- What is lupus?
- Understanding the Signs, Symptoms & Diagnosis of Lupus
- How Lupus Affects the Body
- Lifestyle & Additional Information
- Mood Disorders and Lupus
- Defining mood disorders
- How lupus affects the nervous system
What is lupus?
Lupus may develop in response to a number of factors. These may be hormonal, genetic, environmental, or a combination of these.
Hormones are chemical substances that the body produces. They control and regulate the activity of certain cells or organs.
Hormonal activity could explain the following risk factors:
Sex: The U.S. National Institutes of Health note that females are nine times more likely to have lupus than males.
Age: Symptoms and diagnosis often occur between the ages of 15 and 45 years, during the childbearing years. However, 20 percent of cases appear after the age of 50 years, according to Genetics Home Reference.
As 9 out of 10 occurrences of lupus affect females, researchers have looked at a possible link between estrogen and lupus. Both men and women produce estrogen, but women produce more.
In a review published in 2016, scientists observed that estrogen can affect immune activity and induce lupus antibodies in mice that are susceptible to lupus.
This may explain why autoimmune diseases are more likely to affect women than men.
In 2010, researchers who published a study on self-reported flares in the journal Rheumatology found that women with lupus report more severe pain and fatigue during menstruation. This suggests that flares may be more likely at this time.
There is not enough evidence to confirm that estrogen causes lupus. If there is a link, estrogen-based treatment could regulate the severity of lupus. However, more research is necessary before doctors can offer it as a treatment.
2) Genetic factors
Researchers have not proved that any specific genetic factor causes lupus, although it is more common in some families.
Genetic factors may be the reason why the following are risk factors for lupus:
Race: People of any background can develop lupus, but it is two to three times more common in people of color, compared with the white population. It is also more common in Hispanic, Asian, and Native American women.
Family history: A person who has a first- or second-degree relative with lupus will have a higher risk of developing it.
Scientists have identified certain genes that may contribute to the development of lupus, but there is not enough evidence to prove that they cause the disease.
In studies of identical twins, one twin may develop lupus while the other does not, even if they grow up together and have the same environmental exposures.
If one member of a twin pair has lupus, the other has a 25-percent chance of developing the disease, according to a study published in Seminars in Arthritis and Rheumatism in 2017. Identical twins are more likely to both have the condition.
Lupus can happen in people with no family history of the disease, but there may be other autoimmune diseases in the family. Examples include thyroiditis, hemolytic anemia, and idiopathic thrombocytopenia purpura.
Some have proposed that changes in the x-chromosomes might affect the risk.
Environmental agents — such as chemicals or viruses — may contribute to triggering lupus in people who are already genetically susceptible.
Possible environmental triggers include:
Smoking: A rise in the number of cases in recent decades may be due to higher tobacco exposure.
Exposure to sunlight: Some suggest that this may be a trigger.
Medication: Around 10 percent of cases may be drug-related, according to Genetics Home Reference
Viral infections: These may trigger symptoms in people who are prone to SLE.
Lupus is not contagious, and a person cannot transmit it sexually.
Recently, scientists have been looking at gut microbiota as a possible factor in the development of lupus.
Scientists who published research in Applied and Environmental Microbiology in 2018 noted that specific changes in gut microbiota feature in both people and mice with lupus.
They call for more research into this area.
Are children at risk?
Lupus is rare in children under the age of 15 years unless their birth mother has it. In this case, a child may have lupus-related heart, liver, or skin problems.
Infants with neonatal lupus may have a higher chance of developing another autoimmune disease later in life.
Your primary care doctor should coordinate care between your different health care providers and treat other problems as they come up. Your doctor will develop a treatment plan to fit your needs. You and your doctor should review the plan often to be sure it is working. You should report new symptoms to your doctor right away so that your treatment plan can be changed if needed.
The goals of the treatment plan are to
- Prevent flares
- Treat flares when they occur
- Reduce organ damage and other problems
Treatments may include drugs to
- Reduce swelling and pain
- Prevent or reduce flares
- Help the immune system
- Reduce or prevent damage to joints
- Balance the hormones
Besides taking medicines for lupus, you may need to take medicines for problems that are related to lupus such as high cholesterol, high blood pressure, or infection.
Alternative treatments are those that are not part of standard treatment. At this time, no research shows that alternative medicine can treat lupus. Some alternative or complementary approaches may help you cope or reduce some of the stress associated with living with a chronic illness. You should talk to your doctor before trying any alternative treatments.
How can I cope with lupus?
It is important to take an active role in your treatment. It helps to learn more about lupus – being able to spot the warning signs of a flare can help you prevent the flare or make the symptoms less severe.
It is also important to find ways to cope with the stress of having lupus. Exercising and finding ways to relax may make it easier for you to cope. A good support system can also help.
NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
Lupus is a disease in which the immune system begins to recognize and attack the body’s own tissues. This phenomenon is similar to “friendly fire” and causes inflammation in different organs of the body. The nature of lupus is highly individualized, and two patients may experience two sets of totally different symptoms. In the United States, lupus affects roughly 1 in 2000 people, and 9 out of 10 lupus cases occur in women. Although the disease occurs in people of all races and ethnic groups, it occurs more frequently in African Americans.
The first symptoms of lupus usually occur somewhere between the teen years and the 30s and may be mild, severe, sporadic, or continual. Common general symptoms include fatigue, fever, and hair loss. Lupus can also affect individual organs and body parts, such as the skin, kidneys, and joints.
The following pages provide introductory information on lupus for patients, loved ones, and health care providers. Think of this as “Lupus primer.”
Understanding the Signs, Symptoms & Diagnosis of Lupus
- How is Lupus diagnosed?
- Types of Lupus
- Causes of Lupus
- Signs, Symptoms, and Co-occuring conditions
How Lupus Affects the Body
- Antiphospholipid Antibodies
- Cardiovascular System
- Immune System
- Nervous System
Lifestyle & Additional Information
- Lupus and Cancer
- Lupus and Pregnancy
- Things to Avoid
Mood Disorders and Lupus
Defining mood disorders
Mood disorders include depression and generalised anxiety and are one of the most frequently experienced type of psychological problem for people with lupus. Other common neuropsychiatric manifestations of lupus such as cognitive impairment, epilepsy, psychosis and catatonia are outlined elsewhere.
See pages – CNS Involvement in Lupus and Antiphospholipid (Hughes) Syndrome.
It is important to establish diagnostic criteria for mood disorders before it is possible to plan effective strategies to enable people with these conditions to make sustainable improvements in their mood.
An effective initial screening method (prior to appointments) can make use of a retrospective questionnaire assessment such as Zigmond and Snaith’s 14-symptom Hospital Anxiety and Depression Scale, which takes little time to complete. This provides information on how severe these symptoms are but is not a diagnostic tool per se. Simple mood diaries are an effective way of selfmonitoring daily mood; these can be completed as frequently as the person wishes (e.g. three times a day) and giving as much or little detail as they want (e.g. a single numerical rating on a 0-10 scale and/or free narrative).
The terms depressed and anxious have been assimilated into everyday language but the mood disorders these symptoms reflect are based on clear medical diagnoses. Whilst these may be the most salient term for a person experiencing an acute episode of mood disturbance, health professionals must listen to the mood symptoms their patients are describing and map these along the parallel continuums from happiness and calmness to enduring sadness or generalised anxiety. However, people with lupus are rarely at the extreme ends of the continuum and will often report moderately depressed or anxious mood states and judgment is required to determine if these require help.
An episode of major depression is classified by the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM) as a period of at least 2 weeks of having depressed mood or lack of interest in activities and anhedonia (the lack of pleasure from previously enjoyed activities). These problems should be experienced most of the day and every day for this period. In addition to this, classification requires the individual to have four or more of the following associated problems:
• Change in appetite or change in weight
• Hypersomnia or insomnia (especially waking early)
• Restlessness or feeling slowed down
• Fatigue or loss of energy
• Guilt and feelings of worthlessness
• Inability to concentrate or indecisiveness
• Suicidal ideation
The World Health Organization’s International Statistical Classification of Diseases and Related Health Problems (ICD) section on mental and behavioural disorders codes depressive episodes as mild, moderate or severe (F32.0, F32.1 and F32.2, respectively). All three codes are outlined as sharing the features of depressed mood, loss of interest and enjoyment and reduced energy levels leading to diminished activity due to increased fatigability after only slight effort is common. Other common symptoms are reduced concentration and attention, reduced self-esteem and self-confidence, ideas of guilt and unworthiness, bleak and pessimistic views of the future, ideas or acts of self-harm or suicide, disturbed sleep and diminished appetite. For all three severity grades of depressed mood it is stated that a duration of at least 2 weeks is usually required for diagnosis unless the onset is rapid and severe.
The symptoms within both of these sets of diagnostic criteria have to be seen in the context of the disease process where a person with lupus might experience sleep disturbance and diminished appetite, especially within a flare. There is some potential for overlap with fatigue and disability from lupus, but the criterion of feeling slowed down might be best interpreted and explained as referring to a cognitive experience rather than as physical problems. These symptoms are defined as ‘somatic’ in the ICD and consideration of these will help avoid ‘false positive’ diagnoses. It is assumed that these criteria are being applied to individuals who have already received a diagnosis of lupus. Research indicates that people with lupus in their early journey to obtaining the diagnosis, when symptoms may fluctuate and objective tests prove inconclusive, can be wrongly misdiagnosed with a mood disorder and this may impact on satisfaction with healthcare interactions in the future.
