Psychiatric and cardiovascular comorbidities as causes of long-term work disability among individuals with recent-onset rheumatoid arthritis.

OBJECTIVES: With the ameliorating prognosis of rheumatoid arthritis (RA), the role of comorbidities as causes of work disability (WD) may increase. The aim of this study was to determine the contribution of psychiatric and cardiovascular (CV) comorbidities as the leading causes of long-term WD among patients with recent-onset RA. METHOD: Between 2000 and 2007, all incident, working-age and non-retired RA patients were identified from a Finnish nationwide register. From other registers, we identified the RA patients who were granted a permanent or temporary disability pension by 31 December 2008. The incidences of disability pensions with CV diseases (ICD-10 codes I00-I99) or psychiatric disorders (F20-F69) as the leading causes were assessed and compared with the general population. RESULTS: We identified a cohort of 7831 patients with RA. During follow-up, 1095 patients were granted a disability pension. After adjusting for competing risks, the 9-year cumulative incidence of WD caused by RA, a psychiatric comorbidity, or a CV disease was 11.9, 1.3, and 0.5%, respectively. Compared to the general population, the age- and sex-specific standardized incidence ratio (SIR) of WD due to psychiatric comorbidities was 0.99 [95% confidence interval (CI) 0.80-1.23] and due to CV disease 1.75 (95% CI 1.23-2.51). CONCLUSIONS: In the study cohort with recent-onset RA, the 9-year cumulative incidence of disability pensions caused by psychiatric or CV comorbidities was only 11% or 4%, respectively, of that caused by RA itself. Compared to the general population, the risk of WD due to CV disease was increased.

Inhibitory effect of the angiotensin converting enzyme inhibitors captopril and enalapril on the conversion of procollagen to collagen.

OBJECTIVE AND DESIGN: Angiotensin converting enzyme inhibitors are reported to inhibit the collagen accumulation involved in left ventricular hypertrophy. We tested the effect of captopril and enalapril on the conversion of procollagen to collagen in short-term tissue cultures in order to study the possible mechanisms by which the antifibrotic effect of this group of inhibitors takes place. METHODS: We employed short-term cartilage and tendon tissue cultures to monitor the conversion of procollagen to collagen. After pulse-labelling with [14C]-proline, the cultures were incubated further with the test compounds in different concentrations for a 180 min chase period. The reaction was stopped and radioactive collagenous peptides were analysed by gel electrophoresis. The amounts of collagenous proalpha and alpha chains were estimated, and the inhibition of procollagen to collagen conversion was calculated relative to 0 min control (100% inhibition) and 180 min control (0% inhibition) samples. RESULTS: Inhibition (50%) was obtained with 7 mmol/l captopril and 22 mmol/l enalapril in the cartilage cultures. Both compounds seemed to inhibit the conversion in clearly lower concentrations in tendon cultures, 4 mmol/l and 7 mmol/l, respectively, were sufficient for 50% inhibition. Angiotensin I, II, saralasin and bradykinin did not have any effect on conversion at 3.5, 9, 2 and 4 mmol/l concentrations, respectively. CONCLUSION: The peptidase inhibitors captopril and enalapril are able to inhibit the conversion of procollagen to collagen, which is a proteolytic process, possibly by inhibiting the specific procollagen proteases. Whether this phenomenon is involved in the antifibrotic property of angiotensin converting enzyme inhibitors warrants further study, as does the question of whether new antifibrotic agents could be developed on this basis.

Treatment of Helicobacter pylori in patients with lymphocytic gastritis.

BACKGROUND/AIMS: Lymphocytic gastritis is a subtype of chronic gastritis characterized by a marked increase in the number of intraepithelial lymphocytes in the gastric mucosa. Its etiology is unknown, but a proportion of these patients have Helicobacter pylori infection. The aim was to assess the significance of H. pylori treatment in lymphocytic gastritis patients. METHODOLOGY: The 10 patients with lymphocytic gastritis and either serologically or histologically diagnosed H. pylori infection were treated with a triple therapy and followed by serology and histology after 6-18 months. RESULTS: The levels of IgG antibodies for H. pylori decreased below 50% of the pretreatment values in all patients. The maximum numbers of intraepithelial lymphocytes decreased significantly (P = 0.005) from the pretreatment values. CONCLUSIONS: Treatment of H. pylori infection cures lymphocytic gastritis associated with H. pylori infection. H. pylori appears to be one etiological cause of lymphocytic gastritis.

Blood leukocyte differential in Helicobacter pylori infection.

