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Purpose Ocular manifestations of syphilis have been reported in 2–10% of systemic infection. The purpose of this study was to report the incidence of ocular syphilis and various ocular manifestations, particularly optic nerve involvement, in newly diagnosed cases. Methods This was a retrospective study. Medical records of newly diagnosed syphilis patients between January 2009 and January 2017 in a tertiary medical centre were reviewed. Results There were 123 new systemic syphilis cases out of 569,222 (0.02%) admissions to the Tel Aviv Medical Center during the study period. Ninety‐three of the 123 patients (76%) underwent ophthalmological examination. Twenty‐three of the 93 patients (25%, mean age 48.6 ± 12.9 years, 20 males) had ocular syphilis, and in 12/23 (52%) patients, the ocular symptoms and findings prompted syphilis investigation. Eighteen of the 23 (78%) had optic nerve involvement, and the most common was inflammatory disc oedema. Older age (p = 0.0005) and tertiary stage disease (p = 0.0441) were associated with ocular manifestations and the presence of optic nerve findings. Human immunodeficiency virus (HIV) was associated with ocular but not optic nerve findings. Treatment included intravenous penicillin G, and four patients with severe optic neuropathy were also treated with systemic corticosteroids. Visual acuity significantly improved in most patients (p < 0.05). Conclusion Ocular syphilis was found in one‐quarter of the patients diagnosed with systemic syphilis and preceded the diagnosis of systemic disease in one‐half of them. Optic nerve involvement was a common manifestation. A high index of suspicion for Treponema infection is required in patients presenting with optic nerve involvement to facilitate prompt diagnosis and treatment. Post‐treatment visual outcome was good.

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Increased levels of circulating androgens are associated with earlier age of onset of IIH in women.

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SummaryUp to 20% of Crohn's disease (CD) patients respond poorly to glucocorticoids (GC). A product of an alternative splicing of the glucocorticoid receptor (GR) premRNA, GR b , may play a role as a dominant inhibitor of the glucocorticoid response. Increasing evidence suggests that inflammatory cytokines such as interleukin (IL)-18 alternate the splicing of the primary transcript between the two isoforms GR b and GR a in hGR gene of CD patients. The aim of this study is to assess the expression of GR a and GR b in patients with CD and to look for a possible correlation between these receptors and the response to glucocorticoid treatment. Forty-two CD patients and 17 healthy volunteers were studied. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed using real-time PCR techniques. Serum IL-18 protein levels were measured by enzyme-linked immunosorbent assay (ELISA). The amount of hGR a -mRNA in patients in remission was significantly lower than in controls ( P < 0·05). The amount of hGR b -mRNA was significantly higher in GC-resistant patients in the active stage of disease compared with all other groups ( P < 0·05). Patients in the active stage of the disease had higher levels of IL-18 than patients in remission and both had higher levels than controls ( P < 0·05). The amounts of IL-18 were directly correlated with the amount of hGR b mRNA in GC-resistant patients with an active disease. High levels of hGR b might be connected to GC resistance. IL-18 might participate in the alternative splicing of the hGR preliminary mRNA of CD patients. The results support the theory that augmented hGR b mRNA expression level in PBMC is connected with GC-resistance of CD patients.

A patient with essential mixed cryoglobulinaemia (EMC) type II and hepatitis C virus (HCV) infection, in whom immunophenotypic and genotypic studies demonstrated a clonal proliferation of B lymphocytes, is described. Fluorescent in situ hybridization with probes to Ig heavy chain gene and to the oncogene bcl-2 demonstrated a translocation of bcl-2 to the immunoglobulin heavy chain locus on chromosome 14. A sharp rise in the level of the monoclonal IgM was associated with a second genetic aberration [t(8:22) (q24:q11)]. No other clinical evidence of disease progression could be demonstrated. Low grade lymphoproliferative disorder with typical cytogenetic abnormalities developed on the background of EMC and HCV. Clinical progression was associated with a second genetic abnormality involving the myc oncogene. It is possible that HCV chronic infection may indirectly influence oncogenes associated with lymphoma.