A less intense but prolonged version of depression is called dysthymic disorder or minor depression; this is classified as depressed mood most of the day, more days than not for at least 2 years in the DSM, and very similarly in the ICD where it is not so strictly defined (code F34.1).This will probably be the most common type of depressed mood that will be seen in a clinical practice.
Generalised anxiety disorder is distinct from phobias and pure obsessive thought disorders and can be classified in a very similar way to depression. The DSM classifies this using the criteria of excessive, uncontrollable worry about several events (which could include one’s state of health) more days than not for a period of at least 6 months that has an impact on social functioning or work ability. In addition to this, to be classified the individual is required to have four or more of the following associated problems:
• Feeling restless or ‘edgy’
• Experiencing fatigue easily
• Having difficulty concentrating
• Being irritable without reason
• Experiencing muscle tension (particularly of the shoulders/neck)
• Having disturbed sleep (especially onset insomnia)
The criterion of muscle tension may be experienced in rheumatic disease. It is also clear that (major) depression and (generalised) anxiety have a large overlap in content of their listed symptom and associated thought processes. This will, hopefully, be clarified in the forthcoming revision to the DSM criteria, which are being redeveloped.The ICD already defines concomitant anxiety and depressive disorder (code F41.2). Fortunately, both conditions can be tackled by similar medical treatments and psychological therapies.
Given that there are problems with accurate recall of psychological processes, the criteria for depression and anxiety ideally require some form of daily mood assessment. There are many good measures of mood available; two classic measures are Watson and colleagues’ Positive and Negative Affect Schedule and Lorr and McNair’s Profile of Mood States. Both of these questionnaires cover depression (versus elation) and anxiety (versus calmness) although it is feasible, and indeed may be preferable, to allow patients to define a diary system for recording aspects of their mood without the formality of such scales.
A further simple method of getting to the heart of the issue of depression (reflecting the above criteria) is the use of two screening questions composed by Arroll and colleagues:
• “During the past month have you often been bothered by feeling down, depressed, or hopeless?”
• “During the past month have you often been bothered by little interest or pleasure in doing things?”
These questions can allow therapeutic skills to be directed to either or both of these issues, as will now be considered further. Alternatively, patients’ responses to these questions may be used as the basis for suggesting a referral to local psychological services.
How lupus affects the nervous system
Lupus is an autoimmune disease that can affect almost any part of your body, including your joints, skin, kidneys, heart, lungs, or blood. Lupus can also affect the nervous system and brain. There are several terms doctors use to describe this: neuropsychiatric lupus (NPSLE), neurocognitive dysfunction, or central nervous system lupus (CNS lupus).
The nervous system has three parts, any of which may be affected by lupus:
- The central nervous system (CNS)—The brain and spinal cord.
- The peripheral nervous system (PNS)—The network of nerves that connects the brain and spinal cord to the rest of the body, and gives skin and muscles the signals needed for sensation and movement.
- The autonomic nervous system (ANS)—Allows communication between spinal and peripheral nerves and the brain and internal organs, and controls functions like breathing, blood flow, and heart rate.
People with lupus can experience a number of complications when their nervous system is affected. The symptoms may come on suddenly or may come and go, but they will vary depending upon the location and extent of the tissue injury. These symptoms also can be present in other diseases, so diagnosing lupus-related nervous system disorders is often difficult.
Neurologists are physicians who specialize in the nervous system. They may rely on a number of diagnostic tools to determine whether lupus is involved in cognitive problems:
- Brain scans (magnetic resonance imaging (MRI) and computed tomography (CT)
- Electroencephalograms (to capture the electrical pattern of brain activity)
- Spinal tap (to examine fluid in the spinal column)
Behavioral and cognitive tests may also be done to find out if your memory or other mental abilities have been affected.
Depending on the symptoms, a variety of medications are available to treat lupus-related nervous system disorders, including non-steroidal anti-inflammatory drugs, antimalarials, and steroids. Your response to treatment may be rapid or gradual over several months.
For many people with lupus, nervous system involvement is completely reversible.
Central Nervous System (CNS) impacts
When lupus affects your central nervous system, many symptoms may occur, including:
- Vision problems
- Mood swings
- Difficulty concentrating
Lupus fog or cognitive dysfunction
As many as half of all people with lupus describe feelings of confusion, fatigue, memory loss, and difficulty expressing their thoughts. This collection of symptoms is termed cognitive dysfunction, although many people with lupus call it “lupus fog.” Cognitive dysfunction most often affects people with mild to moderately active lupus. The causes of these symptoms, and the reasons the symptoms tend to come and go, are unknown. Living with cognitive dysfunction can be very frustrating. However, you can learn to improve your concentration and lessen confusion and memory loss with a variety of coping skills, including puzzles, games, biofeedback, using a daily appointment calendar, and balancing daily activities to reduce stress.