Helicobacter pylori causes a chronic infection in gastric mucosa, but its systemic effects are largely unknown. Our aim was to characterize the effect of H. pylori infection and gastric mucosal inflammation on the peripheral blood leukocyte count. An endoscopic series of 96 patients (40 men and 56 women), with a mean age of 62 years (range 49-80) was studied. Endoscopy with eight stepwise biopsies was performed and the occurrence of H. pylori was studied from sections stained with Warthin-Starry. The severity of inflammation in antral and body mucosa was estimated. The peripheral blood leukocyte count and differential count were determined by the automatic flow cytometric method. The total number of blood leukocytes and the numbers of lymphocytes and basophils were significantly increased in H. pylori-positive patients (N = 58), as compared with H. pylori-negative ones (N = 38). The total number of blood leukocytes correlated with the numbers of neutrophils, eosinophils, and mononuclear cells in the gastric mucosa. The number of basophils correlated with the number of mucosal neutrophils and mononuclear inflammatory cells. The results show that mucosal inflammation due to H. pylori infection is reflected in the amount of peripheral blood leukocytes. Basophilia suggests involvement of allergic mechanisms in H. pylori gastritis.

Ten year follow up study of lymphocytic gastritis: further evidence on Helicobacter pylori as a cause of lymphocytic gastritis and corpus gastritis.

AIMS: To examine the course of lymphocytic gastritis and its relation to Helicobacter pylori (H pylori) infection in a 10 year follow up. METHODS: Ninety six patients were originally examined for dyspepsia in 1981. Gastroscopies with stepwise biopsies were performed on all the patients initially and after an interval of 10 years. RESULTS: Nine per cent of the patients (9/96) had features of lymphocytic gastritis in gastric biopsy at the first examination, and 12.5% (12/96) at the second examination; 7/9 patients (78%) had persistent lymphocytic gastritis during the follow up; in two the diagnostic features of lymphocytic gastritis had disappeared, and five had a new diagnosis of lymphocytic gastritis at the second examination. At the second examination 9/12 lymphocytic gastritis patients (75%) were H pylori positive histologically, while all had specific antibodies to H pylori. The lymphocytic gastritis patients had higher grades of gastritis (p = 0.009), neutrophilic and eosinophilic granulocytes, mononuclear inflammatory cells, and foveolar hyperplasia in the corpus mucosa, but smaller numbers of H pylori, than the H pylori positive patients without lymphocytic gastritis. The appearance of lymphocytic gastritis during the 10 year interval was associated with increases in the grades of corpus gastritis and neutrophilic granulocytes (p = 0.043 for both). During the follow up, the patients with lymphocytic gastritis, but not the H pylori positive patients without lymphocytic gastritis, appeared to have a significant increase in the grade of intestinal metaplasia in the corpus mucosa (p = 0.043). CONCLUSIONS: In some patients H pylori may cause a gastritis that predominates in the corpus and is associated with an increase in the intraepithelial lymphocyte count. This form of gastritis may cause progression of intestinal metaplasia.

Helicobacter pylori-associated gastritis. Evolution of histologic changes over 10 years.

BACKGROUND: Helicobacter pylori seems to be the commonest cause of chronic gastritis, but the natural course of H. pylori-associated gastritis is largely obscure. METHODS: We present a histologic follow-up of 39 patients with H. pylori-positive gastritis. Gastroscopies with stepwise biopsies were performed in all the patients at an interval of 10 years. RESULTS: Of the patients 87% (34/39) had a persistent infection and showed a significant decrease in the grades of antral gastritis, eosinophilic granulocytes, corpus eosinophilic granulocytes, and foveolar hyperplasia and a significant increase in the grade of corpus neutrophilic granulocytes. The quantities of H. pylori as estimated histologically did not change significantly during the follow-up period in patients with a persistent infection. In the five other patients (13%) the H. pylori infection had apparently disappeared spontaneously, and this was accompanied by decreases in the amount of inflammatory cells in the gastric mucosa. CONCLUSIONS: H. pylori infection in the gastric mucosa is chronic and may be associated with both regressive and progressive histologic changes. Spontaneous healing of H. pylori infection is possible and is associated with partial resolution of the inflammatory changes in the gastric mucosa.

Chronic gastritis in patients with gastric ulcer; a 10-year follow-up.

