Systemic lupus erythematosus natural history, complications and prognosis: Difference between revisions

Jump to navigation Jump to search
Line 3: Line 3:
{{CMG}}; {{AE}}{{MIR}}
{{CMG}}; {{AE}}{{MIR}}
==Overview==
==Overview==
Common complications of systemic lupus erythematosus include dermatitis, nephritis and arthiritis. Prognosis is generally poor, and the 10-year mortality rate of patients with systemic lupus erythematosus is approximately 40%. The disease course can be divided into 4 subcategories based on the course of the disease: developmental phase, preclinical phase, clinical phase, and comorbid complication phase.
Common complications of systemic lupus erythematosus include [[dermatitis]], [[nephritis]] and [[arthritis]]. [[Prognosis]] is generally poor, and the 10-year [[mortality rate]] of patients with systemic lupus erythematosus is approximately 40%. The disease course can be divided into 4 subcategories based on the course of the disease: developmental phase, preclinical phase, clinical phase, and comorbid complication phase.
==Natural History==
==Natural History==
*Systemic lupus erythematosus (SLE) is an [[autoimmune disease]]. SLE is a disease of waxing and waning, with possible flare up episodes. SLE usually develops in the second and third decade of life, although it can presents any age, and start with mild symptoms such as [[fatigue]], fever, and skin [[rashes]]. Without treatment, the patient will develop symptoms of end organ damage, which will eventually lead to death in most of the patients.
*Systemic lupus erythematosus (SLE) is an [[autoimmune disease]]. SLE is a disease of waxing and waning, with possible flare up episodes. SLE usually develops in the second and third decade of life, although it can presents any age, and start with mild symptoms such as [[fatigue]], [[fever]], and skin [[rashes]]. Without treatment, the patient will develop symptoms of [[end organ damage]], which will eventually lead to death in most of the patients.
*The disease course can be divided into 4 subcategories based on the course of the disease:
*The disease course can be divided into 4 subcategories based on the course of the disease:
   
   
Line 16: Line 16:
*Mostly associated with [[auto-immune]] [[antibody]] production
*Mostly associated with [[auto-immune]] [[antibody]] production
*[[Autoantibodies]] common to other systemic autoimmune diseases
*[[Autoantibodies]] common to other systemic autoimmune diseases
*Proceeds with a more disease-specific clinically overt autoimmune phase
*Proceeds with a more disease-specific clinically overt [[Autoimmune disease|autoimmune phase]]
   
   
===== Clinical phase: =====
===== Clinical phase: =====
*The phase due to damages of the auto-antibodies to the body tissues (mostly related to disease itself)
*The phase due to damages of the [[autoantibodies]] to the body tissues (mostly related to disease itself)
*[[Inflammation]]
*[[Inflammation]]
*Involvement of first organs
*Involvement of first organs
*Flares
*Flares
*Involvement of additional organs
*Involvement of additional organs
*Early damages (e.g. alopecia, fixed erythema, cognitive dysfunction, valvular heart disease, avascular necrosis, tendon rupture, Jaccoud’s arthropathy, and osteoporosis)
*Early damages (e.g. [[alopecia]], [[Erythema|fixed erythema]], [[Cognitive disorder|cognitive dysfunction]], [[valvular heart disease]], [[avascular necrosis]], [[Tendonitis|tendon rupture]], [[Jaccoud's arthropathy|Jaccoud’s arthropathy]], and [[osteoporosis]])
   
   
===== Comorbidity-complication phase =====
===== Comorbidity-complication phase =====
*The phase of damages due to complications of longstanding disease, [[immunosuppressive therapy]], and end organ damages (irreversible damages and complications)
The phase of damages due to complications of longstanding disease, [[immunosuppressive therapy]], and [[End organ damage|end organ damages]] (irreversible damages and complications)
*Infections
*[[Infections]]
*[[Atherosclerosis]]
*[[Atherosclerosis]]
*[[Malignancies]]
*[[Malignancies]]
Line 37: Line 37:
* [[Ultraviolet]] light
* [[Ultraviolet]] light
* [[Infection]]
* [[Infection]]
* Injuries
* [[Injuries]]
* [[Surgery]]
* [[Surgery]]
* [[Pregnancy]]
* [[Pregnancy]]
* Abrupt discontinuation of medications
* Abrupt discontinuation of medications
* Treatment noncompliance
* Treatment noncompliance
* Medications
* [[Medications]]
* Immunizations
* [[Immunization|Immunizations]]


