whereas further estrogen pretreatment seemed to reduce avidin production. Progesterone did not enhance avidin production with or without estrogen priming but, due to its inhibition of growth, clearly inhibited avidin when it was continuously in the culture medium. It is concluded that chick oviductal fibroblasts have an inherent capacity for avidin production and that this is independent of progesterone.

Animals↗
PubMed1981

Ultrastructural changes in immature chick oviduct epithelium during avidin induction by actinomycin D.

Avidin induction by actinomycin D may be mediated through cell damage. So the morphology of chick oviduct epithelium was studied 0-24 h after administration of actinomycin D (0.2 mg/kg, i.p.). The avidin content of the oviducts was measured by radioimmunoassay. There were several changes indicating cell damage in both the cytoplasm and nucleus. Marked vesiculation in and around Golgi complexes and the appearance of groups of light vacuoles occurred within 7 h of treatment. Swelling and breakage of mitochondria were found, the perinuclear cleft was enlarged and autophagosomes developed after 12 h. Invagination and swelling of the nucleus occurred during the experimental period. An increase in nuclear pores, polysomes and rough endoplasmic reticulum probably reflected the reparative processes of the cells. Ne secretory granules could be seen. Avidin accumulation began 7 h after actinomycin D, beginning simultaneously with the cell damage and earlier than the marks of regeneration. It is concluded that the avidin induced by actinomycin D is implicated in the severe cell damage caused by the drug.

Animals↗