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Biomedical subjects

R Jansson

Publications and source records attributed to R Jansson.

At least 19 recordsLinked to original sources
PubMed1991

Stressful life events and Graves' disease.

The role of stressful life events in the onset of Graves' disease (toxic diffuse goitre) is controversial. However, the numerous early clinical reports that supported such an association were not adequately controlled and specificity of the diagnosis could be questioned. Later studies have not shown a causal relation, but these studies were small, did not have proper controls, or epidemiological methods were inappropriate. To assess possible associations between life events, heredity, social support, and Graves' disease, we have done a population-based case-control study in a defined area with about 1 million inhabitants. Over 2 years, 208 (95%) of 219 eligible patients with newly-diagnosed Graves' disease and 372 (80%) of all selected matched controls answered an identical mailed questionnaire about marital status, occupation, drinking and smoking habits, physical activity, familial occurrence of thyroid disease, life events, social support, and personality. Compared with controls, patients claimed to have had more negative life events in the 12 months preceding the diagnosis, and negative life-event scores were also significantly higher (odds ratio 6.3, 95% confidence interval 2.7-14.7, for the category with the highest negative score). Individuals who had relatives with thyroid disease (especially first-degree and second-degree relatives) were more likely to have Graves' disease (3.6, 2.2-5.9). Slightly more patients than controls were divorced (1.8, 1.0-3.3) and reported a less frequent intake of alcohol (0.4, 0.2-0.8). When results were adjusted for possible confounding factors in multivariate analyses, risk estimates were almost unchanged. These findings indicate that negative life events and hereditary factors may be risk factors for Graves' disease.

Adult↗
PubMed1991

Effect of short-term indomethacin treatment on the clinical course of acute obstructive cholecystitis.

In acute obstructive cholecystitis the increased intraluminal pressure in the gallbladder is reduced by nonsteroid anti-inflammatory drugs which effectively relieve biliary pain. To investigate if such drugs influence the clinical course, a double-blind study was performed in which indomethacin (suppositories 75 mg b.d.) was tested against placebo in 34 patients with acute obstructive cholecystitis. During the 3-day treatment period both the indomethacin and the placebo group improved significantly as regards pyrexia, pain, abdominal tenderness and leukocytosis. The indomethacin group showed significantly greater improvement than the placebo group in temperature, pain and white blood cell count on day 1, and significantly greater reduction of abdominal tenderness on day 2. The serum bilirubin fell significantly during the 3-day period in the indomethacin, but not the placebo group. The hospital stay in cases without early surgery was significantly shorter in the indomethacin group (5.4 vs. 8.5 days). Because of its favourable effect on the clinical course of acute cholecystitis, rectally administered indomethacin is useful for patients awaiting operation or scheduled for later elective surgery.

Acute Disease↗
PubMed1990

Is a more active attitude warranted in patients with subclinical thyrotoxicosis?

In 1985 one of the new sensitive thyroid stimulating hormone (TSH) assays was introduced as part of our laboratory routine for thyroid function testing. Consequently, we now routinely identify a small but not insignificant group of patients with 'subclinical thyrotoxicosis', i.e. a low serum TSH in conjunction with a normal serum free T4. We here present the results of a 2-year follow-up investigation, which includes 40 patients with subclinical thyrotoxicosis and 40 euthyroid control patients. The group with subclinical thyrotoxicosis was characterized by a mean age of 65 years and a high prevalence of nodular goitre. Twelve (30%) of the patients but none of the individuals in the control group were treated during the follow-up period because of clinical thyroid disease. Atrial fibrillation was found in 11 (28%) patients compared to four (10%) of the controls. Therapy should be considered more often than previously in patients with nodular goitre and subclinical thyrotoxicosis, particularly in conjunction with atrial fibrillation.

Aged↗
PubMed1990

Effects of L-thyroxine and iodide on the development of autoimmune postpartum thyroiditis.