BACKGROUND: The course of gastric ulcer disease and its relations to certain indicators of inflammation and Helicobacter pylori in the gastric mucosa were examined in a 10-year follow-up. METHODS: Thirty-three patients with gastric ulcer were examined endoscopically with biopsies in 1981-82 and invited for re-examination in 1991-92. Twenty-one of them were able to comply with the invitation. A gastroscopy with biopsies was performed on each of these, and the results were compared with those of age- and sex-matched control patients with non-ulcer H. pylori-positive gastritis. RESULTS: All the patients were H. pylori-positive at the first examination and had a persistent infection at the second examination, if they had not undergone a gastric resection. Thirteen patients had a non-operated stomach at the second examination. The grades of gastritis and intestinal metaplasia in the antrum at the second examination were significantly higher in the ulcer patients than in the controls (p = 0.009 and p = 0.04, respectively). Eosinophilic granulocytes in both the antral and the corpus mucosa had decreased significantly in the controls (p = 0.002 and p = 0.04, respectively) but not in the ulcer patients. CONCLUSIONS: The results suggest that the course of ulcer-associated H. pylori-positive gastritis is different from that of non-ulcer-associated H. pylori-positive gastritis and that abnormal eosinophilic infiltration persists in patients with gastric ulcer.

Pleuro-pulmonary aspergillosis. US and US-guided biopsy as an aid to diagnosis.

We reviewed the US findings and the diagnostic yield of fine-needle aspiration biopsy (FNAB) for cytologic and microbiologic samples in 4 patients with pulmonary or pleural aspergillosis. All 3 apical Aspergillus abscesses were round, hypoechoic with irregular margins and one contained echo-densities with shadowing consistent with air. One pleural empyema was oval and hypoechoic. Cytology suggested inflammation in all cases and Aspergillus hyphae were detected in 2 of 4 aspirates. Culture of the aspirate was positive for Aspergillus in 3 of 4 cases, while one diagnosis was made after surgery. No complications occurred. Apico-pleural Aspergillus lesions are suitable targets for US-guided FNAB, thus avoiding more invasive methods. Our results suggest wider use of this procedure.

Smoking and the pulmonary mineral particle burden.

The total pulmonary mineral particle burden and types of environmental particles were assessed in relation to smoking in 11 unselected autopsy lungs from adult male smokers and paired male non-smokers matched by age and lung. The lungs were fixed intrabronchially with formalin-polyethylene glycol-alcohol solution at a standard pressure and air-dried. A sample of 1-2 cm3 was taken from the posterior or apicoposterior segment of the right/left upper lobe and plasma ashed at low temperature. The mineral particles were identified by scanning transmission electron microscopy (STEM), electron microprobe analysis and electron diffraction. The number, mass and volume were calculated from the STEM image. The smokers' lung tissue had a lower number (54 +/- 15 X 10(6), mass (5.1 +/- 3.2 micrograms), volume (183 +/- 122 X 10(-5) mm3) and surface area (104 +/- 44 mm2/cm3 of lung tissue) of particles than the non-smokers' lung tissue (68 +/- 42 X 10(6), 12.6 +/- 13.4 micrograms, 468 +/- 501 X 10(-5) mm3 and 191 +/- 167 mm2/cm3 of lung tissue, respectively). All mineral types except talc were more numerous in the non-smokers' than in the smokers' lung tissue. The mineral particles were typical of the Finnish bedrock: quartz 15 +/- 7%, plagioclase 8 +/- 4%, microcline 13 +/- 5%, micas 22 +/- 10%, talc 4 +/- 4% and kaolinite 10 +/- 5%. Fibres were observed in only 2 cases, amounting to 1% in each. The lower mineral particle content of the smokers' lungs probably reflects more active clearance mechanisms caused by cigarette smoke.

Hepatic glucose-6-phosphatase activity in non-insulin dependent diabetics. Effect of enzyme-inducing drugs.

The role of glucose-6-phosphatase (G6Pase) in postreceptional glucose handling in non-insulin dependent diabetics ( NIDDs ) was in investigated by comparing the enzyme values in diagnostic liver biopsy samples with fasting blood glucose (BG), immunoreactive insulin (IRI) and plasma antipyrine half-life (T/2). The NIDDs , treated with sulphonylureas, had elevated serum aminotransferase and alkaline phosphatase values associated with fatty liver with or without fibrosis. G6Pase activity was reduced in the NIDDs compared with subjects who had undergone gallstone surgery (p less than 0.001), insulin dependent diabetics (p less than 0.001), and age- and sex-matched non-diabetics (p less than 0.001). G6Pase was inversely related to BG and antipyrine T/2, but not to IRI or conventional liver function tests. Therapy with phenobarbital and medroxyprogesterone acetate, known inducers, increased G6Pase activity, shortened antipyrine T/2, reduced BG and did not alter IRI, in four NIDDs . Low liver G6Pase activity in NIDDs may hence be one factor underlying the impaired glycemic control.