News Prognostic Indicators Of Hospitalized Patients With Systemic Lupus Erythematosus A Large Retrospective Multicenter Study In China

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Abbreviation: NA, not available.

a Inferred from data presented; includes patients in whom no pathogen was isolated but who responded to antibiotic treatment. b Mycobacterium tuberculosis is the most frequent isolate. c Only major infections included. d Minor and major infections included.

Lupus Erythematosus Disseminatus

Fig. 1. Lateral radiograph of the thoracic spine. There is loss of intervertebral disc space at T7-8 with loss of the endplate cortex anteriorly and little reactive bone formation (Courtesy of Robert Lopez-Ben, Division of Diagnostic Radiology, Department of Radiology, The University of Alabama at Birmingham, Birmingham, Alabama).

Fig. 1. Lateral radiograph of the thoracic spine. There is loss of intervertebral disc space at T7-8 with loss of the endplate cortex anteriorly and little reactive bone formation (Courtesy of Robert Lopez-Ben, Division of Diagnostic Radiology, Department of Radiology, The University of Alabama at Birmingham, Birmingham, Alabama).

Viral infections

Herpes zoster is the most frequent viral infection [5,11,13,17,58,62], occurring mainly in patients who have SLE with previous histories of nephritis, hemolytic anemia, thrombocytopenia, and previous use of cyclophosphamide [95]. Localized HZ is the most common clinical presentation and generally occurs during periods of disease quiescence and in patients receiving 20 mg or less of prednisone per day [95]. Disseminated HZ and bacterial superinfection also may occur and usually are related to the use of high doses of corticosteroids (prednisone > 60 mg/d) or immunosuppressants [58,95].

Cytomegalovirus (CMV) is another opportunistic infection occurring in patients who have SLE, especially in those receiving cyclophosphamide or high doses of corticosteroids [16,18,96-98] or in patients receiving plasmapheresis [62]. Pneumonia and encephalitis produced by CMV are fatal in most cases [16,19]. Risk behaviors leading to infection by retroviruses are not believed to be increased in SLE patients [99]; thus, retroviral infections have not been described with increased frequency. Case reports, however, are emerging [100,101]. Nevertheless, infections with the human immunodeficiency virus need to be distinguished from SLE, because the illnesses share some clinical characteristics and some of the same autoantibodies [102,103].

Human parvovirus B19 DNA has been detected in patients who have SLE, but its clinical relevance is unclear to date [104].

Fungal infections

Fungal infections can occur frequently in patients who have SLE who are receiving high doses of corticosteroids or immunosuppressive therapy

Lupus Erythematosus Disseminatus

Fig. 2. Magnetic resonance image of the thoracic spine. (A) Sagittal Tl-weighted MR image of the thoracic spine. There is marked marrow edema in T7 and T8 vertebral bodies. An epidural mass bulges the posterior longitudinal ligament and compresses the spinal cord at this level. (B) Sagittal Tl-weighted MR image of the thoracic spine with fat suppression after intravenous administration of gadolinium contrast. There is marked contrast enhancement of the vertebral bodies of T7 and T8. There is rim enhancement of the epidural mass and the contiguous posterior disc space is better appreciated (Courtesy of Robert Lopez-Ben, Division of Diagnostic Radiology, Department of Radiology, The University of Alabama at Birmingham, Birmingham, Alabama).

Fig. 2. Magnetic resonance image of the thoracic spine. (A) Sagittal Tl-weighted MR image of the thoracic spine. There is marked marrow edema in T7 and T8 vertebral bodies. An epidural mass bulges the posterior longitudinal ligament and compresses the spinal cord at this level. (B) Sagittal Tl-weighted MR image of the thoracic spine with fat suppression after intravenous administration of gadolinium contrast. There is marked contrast enhancement of the vertebral bodies of T7 and T8. There is rim enhancement of the epidural mass and the contiguous posterior disc space is better appreciated (Courtesy of Robert Lopez-Ben, Division of Diagnostic Radiology, Department of Radiology, The University of Alabama at Birmingham, Birmingham, Alabama).