==Complications==
==Complications==
Line 56: Line 56:
|[[Dysphagia]]
|[[Dysphagia]]
|
|
* The most frequent gastrointestinal complaint and is usually due to an underlying esophageal motility disorder, concomitant [[gastroesophageal reflux disease]].
* Usually due to an underlying [[esophageal motility disorder]]
|
* Concomitant [[gastroesophageal reflux disease]]
|↑↑
|-
|-
|[[Peptic ulcer disease]]
|[[Peptic ulcer disease]]
|
|
* May be due to the disease itself or the effect of SLE treatment.
* Due to
|
** The disease itself
** The effect of SLE treatment
|
|-
|-
|[[Intestinal pseudo-obstruction|Intestinal pseudo-obstruction]]
|[[Intestinal pseudo-obstruction|Intestinal pseudo-obstruction]]
|
|
* A rare complication of SLE and lead to mechanical obstruction of the small or large bowel in the absence of an anatomic lesion obstructing the flow of intestinal contents.
* May lead to [[Gastrointestinal obstruction|mechanical obstruction]] of the small or large bowel in the absence of an anatomic lesion
|
* Obstructing the flow of intestinal contents
|↓↓
|-
|-
|[[Protein-losing enteropathy|Protein-losing enteropathy]]
|[[Protein-losing enteropathy|Protein-losing enteropathy]]
|
|
* It typically occurs in patients with clinically severe SLE with multi-organ involvement and characterized with the onset of profound edema and [[hypoalbuminemia]] in the absence of nephrotic range [[proteinuria]].
* Occurs in patients with clinically severe SLE with multi-organ involvement
|
* Characterized by:
** [[Edema|Profound edema]]
** [[hypoalbuminemia]]
* The absence of [[nephrotic]] range [[proteinuria]]
|
|-
|-
|[[Hepatitis]]
|[[Hepatitis]]
|
|
* May be due to a wide range of factors including drug-induced damage, steatosis, viral hepatitis, vascular thrombosis, overlap with autoimmune hepatitis, or SLE itself.
* May be due to:
|
** [[Drug-induced lupus erythematosus|Drug-induced damage]]
** [[Steatosis]]
** [[Viral hepatitis]] (concomitant with SLE)
** [[Thrombosis|Vascular thrombosis]]
** Overlap with [[autoimmune hepatitis]] due to SLE itself
|
|-
|-
|[[Acute pancreatitis|Acute pancreatitis]]
|[[Acute pancreatitis|Acute pancreatitis]]
|
|
* It occurs usually in the setting of active SLE.
* Occurs usually in the setting of active SLE
|
|
|-
|-
|[[Mesenteric vascular occlusion|Mesenteric vasculitis]]
|[[Mesenteric vascular occlusion|Mesenteric vasculitis]]
|
|
* Most often this involves medium-sized branches of the [[Celiac artery|celiac]], [[Superior mesenteric artery|superior mesenteric]], and [[Inferior mesenteric artery|inferior mesenteric arteries]]. Features of [[mesenteric]] [[vasculitis]] include [[abdominal pain]] or [[gastrointestinal bleeding]] with [[intestinal ischemia]], infarction, perforation, or [[pancreatitis]].
* Mostly involve:
* [[SBP|Primary spontaneous peritonitis]]: an infection that develops in the [[peritoneum]] mainly due to lupus [[vasculitis]].
** Medium-sized branches of the [[Celiac artery|celiac artery]]  
** [[Superior mesenteric artery|Superior mesenteric artery]]
** [[Inferior mesenteric artery|Inferior mesenteric artery]]  
* Features of [[mesenteric]] [[vasculitis]] include:
** [[abdominal pain]]  
** [[gastrointestinal bleeding]]  
** [[intestinal ischemia]], [[infarction]], [[perforation]]
** [[pancreatitis]]  
** [[SBP|Primary spontaneous peritonitis]]:  
*** An [[infection]] that develops in the [[peritoneum]] mainly due to lupus [[vasculitis]]  
|
|
|-
|-
|[[Acute cholecystitis]]
|[[Acute cholecystitis]]
|
|
* Due to periarterial [[fibrosis]] and acute vasculitis
* Due to periarterial [[fibrosis]] and [[Vasculitis|acute vasculitis]]
* It can progress to [[gangrene]], perforation, and [[sepsis]].
* May progress to [[gangrene]], [[perforation]], and [[sepsis]]
|
|
|-
|-
Line 99: Line 121:
|[[Pleural disease|Pleural disease]]
|[[Pleural disease|Pleural disease]]
|
|
* [[Pleuritis]] can lead to [[pleuritic chest pain]] with or without radiographic evidence of a [[pleural effusion]]. Pleuritis is a disease state in which there is [[inflammation]] of the [[pleura]], the lining of the [[pleural cavity]], surrounding the [[Lung|lungs]].
* May lead to:
* [[Pneumothorax]]: a collection of air within the pleural cavity.
** [[pleuritic chest pain]] with or without [[radiographic]] evidence of a [[pleural effusion]]
* [[inflammation]] of the [[pleura]], the lining of the [[pleural cavity]], surrounding the [[Lung|lungs]]
