Salivary gland scintigraphy in Sjögren's syndrome and patients with sicca symptoms but without Sjögren's syndrome: the psychological profiles and predictors for salivary gland dysfunction.

OBJECTIVE: To characterise the psychological profiles of Sjögren's syndrome (SS) and patients with sicca symptoms but without SS; to find predictors for salivary gland function; to evaluate salivary scintigraphy as a method to differentiate between SS and patients with sicca symptoms but without SS. PATIENTS AND METHODS: Psychological tests (Medical Outcomes Study Short Form General Health Survey (SF-36), Jenkins Activity Survey, Toronto Alexithymia Scale, and Maastricht Questionnaire for vital exhaustion) were performed and assessment of the function of the salivary glands made in 26 patients with primary SS, 8 with secondary SS, and 9 with sicca symptoms but without SS. Data were analysed with BMDP new system version 1.0 statistical program. RESULTS: Psychological profiles were similar in all groups. Hb, RF, ANA, and SSA differentiated between the groups. Results of salivary scintigraphy were predicted to 51% by ANA, SSA, SSB, IgG, IgA, diagnosis, vitality, and role limitations due to emotional problems. No predictors were found for the resting salivary flow. Salivary scintigraphy was pathological in 21/26 (81%) and in 8/8 (100%) patients with secondary SS, but only in 2/9 (22%) patients with sicca symptoms without SS (p=0.002) (sensitivity 85.3%, specificity 77.8%). CONCLUSIONS: Patients with sicca symptoms but without SS have sickness behaviour similar to that of patients with SS. The results of salivary scintigraphy can be predicted by diagnosis and autoimmune findings; psychological characteristics added 20% to this predictive value. Distinction between SS and patients with sicca symptoms but without SS is difficult, but in addition to autoantibodies, salivary scintigraphy can be used for this purpose.

Evaluation of Pyloriset Screen, a rapid whole-blood diagnostic test for Helicobacter pylori infection.

Helicobacter pylori infection can be detected by several invasive tests based on gastroscopy and by noninvasive methods such as serologic assays. Noninvasive tests can be used not only in addition to invasive tests but also by themselves to screen for H. pylori infection in patients who are not in urgent need of endoscopy. Lately, rapid qualitative serologic tests have been developed. In the present study, the accuracy of a novel rapid whole-blood test, Pyloriset Screen, detecting immunoglobulin G (IgG) and IgA antibodies against H. pylori was evaluated. A total of 207 consecutive adult outpatients referred for upper endoscopy were enrolled. Gastric biopsy specimens were taken from the antrum and corpus for histologic examination and rapid urease testing. Cultures were available for 113 patients. Serum samples collected from all patients were tested for H. pylori antibodies by two enzyme immunoassays (EIAs) (Pyloriset EIA and an in-house EIA), a rapid latex agglutination test (Pyloriset Dry), and Pyloriset Screen. Patients were considered H. pylori positive if helicobacters were seen on histologic examination (77 patients) or, if in combination with histologically verified (although helicobacter-negative) gastritis, their IgG antibody titers were elevated in the two EIAs (five patients). The Pyloriset Screen test had a sensitivity of 95%, a specificity of 94%, a positive predictive value of 91%, and a negative predictive value of 97%. Among 63 patients under the age of 45 years, the Pyloriset Screen test did not miss a single H. pylori diagnosis, and only 1 patient had a false-positive result. Pyloriset Screen could be used reliably to screen for H. pylori infection.

Urine trypsinogen-2 as marker of acute pancreatitis.

We examined the clinical utility of urine trypsinogen-2 as a marker of acute pancreatitis (AP). Fifty-nine patients with AP, 42 with acute abdominal diseases of extrapancreatic origin, and 63 without evidence of acute abdominal disease were studied. Urine trypsinogen-2 was determined by a time-resolved immunofluorometric assay. As reference methods we used serum trypsinogen-2, urine amylase, and serum amylase. The diagnostic accuracy of the markers was evaluated by receiver-operating characteristic (ROC) analysis. At admission, urine trypsinogen-2 differentiated patients with AP from controls with high accuracy. The area under the ROC curve (AUC) was 0.978, which was equal to that of serum trypsinogen-2 (0.998) and serum amylase (0.969) and significantly larger than that of urine amylase. For differentiation between severe and mild AP, urine trypsinogen-2 (0.730) was equal to serum trypsinogen-2 (0.721), and clearly better than amylase in serum and urine. These results suggest that determination of urine trypsinogen-2 is a useful test to detect AP and to evaluate disease severity.

Diagnosis of Lyme borreliosis: non-specific serological reactions with Borrelia burgdorferi sonicate antigen caused by IgG2 antibodies.

