Atorvastatin-induced reversible positive antinuclear antibodies

Jiménez-Alonso, J; Jáimez, L; Sabio, José Mario; Hidalgo, Carmen; Leon, L L

doi:10.1016/s0002-9343(01)01102-0

Cited by 22 publications

(11 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Statins are known to induce many autoimmune diseases, as discussed previously 14,18. Statins also have immunomodulatory properties, including loss of immune tolerance and production of pathogenic autoantibodies 6. AChR-ab titer increase in our 2 cases favors this theory.…”

Section: Discussionmentioning

confidence: 54%

Statins may aggravate myasthenia gravis

Dhall

Young

et al. 2008

Muscle and Nerve

View full text Add to dashboard Cite

Statin-induced myopathy is well-known, but the effect of cholesterol-lowering agents on myasthenia gravis (MG) has not been studied in detail. We investigated statin use and its effects on MG among patients with this disease. Statin information was systemically obtained from 170 patients being treated at the Neuromuscular Disease Clinic at the University of Alabama at Birmingham. When a new myalgic syndrome or worsening of MG developed within 4 months after statin treatment, no other likely cause was found, and clinical improvement occurred either with or without discontinuation of the statin, we considered these symptoms to be statin-induced. Fifty-four patients (31%) were on statins. The statin group had proportionally more males, and older patients compared with the non-statin group. A myalgic syndrome was noted in 7 (13%) patients, but it resolved without any sequelae after withdrawal of the statin. MG worsening occurred in 6 (11%) patients without regard to type of MG or brand of statin. MG worsening occurred independently of myalgic syndrome and involved predominantly oculobulbar symptoms within 1-16 weeks of statin treatment. In 4 patients, additional treatment was needed to reverse MG worsening. Statins are safe in the majority of MG patients, but their use must be accompanied by close observation for possible MG worsening.

show abstract

Section: Discussionmentioning

confidence: 54%

Statins may aggravate myasthenia gravis

Dhall

Young

et al. 2008

Muscle and Nerve

View full text Add to dashboard Cite

show abstract

“…However, the development of anti-nuclear Abs and a lupus-like syndrome has been reported in patients receiving statin therapy (12,13). Thus, to examine the potential immunomodulatory effect of atorvastatin in lupus we have used NZB/W F 1 female mice.…”

mentioning

confidence: 99%

Atorvastatin Inhibits Autoreactive B Cell Activation and Delays Lupus Development in New Zealand Black/White F1 Mice

Lawman

Mauri

Jury

et al. 2004

The Journal of Immunology

109

View full text Add to dashboard Cite

Systemic lupus erythematosus is a multisystem autoimmune disease characterized by a wide range of immunological abnormalities that underlie the loss of tolerance. In this study we show that administration of atorvastatin to lupus-prone NZB/W F1 mice resulted in a significant reduction in serum IgG anti-dsDNA Abs and decreased proteinuria. Histologically, the treatment was associated with reduced glomerular Ig deposition and less glomerular injury. Disease improvement was paralleled by decreased expression of MHC class II on monocytes and B lymphocytes and reduced expression of CD80 and CD86 on B lymphocytes. Consequent upon this inhibition of Ag presentation, T cell proliferation was strongly impaired by atorvastatin in vitro and in vivo. A significant decrease in MHC class II expression was also observed in the target organ of lupus disease (i.e., the glomerulus). Serum cholesterol in atorvastatin-treated lupus mice fell to the level found in young NZB/W mice before disease onset. This is the first demonstration that atorvastatin can delay the progression of a spontaneous autoimmune disease and may specifically benefit patients with systemic lupus erythematosus.

show abstract

“…These findings underscore two important points that clinicians should note: [1] the need to use clindamycin more discriminately in spite of its excellent coverage as a broad-spectrum antibiotic, and [2] to be more alert in recognising the potential risk of CA-CDI progressing to severe complicated CDI in young adults. Additionally, clinicians and other healthcare providers should be prudent to employ appropriate patient management to reduce the morbidity and mortality rate among hospitalised C. difficile infected individuals.…”

Section: Discussionmentioning

confidence: 75%

“…difficile ) is the major cause of nosocomial antibiotic-associated diarrhoea [1,2], while secondary Gram-negative shock in community-acquired Clostridium difficile infection (CA-CDI) may occur following bowel perforation in hospitalised patients [3]. CA-CDI is defined as symptoms that occur in the community or within 48 hours of admission to a hospital, provided symptoms from onset were > 12 weeks after the last discharge from a hospital [3].…”

Section: Introductionmentioning

confidence: 99%

A unique strain of community-acquired Clostridium difficile in severe complicated infection and death of a young adult

et al. 2013

View full text Add to dashboard Cite

BackgroundClostridium difficile is the major cause of nosocomial antibiotic-associated diarrhoea with the potential risk of progressing to severe clinical outcomes including death. It is not unusual for Clostridium difficile infection to progress to complications of toxic megacolon, bowel perforation and even Gram-negative sepsis following pathological changes in the intestinal mucosa. These complications are however less commonly seen in community-acquired Clostridium difficile infection than in hospital-acquired Clostridium difficile infection. To the best of our knowledge, this was the first case of community-acquired Clostridium difficile infection of its type seen in Jamaica.Case presentationWe report a case of a 22-year-old female university student who was admitted to the University Hospital of the West Indies, Jamaica with a presumptive diagnosis of pseudomembranous colitis PMC. She presented with a 5-day history of diarrhoea following clindamycin treatment for coverage of a tooth extraction due to a dental abscess. Her clinical condition deteriorated and progressed from diarrhoea to toxic megacolon, bowel perforation and Gram-negative sepsis. Clostridium difficile NAP12/ribotype 087 was isolated from her stool while blood cultures grew Klebsiella pneumoniae. Despite initial treatment intervention with empiric therapy of metronidazole and antibiotic clearance of Klebsiella pneumoniae from the blood, the patient died within 10 days of hospital admission.ConclusionsWe believe that clindamycin used for coverage of a dental abscess was an independent risk factor that initiated the disruption of the bowel micro-flora, resulting in overgrowth of Clostridium difficile NAP12/ribotype 087. This uncommon strain, which is the same ribotype (087) as ATCC 43255, was apparently responsible for the increased severity of the infection and death following toxic megacolon, bowel perforation and pseudomembranous colitis involving the entire large bowel. K. pneumoniae sepsis, resolved by antibiotic therapy was secondary to Clostridium difficile infection. The case registers community-acquired Clostridium difficile infection as producing serious complications similar to hospital-acquired Clostridium difficile infection and should be treated with the requisite importance.

show abstract

Atorvastatin-induced reversible positive antinuclear antibodies

Cited by 22 publications

References 9 publications

Statins may aggravate myasthenia gravis

Statins may aggravate myasthenia gravis

Atorvastatin Inhibits Autoreactive B Cell Activation and Delays Lupus Development in New Zealand Black/White F1 Mice

A unique strain of community-acquired Clostridium difficile in severe complicated infection and death of a young adult

Contact Info

Product

Resources

About