* [[Pneumothorax]]: a collection of air within the [[pleural cavity]]
|
|
|-
|-
|[[Pneumonitis|Acute pneumonitis]]
|[[Pneumonitis|Acute pneumonitis]]
|
|
* A rare and fulminant form of diffuse lung injury that generally occurs in previously healthy individuals and has a rapid onset with [[fever]], [[cough]], and [[Dyspnea|shortness of breath]].
* Fulminant form of diffuse lung injury
|
* Characterized by rapid onset with [[fever]], [[cough]], and [[Dyspnea|shortness of breath]]
|↓↓
|-
|-
|[[Pulmonary hemorrhage]]
|[[Pulmonary hemorrhage]]
|
|
* Pulmonary alveolar hemorrhage:
* Pulmonary alveolar hemorrhage:
** A rare complication
** Acutely ill patients with [[hemoptysis]], [[fever]], [[cough]], and [[hypoxemia]]  
** Acutely ill patients with [[hemoptysis]], [[fever]], [[cough]], and [[hypoxemia]].
** Extensive blood loss
** Blood loss can be extensive.
** Associated with high mortality rates of 70%–90%
** Associated with high mortality rates of 70%–90%
|
|↓↓
|-
|-
|[[Pulmonary hypertension]]
|[[Pulmonary hypertension]]
|
|
* Increased pressure in the [[pulmonary artery]] or [[lung]] [[Pulmonary circulation|vasculature]] presents with exertional [[Dypsnea|shortness of breath]], [[dizziness]], and [[faint]].
* Increased pressure in the [[pulmonary artery]] or [[lung]] [[Pulmonary circulation|vasculature]]  
|
* Characterized by [[Dypsnea|shortness of breath]], [[dizziness]], and [[faint]]
|
|-
|-
|[[Thromboembolic disease]]
|[[Thromboembolic disease]]
|
|
* Chronic [[inflammation]] during the disease flare ups is an important characteristic in SLE patients that increase the risk of thromboembolic events.
* Chronic [[inflammation]] that increase the risk of [[Thromboembolic disease|thromboembolic events]]
|
|
|-
|-
|Shrinking lung syndrome
|Shrinking lung syndrome
|
|
* A rare complication of SLE, that can cause [[dyspnea]] and [[Dyspnea|shortness of breath]] (estimated prevalence approximately 0.5%).
* Characterized by [[dyspnea]] and [[Dyspnea|shortness of breath]] (estimated prevalence approximately 0.5%)
|
|↓↓
|-
|-
| rowspan="5" |Cardiac involvement
| rowspan="5" |Cardiac involvement
Line 140: Line 165:
** [[Subacute bacterial endocarditis]]
** [[Subacute bacterial endocarditis]]
** [[Uremia]]
** [[Uremia]]
** [[Pulmonary arterial hypertension]] with right-sided heart failure
** [[Pulmonary arterial hypertension]] with [[right-sided heart failure]]
** [[Corticosteroid]]-related [[cardiomyopathy]]
** [[Corticosteroid]]-related [[cardiomyopathy]]
|
|
Line 146: Line 171:
|[[Valvular disease]]
|[[Valvular disease]]
|
|
* The most common form of cardiac involvement in SLE
* Different [[Valvular Diseases|valvular]] complications include:
* Different valvular complications include Libman-Sacks vegetations, valve thickening, and valve regurgitation due to [[Immunoglobulin]] and [[complement]] deposition in valvular structure
** [[Libman-Sacks endocarditis|Libman-Sacks vegetations]]
* More frequently affect mitral valve
** Valve thickening
|
** Valve regurgitation
* Mainly due to [[Immunoglobulin]] and [[complement]] deposition in valvular structure
* More frequently affect [[mitral valve]]
|↑↑
|-
|-
|[[Pericardial disease]]
|[[Pericardial disease]]
|
|
* Acute pericarditis
* [[Acute pericarditis]]
* Pericardial effusion
* [[Pericardial effusion]]
|
|
|-
|-
|[[Myocarditis]]
|[[Myocarditis]]
|
|
* It may present with [[chest pain]], [[ST segment elevation]], elevated biomarkers of [[myonecrosis]], [[heart failure]], and/ or [[sudden death]]. The inflammatory response especially during disease flare ups cause [[myonecrosis]] either directly or indirectly as part of an [[autoimmune]] reaction
* Characterized by:
** [[chest pain]]
** [[ST segment elevation]]
** Elevated biomarkers of [[myonecrosis]]
** [[heart failure]]
** [[sudden death]]
* [[myonecrosis]] may happen as a consequence of [[autoimmune]] reaction
|
|
|-
|-
|[[Coronary heart disease|Coronary artery disease]]
|[[Coronary heart disease|Coronary artery disease]]
|
|
* Increased risk of [[Atheroma|atheromatous plaques]] due to autoimmune status of SLE may result in myocardial infarction (MI).
* Mainly as a result of increased risk of [[Atheroma|atheromatous plaques]] due to autoimmune status of SLE
|↑↑
|↑↑
|-
|-
Line 170: Line 204:
|[[Cognitive-shifting|Cognitive dysfunction]]
|[[Cognitive-shifting|Cognitive dysfunction]]