In the present study we examined the influence of L-T4 and iodide on autoimmune postpartum thyroiditis. Women at risk of developing the disease were identified in early pregnancy by the presence of moderate or high titers of antibodies against thyroid peroxidase (TPOAb). They were given no treatment (n = 20), 0.1 mg L-T4 daily (n = 18), or 0.15 mg iodide daily (n = 20) for 40 weeks postpartum. Changes in thyroid function were seen in all women, although in nine hormone values remained within the reference ranges of erthymoid individuals. In each group of women, thyrotoxicosis occurred around 2-3 months postpartum, followed by a gradual rise of TPOAb. Subsequently, around 5-7 months postpartum, a hypothyroid phase was observed. TSH elevations (greater than 5 mU/L) occurred in 9 of 18 women in spite of treatment with 0.1 mg L-T4 although elevations were lower than in the other two groups. Among those women who developed abnormal thyroid function, the hormone changes appeared greater in the iodide-treated group than in the control group, suggesting that in certain patients iodide may aggravate rather than ameliorate the disease. All 58 women showed a reduction of TPOAb during pregnancy and a transient rise during the postpartum year. The extent of TPOAb elevations did not differ between the groups. Thus, the administration of L-T4 prevented hypothyroid symptoms, but did not alter the course of the postpartum thyroiditis, which appears not to be accelerated by events of target cell origin.

Adult↗
PubMed1990

Factors influencing the outcome of thyrostatic drug therapy in Graves' disease.

In patients with Graves' disease, thyrostatic drug treatment may induce definitive remission without the need of more aggressive measures such as surgery or radioiodine. Following drug therapy, however, relapses often occur. In the present study, a multivariate analysis of pretreatment variables was performed, in order to identify individuals running a high risk of an unfavourable outcome of thyrostatic drug therapy. We studied 109 consecutive patients with a mean age of 38 years, range 20-70, over a mean follow-up period of 5.3 years after cessation of therapy. The analysis showed that goitre size, age, thyroid hormone levels, HLA-DR 3 haplotype, and TSH receptor antibody levels were of prognostic significance, whereas HLA-B8 haplotype, a lymphocytic infiltrate at fine needle biopsy, thyroglobulin, and microsomal antibodies had no such value. In particular, patients characterized by young age, large goitre and high hormone values were found to be associated with an unfavourable course.

Adult↗
PubMed1988

Postpartum thyroiditis.

The special characteristics of postpartum thyroid syndromes are summarized in Table 8. Many of the cases will pass unnoticed, although a higher detection rate is to be expected if postpartum thyroid disease becomes better known among physicians and the general public. Screening in early pregnancy of women with a previous or family history of thyroid disease and in women with other autoimmune disorders (such as diabetes mellitus type 1) may be worthwhile. The initial manifestation of postpartum thyroiditis, often appearing during the first three months postpartum, is a thyrotoxic phase characterized by a low RAIU ('painless thyroiditis' or 'destruction-induced thyrotoxicosis'). Subsequently, a transient hypothyroid phase supervenes. In a small proportion of women hypothyroidism becomes permanent. After a subsequent pregnancy recurrence is the rule. Women who are genetically disposed to Graves' disease may experience thyrotoxicosis with a high RAIU usually appearing later than three months postpartum. As the thyroid function abnormalities are usually mild and transient it is often appropriate to withhold treatment. However, in women with pronounced symptoms treatment should be started. When the postpartum period has passed gradual withdrawal of treatment should be attempted. In women who have experienced postpartum thyroid dysfunction, the risk of developing permanent thyroid disease in later life seems important and therefore long-term follow-up is recommended.

Female↗
PubMed1987

The postpartum period constitutes an important risk for the development of clinical Graves' disease in young women.

In the present study, 93 consecutive women, 20-40 years of age, referred to our clinic from 1976-85 with Graves' disease, were examined with respect to a possible relation between onset of disease and previous pregnancy. An increased relative risk of 6.5 (3.8-11.0, 95% confidence interval) of developing Graves' disease within one year following delivery was found. After excluding the nulliparous women, almost 2 out of 3 women who developed Graves' disease in the principal child-bearing age of 20-35 years had a postpartum onset, suggesting an important role of immunomodulatory events following delivery for the development of this disease in young women. Future studies will ascertain to which extent the recognition of postpartum Graves' disease has implications on the choice of therapy in this group of women.