ELISA methods that measure IgG class antibodies to sonicated Borrelia burgdorferi may give false positive results. These errors could be traced to non-specific reactivity in subclass IgG2 in several instances. Sera were sampled randomly from two adult populations, which differed in having a high and low incidence of Lyme disease. If the binding of IgG2 subclass antibodies was left unrecorded in the test by the use of monoclonal reagent antibodies selective for IgG1 and IgG3, the frequency of positivity in the ELISA test decreased in samples from the low risk group. Twenty-one samples were found to be positive in an immunoblot confirmatory test. Correct prediction of positivity was obtained for 15 sera by ELISA restricted to IgG1 plus IgG3, for only four sera by ELISA restricted to IgG2 and for only six sera by IgG subclass non-restricted ELISA. A non-restricted ELISA with purified flagella of B. burgdorferi as the antigen predicted correctly 14 of the immunoblot-positive sera. The results of this ELISA correlated well with those of the IgG1 plus IgG3 subclass restricted ELISA in the high risk population (r = 0.95, prevalence of seropositivity 12%), but was significantly worse for the low risk group (r = 0.47, prevalence 2.9%). IgG subclass restriction also decreased cross-reactions of syphilitic sera in the ELISA with sonicated antigen.

Successful amplification of DNA specific for Finnish Borrelia burgdorferi isolates in erythema chronicum migrans but not in circumscribed scleroderma lesions.

Early diagnosis of Borrelia burgdorferi infection, hampered by the absence of detectable antibodies in most patients with erythema chronicum migrans is important to prevent late-stage neurologic, rheumatologic, and skin disorders. Furthermore, B. burgdorferi has been claimed to be the causative agent in localized scleroderma (morphea). We used PCR amplification to search for B. burgdorferi outer surface protein OspA-specific sequences in DNA obtained from lesional skin biopsies on Finnish patients with clinically suspect erythema chronicum migrans, lymphocytoma, morphea, or with diverse skin manifestations and persistent high antibodies to B. burgdorferi flagellar antigen. Seronegative patients with other skin lesions served as controls. The amplicons obtained with primers specific for B. burgdorferi type strain B31 ospA sequence did not hybridize to the corresponding probes, and thus the DNA amplified from a Finnish B. burgdorferi erythema chronicum migrans skin isolate was sequenced. This 98-nucleotide sequence of ospA (332-429) showed 11% to 14% nucleotide divergence compared with the North American type strain (B31), several European strains, and an East Siberian tick strain. The sequence was almost identical (99%) to a Swedish isolate from acrodermatitis chronica atrophicans. Using oligonucleotides specific for the Finnish strain, a positive polymerase chain reaction-based hybridization was obtained in six of seven untreated erythema chronicum migrans patients infected in Finland or in Estonia, and in the lymphocytoma patient. Only two of the erythema chronicum migrans patients had IgG or IgM antibodies to flagellin. However, all seven morphea lesions as well as the other lesions were polymerase chain reaction negative. Polymerase chain reaction-based hybridization of B. burgdorferi OspA gene from skin-derived DNA thus provides a sensitive and specific diagnostic tool. In conditions not unequivocally known to be caused by B. burgdorferi, like in morphea, this assay was negative. We also demonstrate that peri-Baltic B. burgdorferi isolates show homology in their OspA genes but differ from geographically more distant isolates.

Lyme borreliosis in Finland in 1986-1988.

In 1986-1988 there were 123 patients with positive serology for Lyme borreliosis out of 4000 sera referred to the Department of Bacteriology and Immunology, University of Helsinki. Of the 63 patients with positive serology in 1986-1987 20 showed a predominant involvement of the nervous system, 18 complained of joint symptoms and 11 patients merely showed a skin involvement including 8 patients with erythema chronicum migrans (ECM) and 3 patients with acrodermatitis chronica atrophicans (ACA). Two of the patients had unspecific general symptoms and in 5 patients the type of involvement remained unknown. The serology was considered to be falsely positive in 2 patients with tuberculous meningitis, in one with syphilis and in another with recurrent fever.

Bannwarth's syndrome and Lyme disease in Finland.

Three patients with lymphocytic meningoradiculitis were admitted in 1983-84 to the Department of Neurology, University Central Hospital of Helsinki. Two patients had classical Bannwarth's meningoradiculitis with facial diplegia, and a third patient showed a migrating arthralgia and cardiac involvement compatible with a diagnosis of Lyme disease. Cerebrospinal fluid (CSF) showed initially in all patients a lymphocytic pleocytosis and increased protein with signs of intrathecal IgG synthesis.