[16,19,58]. The most common fungal infections are produced by P carinii and Candida spp. The risk factors for developing PCP are the use of high doses of corticosteroids or of immunosuppressive drugs, and lymphopenia [58,105-110]. Although PCP occurs infrequently, it has a high mortality rate [19,58,106,107]; therefore, PCP prophylaxis may be indicated in patients who have SLE who have these risk factors. Infections by Candida spp (mainly Candida albicans) are common in patients who have SLE [11,17,19,20,58]. The clinical spectrum includes oral and esophageal mucosa infections and infections of the genitourinary tract [17]. Disseminated candi-diasis, which is frequently fatal, occurs less often [16,18-20,58]. Cryptococcal infection has been described in 10 of 17 patients who had CNS involvement observed over a 20-year period [31]. A case of disseminated cutaneous eumy-cotic mycetoma secondary to Cladophialophora bantiana has been described in a woman who had lupus and was receiving corticosteroids [111].

Disease flares, immunosuppressive therapy, leukopenia, and associated bacterial infections are risk factors for the development of aspergillosis in patients who have SLE [112,113]. There are only a few reported cases of aspergillosis; however, most of them have been lethal [16,112].

Parasitic infections

Disseminated strongyloidiasis with massive pulmonary hemorrhage was reported in a patient from Japan who had SLE [114]. Visceral leishmaniasis was reported in a German patient [115]. A case of Trypanosoma cruzi infection with high degree of parasitemia was reported in a Brazilian patient [116]. Encephalitis caused by Toxoplasma gondii has been described in patients who have SLE [117]. The cases of strongyloidiasis and leishmaniasis did not occur in areas where these infections are endemic, and it is unclear how these patients became infected with these pathogens. It is important to take appropriate diagnostic measures, because these parasitic infections can simulate clinical presentations of active SLE when they include neurologic, pulmonary, and gastrointestinal manifestations.

Infections in scleroderma

Predisposing factors

Risk factors associated with infections in patients who have scleroderma include esophageal and pulmonary involvement, severe Raynaud's phenomenon or calcinosis, and the use of specific treatments for the management of the disease. Scleroderma patients who have smooth muscle involvement of the esophagus are at increased risk for aspiration pneumonia, because these patients usually have lower esophageal sphincter dysfunction and severe gas-troesophageal reflux [14,118-120]. To avoid postoperative infections, esoph-ageal involvement should be considered and ruled out in patients who have scleroderma with lung involvement selected to receive lung transplants [119,121]. Pneumonia has been described in patients who have scleroderma with pulmonary involvement, particularly in those who have interstitial lung disease [6], suggesting that pulmonary fibrosis may be a predisposing factor for the development of pulmonary infections. Oftentimes, bronchoalveo-lar lavage is necessary to determine if there is a concomitant infection [122].

In patients who have scleroderma, severe Raynaud's phenomenon with digital ischemia and ulcerations increases the risk for localized superinfections, which may be complicated by gangrene [119]. Severe calcinosis also has been associated with bacterial infections, especially in the soft tissues around the calcific lesions [123]. Although there are no large studies from which to draw conclusive data, some reported cases show that the risk for infection relates to specific treatments. For example, the aggressive use of immunosuppression and autologous stem cell transplantation resulted in a lethal infection in a neutropenic patient who had scleroderma [124]. Pneumonia has been reported with cyclophosphamide and corticosteroid use [125], and local infections have been reported in 10% of patients receiving subcutaneous relaxin [126].

Infections as a cause of death

In patients who have scleroderma, pulmonary complications cause 17% to 24% of the mortality [127,128]. Pneumonia has been described in patients who had scleroderma who died of pulmonary involvement [6]. In the

Swedish scleroderma cohort studied by Hesselstrand and colleagues [6], approximately 12% of deaths were caused by pneumonia and severe lung fibrosis occurring simultaneously. Aspiration pneumonia also has been described as a cause of death in patients who have scleroderma with esoph-ageal involvement, often producing adult respiratory distress syndrome [14,120]. A fatal case of myocardial necrosis has been reported recently in which Staphylococcus lugdunensis and CMV were identified at necropsy [129]. Unlike SLE, however, there are no conclusive data regarding infections as a predictive factor of mortality in scleroderma [6,73,127,128,130].