Adult↗
PubMed1987

Familial and sporadic medullary thyroid carcinoma: clinical and immunohistological findings.

We have studied the clinical and thyroid immunohistological features of 19 patients with sporadic medullary thyroid carcinoma and 16 patients with the hereditary syndrome multiple endocrine neoplasia 2a (MEN 2a). Both groups were identified by family screening using serum calcitonin determinations before and after pentagastrin stimulation. Pheochromocytoma and hyperparathyroidism were associated both with multiple endocrine neoplasia 2a and some cases of sporadic medullary thyroid carcinoma. Hereditary medullary thyroid carcinoma was invariably associated with C-cell hyperplasia, but C-cell hyperplasia was also associated with some sporadic tumours. All tumours were positive for calcitonin and carcinoembryonic antigen (by immunohistological staining) (CEA) and most tumours stained for somatostatin. C-cell hyperplasia also stained for calcitonin, CEA and somatostatin. We conclude that sporadic and familial medullary thyroid carcinoma cannot always be discriminated by clinical or immunohistological methods. Family screening is essential in the diagnosis of hereditary medullary thyroid carcinoma.

Adult↗
PubMed1987

Postpartum activation of autoimmunity: transient increase of total IgG levels in normal women and in women with autoimmune thyroiditis.

The immunoregulatory mechanisms underlying the transient rebound of autoimmune disease activity in the postpartum period were studied by determining serum immunoglobulins, thyroid microsomal antibodies and some viral (cytomegalovirus, Epstein-Barr, varicellae-zoster and mumps) and bacterial (Yersinia enterocolitica and Salmonella) antibodies in women with autoimmune thyroiditis and in healthy postpartum women. A characteristic increase between 2 and 5 months postpartum followed by a decrease to 10-12 months postpartum was observed not only for thyroid microsomal antibody titres in women with autoimmune thyroiditis but also for serum total IgG and IgG subclass levels (but not IgM, IgA or IgE) in both groups of women. This pattern of transient antibody increase was not detected against viral and bacterial antigens. The characteristic alterations of thyroid microsomal antibody titres in the postpartum period of women with autoimmune thyroiditis thus appear to occur as a consequence of an activation of immunoglobulin-producing B cell clones. This activation seems restricted to the IgG class and to certain B cell clones.

Adult↗
PubMed1987

The secretion of cholecystokinin in the gallstone patient before and after removal of a functioning gallbladder.

Cholecystectomy will not always relieve the abdominal symptoms of the patient with gallstones. The functional effects of gallbladder removal in a patient with a patent cystic duct are not known in detail. Studies of the function of the gallbladder and pancreas have suggested feedback mechanisms for the release of cholecystokinin (CCK). A disturbed regulation of CCK release after cholecystectomy might induce pancreaticobiliary and gastrointestinal dysfunctions. In our study the concentrations of CCK in plasma were measured in 17 patients with gallstones. The measurements were taken with gallbladders opacified at cholecystography and with patent cystic ducts at the operation, in the fasting state, and during stimulation before and 17 weeks after the cholecystectomy. The CCK assay used measures sulfated CCK-8, CCK-22, and CCK-33 with equimolar potency but neither nonsulfated CCK nor any gastrins. Emtobil (containing peanut oil and sorbitol) was used for peroral stimulation of the CCK release. The basal concentration of CCK was 4 pmol/L and rose five times during a "test meal." No significant differences were seen in fasting or stimulated concentrations of plasma CCK before and after the cholecystectomy. Thus cholecystectomy in gallstone patients with functioning gallbladders does not seem to influence the regulation of CCK release.

Adult↗
PubMed1986

Subacute thyroiditis: activated HLA-DR and interferon-gamma expressing T cytotoxic/suppressor cells in thyroid tissue and peripheral blood.

