Israel Medical Association Journal

Background: Patients with autoimmune disease (AID) and coronavirus disease 2019 (COVID-19) could have higher mortality due to the co-morbidity and the use of immunosuppressive therapy.

Objectives: To analyze the risk factors and outcomes of patients with AID and COVID-19 versus a control group.

Methods: A prospective cohort study included patients with and without AID and COVID-19. Patients were paired by age and sex. Clinical, biochemical, immunological treatments, and outcomes (days of hospital stay, invasive mechanical ventilation [IMV], oxygen at discharge, and death) were collected.

Results: We included 226 COVID-19 patients: 113 with AID (51.15 ± 14.3 years) and 113 controls (53.45 ± 13.3 years). The most frequent AIDs were Rheumatoid arthritis (26.5%), systemic lupus erythematosus (21%), and systemic sclerosis (14%). AID patients had lower lactate dehydrogenas, C-reactive protein, fibrinogen, IMV (P = 0.027), and oxygen levels at discharge (P ≤ 0.0001) and lower death rates (P ≤ 0.0001). Oxygen saturation (SaO₂) ≤ 88% at hospitalization provided risk for IMV (RR [relative risk] 3.83, 95% confidence interval [95%CI] 1.1–13.6, P = 0.038). Higher creatinine and LDH levels were associated with death in the AID group. SaO₂ ≤ 88% and CO-RADS ≥ 4 were risk factors for in-hospital mortality (RR 4.90, 95%CI 1.8–13.0, P = 0.001 and RR 7.60, 95%CI 1.4–39.7, P = 0.016, respectively). Anticoagulant therapy was protective (RR 0.36, 95%CI 0.1–0.9, P = 0.041)

Conclusions: Patients with AID had better outcomes with COVID-19 than controls. Anticoagulation was associated with a lower death in patients with AID.

Background: Erythema nodosum (EN) is the most common type of panniculitis, commonly secondary to infectious diseases.

Objectives: To elucidate the causative factors and the clinical presentation of patients with EN (2004–2014) and to compare their data to those reported in a previous study.

Methods: A retrospective study was conducted of all patients diagnosed with EN who were hospitalized at Soroka University Medical Center (2004–2014). The clinical, demographic, and laboratory characteristics of the patients were compared to those in a cohort of patients diagnosed with EN from 1973–1982.

Results: The study comprised 45 patients with a diagnosis of EN. The most common symptoms of patients hospitalized with EN were arthritis or arthralgia (27% of patients). Patients with EN, compared to those reported in 1987, has significantly lower rates of fever (18% vs. 62% P < 0.001), streptococcal infection (16% vs. 44%, P = 0.003), and joint involvement (27% vs. 66%, P < 0.001). In addition, fewer patients had idiopathic causes of EN (9% vs. 32%, P = 0.006).

Conclusions: In the past decades, clinical, epidemiological, and etiological changes have occurred in EN patients. The lowering in rate of fever, streptococcal infection, and joint involvement in patients with EN are probably explained by improvements in socioeconomic conditions. The significantly decreasing rate of idiopathic causes of EN is possibly due to the greater diagnostic accuracy of modern medicine. The results of the present study demonstrate the impact of improvements in socioeconomic conditions and access to healthcare on disease presentation.

Behçet’s disease (BD) is a systemic inflammatory disorder characterized by a protean clinical spectrum and an enigmatic pathogenesis. After being classified as an autoimmune disorder, spondyloarthritis and vasculitis, today BD is considered at the crossroad between autoimmune and auto-inflammatory syndromes. Many pathogenetic, clinical and therapeutic clues support this recent interpretation, enabling novel treatment choices such as interleukin (IL)-1 inhibition. Thus, in the last decade the IL-1 receptor antagonist anakinra and the anti-IL-1β monoclonal antibody canakinumab were increasingly administered in BD patients resistant to standard therapies, leading to interesting results and new intriguing pathogenetic implications. However, further studies are essential to both establish how the innate and acquired immune systems interact in BD patients and identify the best way of administering anti-IL-1 agents with regard to dosage, interval of administration and organ response.

Background: Although the presence of bacteria in the cervix is not a sign of disease, the majority of pathogens involved in pelvic inflammatory disease originate from this "normal" flora.

Objectives: To assess the distribution of cervical non-gonococcal and non-chlamydial bacteria in hospitalized women with PID[1] and the bacteria's antibiotic sensitivity.

Methods: We retrospectively evaluated the cultures obtained from the uterine cervix over a 1 year period (2008) at Wolfson Medical Center, Holon. The distribution of cervical non-gonococcal and non-chlamydial bacteria in women with PID and the bacteria's antibiotic sensitivity was compared to that in our previous 1 year study that was performed at Kaplan Medical Center, Rehovot (1988–89). 

Results: In 2008, a total of 412 cultures were obtained of which 126 (30.5%) were sterile. The prevalence of negative cultures was similar in 2008 and in 1988, namely, 30.5% and 33.7%, respectively (P = 0.23). PID was finally diagnosed in 116 patients with positive cultures. The most prevalent bacteria in the 2008 study were Enterococcus species and Escherichia coli – 24.0 % and 26.4% respectively compared to 18.0% and 38.1% in the 1988 study, with the decrease in E. coli isolates being significant (P = 0.0003). In 2008 the antimicrobial sensitivity for various antibiotics ranged from 44.3% to 100.0% (median 90.2%) while in 1988 it ranged from 2.9% to 80.1% (median 51.9%).

Conclusions: The cervical bacterial flora in hospitalized women with PID did not vary significantly between 1988 and 2008. However, antimicrobial sensitivity of the isolated bacteria increased dramatically, probably due to a decrease in resistance to antibiotics.

Objectives: To help clinicians and laboratory scientists recognize and utilize vasculitis-related ANCAs as an aid in diagnostic workup and patient follow-up, and be aware that ANCAs with different characteristics are commonly found in other chronic inflammatory conditions that persistently engage neutrophils in the inflammatory process.

Methods: Indirect immunofluorescence and enzyme immunoassay methods were used to detect ANCAs with both known and unknown neutrophil autoantigenic targets.

Results: Primary necrotizing small vessel vasculitides such as Wegener’s granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, and renal-limited rapidly progressive necrotizing glomerulonephritis target either the serine protease proteinase 3 or myeloperoxidase  in azurophilic granules. In ulcerative colitis and rheumatoid arthritis, we found multiple ANCA targets contained in azurophilic and specific granules, the cytosol and the nucleus, whereas PR3² and MPO³ were not, or only weakly, recognized.

Conclusions: ANCAs typically found in active SVV⁴ are demonstrable both by indirect immunofluorescence and antigen-specific enzyme immunoassay, and strong reactivity to either PR3 or MPO is characteristic. Strong ANCA with MPO reactivity is also found in some patients with drug-induced syndromes (lupus, vasculitis). Intermediate to strong perinuclear ANCAs are found in a substantial proportion of patients with UC⁵ (40–60%) and RA⁶ (30–70%), but in these conditions the ANCAs have many antigen targets that are only weakly recognized.

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¹ ANCA = anti-neutrophil cytoplasm antibody

² PR3 = protease proteinase 3

³ MPO = myeloperoxidase

⁴ SVV = small vessel vasculitides

⁵ UC = ulcerative colitis

⁶ RA = rheumatoid arthritis