|
|
* The mental status of SLE patients can be temporarily affected by multiple, transient metabolic and systemic processes
* May be temporarily affected by multiple, transient [[metabolic]] and systemic processes
|
|
|-
|-
|[[Stroke]]
|[[Stroke]]
|
|
* Thrombotic stroke is increased in SLE due to small vessel vasculopathy.
* Increase risk of [[Ischemic stroke classification|thrombotic stroke]] due to [[Vasculopathy|small vessel vasculopathy]]
|
|
|-
|-
|[[Seizure|Seizures]]
|[[Seizure|Seizures]]
|
|
* Increased intracranial pressure can arise from a hypercoagulability state or thrombosis within the cerebral venous and can be the reason of seizures in these patients
* May happen secondary to [[increased intracranial pressure]]:
** [[Hypercoagulability]] state (due to inflammation)
** [[Thrombosis]] within the [[Cerebral venous sinus thrombosis|cerebral venous]]
|
|
|-
|-
|[[Psychosis]]
|[[Psychosis]]
|
|
* Psychosis is fairly common in SLE and can indirectly influence cognitive performance as well. The psychosis in SLE patients is mostly accompanied by hallucinations
* Can indirectly influence [[Cognition|cognitive performance]]
|
* Mostly accompanied by [[Hallucination|hallucinations]] in SLE
|↑↑
|-
|-
|[[Neuropathies]]
|[[Neuropathies]]
|
|
* Peripheral neuropathy prevalence is high in SLE and it is mostly related to disease activity
* [[Peripheral neuropathy]]
* There is a greater chance for the patients with central nervous system involvement to show manifestation of peripheral neuropathy
* Mostly related to disease activity
* There is a predilection for asymmetric and lower extremities involvement, especially peroneal and sural nerves
* [[Central nervous system]] involvement association
* A predilection for asymmetric and [[lower extremities]] involvement, especially [[peroneal]] and [[Sural nerve|sural nerves]]
|
|
|-
|-
Line 198: Line 236:
|[[Arthritis]]
|[[Arthritis]]
|
|
*Mostly symmetrical and non-erosive
*Mostly symmetrical and non-erosive arthritis
*Arthralgias
*[[Arthralgias]]
*Effusions
*Effusions
*Decreased range of motion of both small and large joints
*Decreased [[range of motion]] of both small and large joints
*Morning stiffness
*Morning stiffness
|
|↑↑
|-
|-
|[[Osteonecrosis]] ([[Avascular necrosis]])
|[[Osteonecrosis]] ([[Avascular necrosis]])
|
|
* Most common in the femoral head
* Most common in the [[Femoral|femoral head]]
* Can involve humeral head, tibial plateau, and scaphoid navicular 
* Can involve [[Humerus|humeral head]], [[Tibial|tibial plateau]], and scaphoid navicular 
* Usually bilateral and is often asymptomatic
* Usually [[bilateral]]
* Glucocorticoids treatment is associated with the greatest risk of developing the disease
* Often [[asymptomatic]]
* [[Glucocorticoids|Glucocorticoids treatment]] is associated with the greatest risk of developing the disease
|
|
|-
|-
|Subcutaneous nodules
|[[Subcutaneous tissue|Subcutaneous nodules]]
|
|
* In association with active disease
* Associated with active disease
|
|
|-
|-
|Osteoporosis  
|[[Osteoporosis]]
|
|
*Mostly due to [[glucocorticoid]] usage
*Mostly due to [[glucocorticoid]] usage
Line 225: Line 264:
|
|
|-
|-
|Skin disorder
| rowspan="5" |Skin disorder
|[[Cutaneous lupus erythematosus]]
|[[Cutaneous lupus erythematosus]]
|
|
*Erythema in a malar distribution over the cheeks and nose (but sparing the nasolabial folds), which appears after sun exposure
*[[Erythema]] in a malar distribution over the cheeks and nose (but sparing the [[nasolabial folds]]), which appears after sun exposure
*
|
|
|-
|-
|[[Photosensitivity]]
|
|
|Photosensitivity
* Common theme for skin lesions associated with SLE
|common theme for skin lesions associated with SLE
|↑↑
|
|-
|-
|[[Alopecia|Non-scarring alopecia]]
|
|
|Non-scarring alopecia
* May occur at some point during the course of their disease
|may occur at some point during the course of their disease
|
|
|-
|-
|oral and/or nasal ulcers
|
|
|oral and/or nasal ulcers
* Usually painless
|usually painless
|
|
|-
|-
|discoid lesions
|
|
|discoid lesions
* More inflammatory
|more inflammatory and which have a tendency to scar
* Have a tendency to scar
|
|
|-
|-
|Very rare disorders
| rowspan="3" |Very rare disorders
|Malignancy
|Malignancy
|
|
|
|
|-
|-
|
|Diabetes mellitus 
|Diabetes mellitus 
|
|
|
|
|-
|-
|
|Premature gonadal failure
|Premature gonadal failure
|
|

