Discrepancies between clinical and pathological findings seen at renal biopsy in rheumatological diseases.

OBJECTIVE: Renal biopsy contributes to the diagnosis, follow-up, and treatment of many rheumatic conditions. This study assessed the diagnostic role and safety of renal biopsies in a tertiary rheumatology clinic. METHODS: Renal biopsies performed between June 2020 and December 2022 were screened, and demographic, clinical, histopathological, and safety data were collected from patient records. RESULTS: In this study, 33 males and 38 females were included. Except for 1 patient who received acetylsalicylic acid, antiaggregant, and/or anticoagulant drugs were stopped before the biopsy. Complications included a decrease of hemoglobin in 8 patients (11.3%) and microscopic hematuria in 40 patients (56.3%). Control ultrasonography was performed in 16 patients (22.5%), and a self-limiting hematoma was found in 4 of them (5.6%) without additional complications. While less than 10 glomeruli were obtained in 9 patients (9.9%), diagnosis success was 94.4%. Histopathological data were consistent with one of the pre-biopsy diagnoses in 54 of 67 cases (80.6%) but showed discrepancies in 19.4% (n=13) of patients. A repeat biopsy was performed in 7 patients for re-staging or insufficient biopsy. CONCLUSIONS: Renal biopsy significantly contributes to rheumatology practice, especially in patients with complex clinical and laboratory findings or in whom different treatments can be given according to the presence, severity, and type of renal involvement. Although the possibility of obtaining insufficient tissue and the need for re-staging and repeat biopsy in the follow-up might be expected, complication risk does not seem to be a big concern. Renal biopsy often evidenced discrepancies between pre-biopsy diagnosis and histopathological findings.

Jaw fractures diagnosed and treated at Malmö University Hospital: a comparison of three decades.

The aim was to report the distribution, frequency and aetiology of jaw fractures in patients treated at the University Hospital, Malmö, 1993-2003 and to compare two previous studies from 1952-1962 and 1975-1985. In 1993-2003, 461 patients, 137 women (mean age 42 years; range 15-82) and 324 men (mean age 28 years; range 17-59) were diagnosed and treated. Women were significantly older than men (P<0.001). The most frequent cause of jaw fractures was falls in women (45%). In men, interpersonal violence (46%) was most common followed by road traffic accidents (RTAs) (24%) mostly involving bicycles (14%). The frequency of falls in women and men was significantly different (P<0.001) as was the difference between violence in men and women (P<0.001). The proportion of fractures caused by RTAs was significantly higher in 1952-1962 than in 1993-2003 (P<0.001). There was a significant increase in the proportion of fractures caused by violence between the two studies (P=0.007). In 1993-2003 the proportion of fractures in women due to falls was significantly higher than in 1952-1962 (P=0.006). Violence has replaced RTAs as the main cause for jaw fractures in men; for women falling is the commonest cause.

Evaluation of plasma fibronectine level as a probable indicator for tympanosclerosis.

OBJECTIVES: Wound healing, epithelial regrowth and collagen synthesis are very important factors in the repair of the traumatised tympanic membrane. The aim of the present study was to determine the role of plasma fibronectine in the aetiopathogenesis of tympanosclerosis. METHODS: This prospective study included 58 patients with and 49 without tympanosclerosis. No inflammation or trauma was noted in either patient group. All patients underwent otoscopic and otomicroscopic examination, and the degree of tympanosclerosis was graded from mild (stage I) to severe (stage III). Following otological examination, blood samples were taken for plasma fibronectine measurement. RESULTS: Following otoscopic and otomicroscopic examinations, patients' tympanosclerosis was graded as follows: 18 patients were stage I; 29 were stage II; and 11 were stage III. Statistical analyses revealed that the plasma fibronectine concentrations were significantly lower in the study group compared with the control group (p = 0.031). In addition, fibronectine levels were lowest in the patients with severest tympanosclerosis (p = 0.0001 in each comparison). CONCLUSION: The results of the present study show that serum fibronectine is important in the development and severity of tympanosclerosis.

Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus.

Deficiency of mannan-binding lectin (MBL) has been reported to impact susceptibility to severe infections and atherosclerosis in systemic lupus erythematosus (SLE). In this study, MBL gene polymorphisms were analysed in 143 SLE patients and the frequency of severe infections and organ damage according to SLICC/ACR Damage Index regarding cerebrovascular accidents, angina pectoris, coronary by-pass surgery, myocardial infarction and peripheral arterial disease leading to significant tissue loss, were recorded during a mean follow-up time of 15 years from diagnosis. In a multiple logistic regression model, smoking (P = 0.001), hypertension (P = 0.030), alcohol intake (P = 0.027) and higher triglyceride concentration (P = 0.026) were associated with cerebrovascular, cardiovascular and peripheral arterial organ damage (CPAD), while the association with MBL deficiency did not reach significance (P = 0.098). Alcohol intake (>15 g/month) was inversely correlated with CPAD (OR = 0.29, 95%CI 0.096-0.87). MBL deficiency was not significantly more common in SLE patients with severe infections in a multivariate analysis (P > 0.3). In conclusion, classical risk factors such as smoking, hypertension, low alcohol intake and elevated triglyceride concentration were relatively more important for development of CPAD than MBL deficiency in SLE. Furthermore, MBL deficiency did not contribute to development of major infections in SLE.