ABSTRACT
BACKGROUND Fibromyalgia (FM) is a common disorder of diffuse musculoskeletal pain. It is distinctly different from polymyalgia rheumatica (PMR), a disease seen in people over the age of 50 years. Hallmark features of PMR are the presence of elevated erythrocytes sedimentation rate (ESR) and/or C-reactive protein (CRP). These markers are normal in FM. Obesity in itself can be associated with elevated CRP and ESR, and when obese patients present with myalgia and elevated inflammatory markers, diagnostic confusion can ensue. CASE REPORT We describe a case of 38-year-old female with diffuse musculoskeletal pain and elevated ESR and CRP who was initially misdiagnosed with PMR and responded partially to steroids. She developed severe adverse effects from chronic steroid use. She was ultimately diagnosed with FM. CONCLUSIONS We highlight features to help clinicians avoid the pitfall of diagnosing PMR in young obese patients with FM and elevated inflammatory markers. In this case report, we discuss the features of FM, PMR, PMR-like symptoms presentation, and the association of obesity with elevated inflammatory markers.
Subject(s)
Blood Sedimentation , C-Reactive Protein/analysis , Fibromyalgia/diagnosis , Myalgia/etiology , Obesity/complications , Adult , Biomarkers/blood , Diagnostic Errors , Female , Fibromyalgia/blood , Humans , Myalgia/complications , Polymyalgia Rheumatica/blood , Polymyalgia Rheumatica/diagnosisABSTRACT
Felty syndrome(FS) is an uncommon, but severe, extra-articular manifestation of rheumatoid arthritis (RA). It occurs in patients with longstanding RA. It is extremely rare for RA to present as FS or develop after initially presenting as neutropaenia and splenomegaly. We describe a case of 47-year-old woman who was diagnosed simultaneously with FS and possible RA after testing positive for anticyclic citrullinated peptide antibody, but a negative rheumatoid factor. She had an excellent response to methotrexate. We review the existing literature of such cases and emphasise the importance of serological testing for RA in patients presenting with neutropaenia and splenomegaly, even in the absence of joint symptoms or prior diagnosis of RA.
Subject(s)
Arthritis, Rheumatoid/diagnosis , Felty Syndrome/diagnosis , Neutropenia/diagnosis , Splenomegaly/diagnosis , Arthritis, Rheumatoid/immunology , Autoantibodies/blood , Diagnosis, Differential , Felty Syndrome/etiology , Felty Syndrome/immunology , Female , Humans , Middle Aged , Neutropenia/immunology , Peptides, Cyclic/immunology , Rheumatoid Factor/blood , Splenomegaly/immunologyABSTRACT
Recently we have established that the kidney tubular epithelium is repaired by surviving epithelial cells. It is not known, however, whether a population of intratubular adult progenitor cells are responsible for this epithelial repair after acute kidney injury. In this study, we used an unbiased DNA analog-based approach that does not rely on candidate markers to track multiple rounds of cell division in vivo. In the proximal tubule, robust thymidine analog incorporation was observed postinjury. Cell division was stochastic and enriched among cells that were injured and dedifferentiated. There was no evidence for the presence of a population of specialized progenitors that repeatedly divide in response to injury. Instead, these results indicate that after injury, new epithelial cells arise from self-duplication of surviving cells, most of which are injured. Because the renal papilla contains DNA label-retaining cells and has been proposed as a stem cell niche, we examined the proliferative behavior of these putative progenitors after ischemia-reperfusion injury. Although label-retaining cells in the renal papilla diminished with time after ischemia-reperfusion injury, they neither proliferated nor migrated to the outer medulla or cortex. Thus, nonlethally injured cells repopulate the kidney epithelium after injury in the absence of any specialized progenitor cell population.