Types of infections occurring in scleroderma

Bacterial infections

Data about common bacterial infections in patients who have scleroderma are limited to case reports. Group G streptococcus pyomyositis was described in a patient who had scleroderma who was receiving chloram-bucil [131], and soft tissue S aureus infection around multiple calcific lesions was reported in a patient who had scleroderma and a long history of Ray-naud's phenomenon [123]. Another patient who had scleroderma with lower gastrointestinal tract involvement was reported to have developed bacterial peritonitis secondary to colon perforation [132].

M avium intracellulare, an opportunistic infection, was the cause of septic arthritis in another patient who had scleroderma; he did not respond to medical treatment, refused surgical intervention, and went on to develop osteomyelitis and subsequently Charcot's arthropathy [133]. M kansasii was the cause of tenosynovitis in a woman who had scleroderma receiving cor-ticosteroids [134]. An ocular infection secondary to nocardia was described in a patient who had scleroderma who was receiving a moderate dose of corticosteroids [135].

A report from Japan describes an increased frequency of Helicobacter pylori infection in patients who have scleroderma; a possible role of this infection in esophageal dysfunction has been suggested but remains unproven for now [136].

Viral and fungal infections

There has been only one case report of viral infections complicating the course of scleroderma. This patient was a 40-year-old who had limited scleroderma and developed a flu-like illness followed by acute heart failure and high IgM anti-adenovirus titer; as serologic conversion to IgG occurred, heart failure resolved [137]. Nevertheless, Epstein-Barr virus and CMV have been described as triggering the onset of scleroderma, particularly in pediat-ric patients [138,139], and parvovirus B19 DNA has been detected in patients who have scleroderma, but the clinical correlate of this finding is unclear at the present [140]. P carinii pneumonia has been reported in some patients who have scleroderma. This infection is rare but has a rapid and usually fatal course. An early diagnosis in patients who have respiratory failure is important if the survival rate is to be improved [141].

Esophageal fungal infections have been described with the same frequency in patients who have scleroderma with and without esophageal involvement [142]; treatment of these fungal infections, however, is not followed by improvement of esophageal motility.

Infections in polymyositis/dermatomyositis

Predisposing factors

Patients PM/DM have a host of predisposing factors placing them at risk for developing infections. These factors include upper esophageal involvement, thoracic muscle myopathy, calcinosis cutis, and the use of immuno-suppressive drugs.

Some patients who have PM/DM have involvement of the striated muscle of the hypopharynx and the upper third of the esophagus resulting in altered swallowing, gastroesophageal reflux, and aspiration, and a greater risk for developing aspiration pneumonia [7,8,14,118,143,144]. Likewise, the myopathy affecting the thoracic muscles, present in less than 5% to 10% of PM/DM patients, creates difficulty in handling bronchial secretions [7,8,143]. This difficulty may lead to the development of atelectasis and ventilatory insufficiency [8,144]. This ventilatory compromise can worsen the course of aspiration pneumonia, thereby increasing the risk for death from this complication [8,144].

Calcinosis cutis, frequently described in patients who have juvenile dermatomyositis [7,143], is a known risk factor for the development of staphylococcal soft tissue and dermal infections around calcinotic lesions [145-147]. This risk probably results from the decreased granulocyte chemo-taxis to S aureus that has been described in these patients [147]. These infections may cause severe growth retardation of the extremities and significant functional impairment, thus worsening the course of the disease [146].

To date, there are no large-scale studies comparing the use of immuno-suppressive drugs and the incidence of infections. Reported case studies, however, suggest that the simultaneous use of corticosteroids and immuno-suppressive drugs in the treatment of PM/DM could increase the risk for infections [148]. For example, a patient who had PM/DM who was treated with methotrexate (22.5 mg/wk) and prednisone (50 mg/d) developed PCP [148], and a pediatric patient who had severe dermatomyositis treated with methotrexate (25 mg/wk) and prednisone (150 mg/d) (extremely high dose verified) developed disseminated nocardiosis [149].

Infections as a cause of death

Malignancy [7,8,143,150] and pulmonary complications [7,8,143,150,151] are the main causes of death among patients who have PM/DM. Aspiration pneumonia is one of the most common pulmonary complications [7,8,14,143,144,150,151] and causes of death in patients who have PM/DM [8,144]. In the study published by Marie and coworkers [8], aspiration pneumonia was reported in 17% of all patients who had PM/DM and was \responsible for 30% of the mortality. Aspiration pneumonia has emerged as an independent predictive factor for PM/DM deterioration and as a risk factor for death in patients who have PM/DM. Patients who have esophageal and respiratory compromise should be diagnosed and treated early to decrease the probability of a fatal outcome [7,8,14,118,143,144].

