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Biomedical subjects

Lisa Christopher-Stine

Publications and source records attributed to Lisa Christopher-Stine.

7 recordsLinked to original sources
PubMed2006

Renal biopsy in lupus patients with low levels of proteinuria.

OBJECTIVE: Early and accurate detection of kidney involvement in systemic lupus erythematosus (SLE) improves outcomes. Renal biopsy is required for definitive diagnosis of lupus nephritis (LN). In the absence of acute renal failure (ARF), moderate levels of proteinuria (> 1000 mg/24 h) have been recommended by some to justify biopsy. We investigated whether patients with lower levels of proteinuria without ARF have significant renal disease and should be routinely biopsied. METHODS: We retrospectively evaluated 21 SLE patients with 24-h urine protein < 1000 mg who underwent kidney biopsies. Indications for biopsy included new-onset proteinuria, increasing proteinuria, or hematuria (> 5 red blood cells per high power field). No patient had ARF. RESULTS: Sixteen of 21 (77%) biopsies were diagnostic of LN: 3 class II, 10 class III (5 superimposed class V), 2 class IV (one superimposed class V), and one with class V. One patient had thrombotic microangiopathy. The remaining 4 (23%) patients had non-lupus renal disease. Thirteen patients with class III or greater LN required alterations in therapeutic regimen because of biopsy findings. Of 7 patients without hematuria at the time of biopsy, 4 (57%) had class III, IV, or V LN. One patient without hematuria and < 500 mg/24 h proteinuria had class III LN. CONCLUSION: We found significant renal involvement (Class III, IV, or V LN) in SLE patients with < 1000 mg proteinuria with or without hematuria. Our findings suggest that biopsy be strongly considered in this patient population.

Adolescent↗
PubMed2006

Statin myopathy: an update.

PURPOSE OF REVIEW: Statin therapy has become the mainstay of treatment for lipid lowering, demonstrating cardiovascular risk reduction. Associated with statin popularity are misconceptions and fears of untoward side effects on muscle. This review clarifies the terminology relating to statin-related muscle disease; explores potential pathogenic mechanisms; reviews current estimates of statin myopathy prevalence; and examines diagnosis and management. RECENT FINDINGS: The fundamental mechanism of statin myopathy remains elusive but is believed to be a class effect. The most common explanation for the cause of toxic muscle injury invokes the deficiency of one of three main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway. Recent studies have revealed several patients with statin-induced rhabdomyolysis who also have metabolic muscle defects, indicating that statin use may unmask presymptomatic metabolic myopathies. Although statin-related myotoxicity is believed to be a noninflammatory, toxic myopathy, experimental evidence suggests that it may be triggered by an autoimmune reaction or, conversely, initiate an autoimmune process. The precise mechanism is uncertain. SUMMARY: As a class, statins appear to be usually safe, well tolerated agents with an excellent risk: benefit profile. The etiology and pathogenesis of statin myopathy are poorly understood owing to the relative rarity of its existence.

Humans↗
PubMed2004

Adult inflammatory myopathies.

The major inflammatory myopathies of adults-dermatomyositis, polymyositis and inclusion body myositis-are uncommon and can be difficult to distinguish from many conditions that mimic them clinically. They have a high morbidity; they are not infrequently the first sign of an associated malignancy; and they may be a part of another connective tissue disease. Their pathogenetic features suggest that they are different illnesses. Dermatomyositis and polymyositis are clearly inflammatory, both clinically and histologically, and both generally respond to therapy directed towards inflammation. Inclusion body myositis is now generally recognized as the most common myopathy presenting in patients over the age of 50 years, and it responds only modestly and sometimes not at all to immunosuppressive therapy. In this review, we have summarised the major newly recognized features of pathogenesis, the involvement of extramuscular organs, the differential diagnosis, diagnostic approaches and the main lines of therapy.

Adult↗
PubMed2004

Myositis: an update on pathogenesis.

PURPOSE OF REVIEW: The etiology and much about the pathogenesis of the inflammatory myopathies remain a mystery. In this review, we investigate recent research efforts to understand the pathogenesis of the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM), diseases that result from interactions between environmental risk factors and genetic susceptibility. RECENT FINDINGS: Over the past year, there has been considerable progress toward better understanding of IBM, with relatively few developments toward understanding PM and DM. Although these diseases may share some common clinical phenotypic and serologic components, they differ on a molecular and cellular level. SUMMARY: The need for definitive, safer therapies in these diseases makes vital the search for defining detailed pathogenesis of inflammation and muscle fiber damage at the molecular level.

Animals↗
PubMed2004

Urine protein-to-creatinine ratio is a reliable measure of proteinuria in lupus nephritis.

OBJECTIVE: To evaluate the 24-hour urine protein-to-creatinine (U pr:cr) ratio compared to 24-h urine total protein excretion as a measure of proteinuria in patients with lupus nephritis. METHODS: Proteinuria in 8 patients with lupus nephritis treated with cyclophosphamide was monitored by total protein excretion and U pr:cr ratio in 24-h urine collections. A median of 16 measurements per patient were collected over a median of 47 months. Adequacy of the 24-h collection was assessed by comparing total urine creatinine to the predicted creatinine. Collections in which the difference between the predicted 24-h urine creatinine and the measured 24-h urine creatinine was greater than or equal to 20% were defined as inadequate collections. RESULTS: Timed 24-h urine collections were frequently inadequate (30.2% of total collections were under-collections, while 14.3% were over-collections). We found 87.5% of patients had at least one under-collection whereas 75% had at least one over-collection. Correlations between total protein and U pr:cr ratio for individual patients ranged from 0.87 to 0.99 (mean 0.95). For the entire sample, the correlation (R2 = 0.89) of total urine protein to Upr:cr ratio was excellent. Excluding the 38 under-collections led to improvement in the overall correlation (0.94). Excluding the 18 over-collections led to a correlation of 0.89. Excluding both under-collections and over-collections led to a correlation of 0.94. CONCLUSION: In patients with lupus nephritis, the 24-h U pr:cr ratio is highly correlated with the 24-h urine protein excretion when the collections are adequate. The error of the estimate is higher when collections are poor.

Adult↗