Using a two-colour direct immunofluorescence staining technique, we investigated activated HLA-DR-expressing T helper and T cytotoxic/suppressor cells in peripheral blood of six patients with subacute thyroiditis at referral and at follow-up and in blood from 20 controls. In three of the patients, thyroid fine-needle aspirates were examined as well. At referral, all patients had elevated blood levels of activated T helper and T cytotoxic/suppressor cells 2 (2-4)%, median and range, vs 0 (0-2)%, P less than 0.001 and 12.5 (2-24)%, vs 0 (0-1)% P less than 0.001). At follow-up, the activated proportion of T helper cells had become normal whereas some activated T cytotoxic/suppressor cells remained, 7 (0-8)%. No significant changes in total T cell number were detected when data at referral and at follow-up were compared. In thyroid aspirates, HLA-DR expressing thyrocytes were observed; the total proportion of T cytotoxic/suppressor cells was elevated (70% compared with 35% in blood) and 70% of the T cytotoxic/suppressor cells were HLA-DR+. Furthermore, 55% of the thyroid-infiltrating lymphoid cells were positive for interferon (IFN-gamma+). The finding of activated T cytotoxic/suppressor cells in the blood and thyroid tissue in subacute thyroiditis is consistent with a viral aetiology. Furthermore, intrathyroidal IFN-gamma+ lymphocytes are likely to contribute to expression of major histocompatibility complex (MHC) class II antigens on thyrocytes. No autoantibodies, however, were detected, which suggests that aberrant expression of MHC class II molecules alone is not sufficient to provoke an autoimmune response.

Adult↗
PubMed1986

Cholecystokinin secretion after oral Emtobil, a gallbladder-contracting formula.

Oral Emtobil, a liquid preparation of sorbitol and peanut oil, has been used in roentgenological practice for several years. Emptying of an opacified gallbladder is seen within 15 min after intake of 100 ml of this solution. The main physiological factor responsible for contraction of the gallbladder is cholecystokinin (CCK). In the present study plasma concentrations of CCK in fasting, healthy subjects were studied in response to oral Emtobil. The radioimmunoassay used measures sulphated CCK-8 and CCK-33 with equimolar potency. Neither non-sulphated CCK nor any gastrins are measured. The average concentration, after an overnight fast in nine healthy subjects without gallstones, was 1.2 pmol/l. A peak concentration was seen within 30 min after 'the test meal' and averaged 8 pmol/l. It is suggested that oral Emtobil contracts the gallbladder by release of CCK. Since Emtobil induces a fast and marked rise in the plasma concentration of CCK, it may be used in test procedures to estimate the secretion of CCK.

Administration, Oral↗
PubMed1986

Postpartum thyroid disease.

Recent epidemiological studies in Japan and Sweden have disclosed a high prevalence of transient thyroid dysfunction in women following delivery. These changes seem to reflect an immunoregulatory "rebound" following pregnancy-induced immunosuppression. Thyroid microsomal antibody titers characteristically decrease during pregnancy and increase again after delivery to maximum levels around six months postpartum. At this time some microsomal antibody-positive women develop goitrous hypothyroidism. Subsequently, the microsomal antibody titers fall, reaching the early pregnancy values one year postpartum by which time hypothyroidism subsides. The severity of hypothyroidism is closely related to the titer of microsomal antibody, especially the immunoglobulin G1 subclass of microsomal antibody, and partly predictable from the titer in early pregnancy. The HLA-DR4 antigen was observed in 58% of microsomal antibody-positive Swedish women as compared to 33.7% in the general population (relative risk = 2.71). This association was even stronger in microsomal antibody-positive women who developed postpartum hypothyroidism (69%; relative risk = 4.36). Finally, postpartum thyrotoxicosis with a high radioiodine uptake may occur in women with latent Graves' disease. In these cases changes of TSH-receptor-stimulating antibodies analogous to microsomal antibodies seem to occur.

Adolescent↗