Types of infections occurring in polymyositis/dermatomyositis

Bacterial infections

Aspiration pneumonia, produced by Gram-positive and anaerobic bacteria, is the most common infection, occurring in 15% to 20% of patients who have PM/DM [8,144].

S aureus infections involving the soft tissue and skin around calcinotic lesions are described frequently in patients who have juvenile dermatomyositis and calcinosis cutis [145,147]. Other bacterial infections in dermatomyositis constitute only isolated reported cases. For example Streptococcus pyogenes myositis has been described in patients who have juvenile and adult DM with or without calcinosis; in these patients the myopathy probably favored the bacterial colonization of muscle from bacteremia originating in dermal lesions [152,153]. Recently the case of a patient who had polymyositis and severe gastric symptoms was reported in which these symptoms resolved after triple therapy to eradicate H heilmanii [154].

Opportunistic infections have been described in about 12% of patients who have PM/DM, being fatal in nearly 28% of these patients in a study from France [155]. Among the opportunistic infections, disseminated Nocar-dia brasiliensis involving the skin and the lungs has been reported in both children and adults who have myositis receiving corticosteroids and immu-nosuppressive therapy [149,156], and extrapulmonary infections produced by M tuberculosis and generalized M avium intracellulare have been described in patients who have PM/DM [157,158]. Other atypical mycobac-terial infections also have been described [156]. Although opportunistic infections in these patients are uncommon, early diagnosis and adequate treatment are essential to improve survival.

Viral infections

HZ is a common viral infection in patients who have PM/DM and usually occurs during periods of disease inactivity [159]. CMV is an uncommon opportunistic viral infection in patients who have PM/DM; however, some cases of severe and fatal infection, such as interstitial pneumonia, have been noted in patients receiving corticosteroid or immunosuppressive therapy [160-163]. Some studies have demonstrated a temporal relationship between coxsackievirus, parvovirus B19, hepatitis C, and other enterovirus infections and the onset of PM/DM; however, the role of these pathogens in the cause of PM/DM remains speculative [164-166].

Fungal infections

PCP is frequently fatal in patients who have PM/DM. This infection has a rapid and severe course, and most patients require critical care support [105,110,167]. Known risk factors for the development of PCP are interstitial pulmonary disease [106], lymphopenia [105,106,167], and the use of corticosteroids [105,167] and immunosuppressive drugs [105]. Based on the often fatal course of PCP, patients who have these risk factors can benefit from the initiation of PCP prophylaxis, although there are no definite published guidelines.

Candidiasis is another fungal infection occurring in patients who have dermatomyositis. In a large study of more than 40,000 patients who had various skin disorders, the frequency of mucocutaneous candidiasis was three times higher in patients who had dermatomyositis, bullous pemphigoid, tinea inguinalis, or condylomata acuminata than in the general population, suggesting that preexisting dermal involvement may increase the susceptibility of patients who have dermatomyositis to this infection [168].

Finally, disseminated histoplasmosis involving the muscles and fascia has been reported in a patient who had dermatomyositis being treated with cortico-steroids and methotrexate, who was initially believed to have a disease flare [169].

Summary

In SLE, scleroderma, and PM/DM, infections are important causes of morbidity and mortality. This increased risk for developing infections is the result of immune abnormalities and of organ system manifestations associated with these diseases and their treatments. Common bacteria are responsible for most mild and lethal infections; however, opportunistic microorganisms cause death in some patients, particularly in those receiving high doses of corticosteroid and immunosuppressive therapy. Various viral and fungal infections also contribute to the morbidity and mortality associated with these diseases. Regardless of the cause of infections, adequate and prompt recognition and proper treatment of the infected patient are imperative. Patients who have these diseases, especially when receiving high doses of corticosteroids and immunosuppressive therapy, need to be monitored closely for these infections. This care and concern is necessary to ensure optimal patient outcomes, both in morbidity and mortality.

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