Revision as of 04:07, 26 July 2017

Systemic lupus erythematosus Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Systemic lupus erythematosus from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Lupus and Quality of Life

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Systemic lupus erythematosus natural history, complications and prognosis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Systemic lupus erythematosus natural history, complications and prognosis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

National Guidelines Clearinghouse

NICE Guidance

FDA on Systemic lupus erythematosus natural history, complications and prognosis

on Systemic lupus erythematosus natural history, complications and prognosis

Systemic lupus erythematosus natural history, complications and prognosis in the news

Blogs onSystemic lupus erythematosus natural history, complications and prognosis

Directions to Hospitals Treating Systemic lupus erythematosus

Risk calculators and risk factors for Systemic lupus erythematosus natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Common complications of systemic lupus erythematosus include dermatitis, nephritis and arthritis. Prognosis is generally poor, and the 10-year mortality rate of patients with systemic lupus erythematosus is approximately 40%. The disease course can be divided into 4 subcategories based on the course of the disease: developmental phase, preclinical phase, clinical phase, and comorbid complication phase.

Natural History

  • Systemic lupus erythematosus (SLE) is an autoimmune disease. SLE is a disease of waxing and waning, with possible flare up episodes. SLE usually develops in the second and third decade of life, although it can presents any age, and start with mild symptoms such as fatigue, fever, and skin rashes. Without treatment, the patient will develop symptoms of end organ damage, which will eventually lead to death in most of the patients.
  • The disease course can be divided into 4 subcategories based on the course of the disease:
Developmental phase:
Preclinical phase:
Clinical phase:
Comorbidity-complication phase

The phase of damages due to complications of longstanding disease, immunosuppressive therapy, and end organ damages (irreversible damages and complications)

Factors associated with flare up:

