Citations

Abstract Inhibitors of tumor necrosis factor-α (TNFIs) have revolutionized the treatment for patients with a variety of inflammatory illnesses, including rheumatoid arthritis, psoriasis and psoriatic arthritis, ankylosing spondylitis, and other inflammatory diseases, and have improved the outcomes and quality of life for such patients. Endemic fungal infections, such as coccidioidomycosis, are observed to occur in persons who are treated with these agents and who live in the Coccidioides-endemic area with similar frequency as persons in the general, healthy public but with an increased likelihood of symptomatic infection and extrapulmonary dissemination. Because the control of coccidioidal infections requires the formation and maintenance of granuloma, it is not unexpected that TNFIs, which inhibit granuloma formation, seem to increase the risk of clinical disease. No guidelines exist to address the prevention and management of disease in patients whose treatment course with TNFIs is complicated by subclinical or clinical coccidioidal infection. Therefore, we reviewed the available medical literature and offer suggestions to the approach and treatment of patients with various forms of coccidioidomycosis before and during therapy with TNFIs.

Abstract An elderly woman underwent an uncomplicated right hip replacement (total hip arthroplasty) in 2005 and returned 5 years later with cellulitis of the right hip. Treatment with oral antibiotics was initiated. Septic arthritis of the right hip joint was diagnosed ultimately, and she had surgical removal (explant) of the right hip prosthesis in 2011. Recurrent right hip infections ensued on several occasions with multiple antibiotic courses over the next 4 years. Although she had intermittent infections with methicillin-susceptible Staphylococcus aureus and methicillin-resistant Staphylococcus aureus, she had consistent and persistent isolation of Clostridium cadaveris from the hip beginning in 2013. After prolonged surgical interventions and several courses of antibiotics, C. cadaveris was eradicated; she has undergone implantation for a second stage implant (total hip arthroplasty) of the affected hip and remains stable to date.

AimThe p.P301L mutation in microtubule‐associated protein tau (MAPT) is a common cause of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP‐17). We compare clinicopathologic features of five unrelated and three related (brother, sister and cousin) patients with FTDP‐17 due to p.P301L mutation.MethodsGenealogical, clinical, neuropathologic and genetic data were reviewed from eight individuals.ResultsThe series consisted of five men and three women with an average age of death of 58 years (52–65 years) and average disease duration of 9 years (3–14 years). The first symptoms were those of behavioural variant frontotemporal dementia in seven patients and semantic variant of primary progressive aphasia in one. Three patients were homozygous for the MAPT H1 haplotype; five had H1/H2 genotype. The apolipoprotein E genotype was ϵ3/ϵ3 in seven and ϵ3/ϵ4 in one. The average brain weight was 1015 g (876–1188 g). All had frontotemporal lobar or more diffuse cortical atrophy. Except for one patient, the hippocampus and parahippocampal gyrus had minimal atrophy, whereas there was atrophy of middle and inferior temporal gyri. Dentate fascia neuronal dispersion was identified in three patients, two of whom had epilepsy. In one patient there was extensive white matter tau involvement with Gallyas‐positive globular glial inclusions typical of globular glial tauopathy (GGT).ConclusionsThis clinicopathologic study shows inter‐ and intra‐familial clinicopathologic heterogeneity of FTDP‐17 due to MAPT p.P301L mutation, including GGT in one patient.