Complications

Complications that can develop as a result of prolonged activation of systemic lupus erythematosus or the SLE therapy are:

Organ Disease Description Frequency
Gastrointestinal system Dysphagia ↑↑
Peptic ulcer disease
  • Due to
    • The disease itself
    • The effect of SLE treatment
Intestinal pseudo-obstruction
  • May lead to mechanical obstruction of the small or large bowel in the absence of an anatomic lesion
  • Obstructing the flow of intestinal contents
↓↓
Protein-losing enteropathy
Hepatitis
Acute pancreatitis
  • Occurs usually in the setting of active SLE
Mesenteric vasculitis
Acute cholecystitis
Pulmonary involvement Pleural disease
Acute pneumonitis ↓↓
Pulmonary hemorrhage
  • Pulmonary alveolar hemorrhage:
↓↓
Pulmonary hypertension
Thromboembolic disease
Shrinking lung syndrome ↓↓
Cardiac involvement Cardiomegaly
Valvular disease ↑↑
Pericardial disease
Myocarditis
Coronary artery disease ↑↑
Neurological involvement Cognitive dysfunction
  • May be temporarily affected by multiple, transient metabolic and systemic processes
Stroke
Seizures
Psychosis ↑↑
Neuropathies
Musculoskeletal involvement Arthritis
  • Mostly symmetrical and non-erosive arthritis
  • Arthralgias
  • Effusions
  • Decreased range of motion of both small and large joints
  • Morning stiffness
↑↑
Osteonecrosis (Avascular necrosis)
Subcutaneous nodules
  • Associated with active disease
Osteoporosis
Skin disorder Cutaneous lupus erythematosus
  • Erythema in a malar distribution over the cheeks and nose (but sparing the nasolabial folds), which appears after sun exposure
Photosensitivity
  • Common theme for skin lesions associated with SLE
↑↑
Non-scarring alopecia
  • May occur at some point during the course of their disease
oral and/or nasal ulcers
  • Usually painless
discoid lesions
  • More inflammatory
  • Have a tendency to scar
Very rare disorders Malignancy
Diabetes mellitus 
Premature gonadal failure

Prognosis

The prognosis of systemic lupus erythematosus is ranging from a benign illness to an extremely rapid progressive disease that can lead to a fulminant organ failure and death. Without treatment, systemic lupus eryhtematosus will result in a very high mortality rate, with a report of more than 60% mortality rate during the mid-20th century. SLE is associated with a 10 year mortality of more than 50% among patient with nephritis. The presence of nephritis is associated with a particularly poor prognosis among patients with SLE. The increase in survival rate of patients and better prognosis may be due to increased disease recognition with more sensitive diagnostic tests, earlier diagnosis or treatment, the inclusion of milder cases, increasingly judicious therapy, and prompt treatment of complications. Although improvement in SLE diagnosis have led to better prognosis, the mortality rate among SLE patients is still 5 times more than normal population.

Poor prognostic factors for SLE survival:
  • Presence of nephritis (especially diffuse proliferative glomerulonephritis)
  • Hypertension
  • Male sex
  • Young age
  • Older age at presentation
  • Low socioeconomic status
  • Black race: Higher rate of nephritis
  • Presence of antiphospholipid antibodies
  • High overall disease activity
Prognosis markers:
  • Serum anti ds-DNA titres correlated with:
    • Lupus nephritis
    • Progression to end-stage renal disease
    • Increased disease severity
    • Damage or poor survival
  • Antiphospholipid antibodies correlated with:
    • Features of the antiphospholipid syndrome (APS) (arterial/ venous thrombosis, fetal loss, thrombocytopenia)
    • CNS involvement (especially cerebrovascular disease)
    • Severe lupus nephritis
    • Damage accrual
    • Increase in mortality rate
SLE in men compared to women:
  • Less photosensitivity
  • More serositis
  • Older age at diagnosis
  • Higher 1 year mortality compared to women.
SLE in the elderly (>65) compared to middle age prevalency:
  • Lower incidence of:
    • Malar rash
    • Photosensitivity
    • Purpura
    • Alopecia
    • Raynaud’s phenomenon
    • Renal system involvement
    • Central nervous system involvement
  • Greater prevalence of:
    • Serositis
    • Pulmonary involvement
    • Sicca symptoms
    • Musculoskeletal manifestations

References

2