Lupus fog can be frustrating but there are a variety of coping skills that can help you learn to improve your concentration and lessen confusion.
Compared with the general population, people with lupus may be twice as likely to experience migraine-like lupus headaches, commonly known as lupus headaches. The features of lupus headaches are similar to migraines and may be seen more often in people who also have Raynaud’s phenomenon. However, headaches can also be caused by vasculitis, a symptom of active lupus due to inflammation of the blood vessels. If you are experiencing headaches that are not improved by an over-the-counter headache medication, be sure to tell your doctor.
Medication side effects
Medications used to treat lupus can cause side effects that are similar to the symptoms of CNS lupus. If you have symptoms of CNS lupus you should consult a neurologist who can determine which symptoms are side effects of medication and which are due to lupus. The drugs most known for causing symptoms like those of CNS lupus are:
- Non-steroidal anti-inflammatory drugs (NSAIDs) – May cause headache, dizziness, confusion, and in rare instances, meningitis-like symptoms
- Antimalarials – Very high doses (not usually given for lupus) may cause manic behavior, seizures, psychosis
- Corticosteroids – May cause agitation, confusion, mood swings, psychosis, depression
- Anti-hypertensive medications – May cause depression or loss of sex drive
A serious form of lupus called CNS vasculitis may occur when there is inflammation of the blood vessels of the brain. Characterized by high fevers, seizures, psychosis, and meningitis-like stiffness of the neck, CNS vasculitis is the most dangerous form of lupus involving the nervous system and usually requires hospitalization and high doses of corticosteroids to suppress the inflammation.
Peripheral Nervous System (PNS) impacts
The nerves of the peripheral nervous system control motor responses and sensation, so symptoms of numbness or tingling, or inability to move a part of your body, may be the result of lupus affecting these nerves. Known as peripheral neuropathies, symptoms of PNS nerve damage are caused by inflammation or compression of the nerves due to swelling in the tissue around them.
The types of symptoms you might experience include:
- Vision problems
- Facial pain
- Ringing in the ears
- Drooping of an eyelid
- Carpel tunnel syndrome
Autonomic Nervous System (ANS) impacts
The autonomic nervous system regulates many of the body’s functions that happen almost automatically: heart rate, blood pressure, feeling hot or cold, bladder and bowel functions, release of adrenaline, breathing, sweating, and muscle movement. Lupus can cause these nerve signals to be overactive, which can lead to a wide range of symptoms:
- Mental confusion
- Gastrointestinal problems such as nausea, vomiting, constipation, or diarrhea
Raynaud’s phenomenon is a condition of ANS involvement caused by inflammation of nerves or blood vessels. Blood vessels in the hands and feet go into spasm and restrict blood flow, usually as a reaction to cold temperatures, with the tips of the fingers or toes turning red, white, or blue. Raynaud’s can also cause pain, numbness, or tingling in fingers and/or toes. People who have Raynaud’s phenomenon are advised to avoid cold conditions when possible, and may have to wear gloves or mittens when in air-conditioned surroundings.
Livedo reticularis and palmar erythema are two other skin disorders that may affect you if you have autonomic nerve damage. Both of these conditions can cause a bluish, lacelike mottling under your skin, especially on your legs, giving your skin a “fishnet” look.
Personality traits and associated changes in women with lupus
Danusa Céspedes Guizzo AyacheI; Izaías Pereira da CostaII
IPsychiatrist; Assistant Psychiatry Professor of the Internal Medicine Department at the Medical School of Universidade Federal de Mato Grosso do Sul (UFMS); Coordenator of the Psychiatry Residency at UFMS; Master Degree in Health Sciences from the Health Sciences Multi-Institutional Post-Graduate Program (UNB-UFG-UFMS)
IIRheumatologist; Associate Professor II, Internal Medicine Department at the Medical School of Universidade Federal de Mato Grosso do Sul (UFMS); Internal Medicine Master Degree and PhD from Universidade de São Paulo (USP); Professor at the Health Sciences Post-Graduate Course – UFMS; Member of the Brazilian College of Rheumatology; Coordinator of the Rheumatology Residency Program at NHU/UFMS
OBJECTIVE: The objective of the present study was to evaluate personality traits and associated changes in female patients with Systemic Lupus Erythematosus (SLE), linking variations in disease activity with alterations in personality traits.
PATIENTS AND METHODS: Twenty patients from the Rheumatology Outpatient Clinic at the University Hospital of Universidade Federal de Mato Grosso do Sul (UFMS) participated in this study. Patients were re-evaluated three and six months after the initial evaluation for the presence of Psychiatric Disorders (especially personality changes) and lupus activity. The Adjustment/Neuroticism Factorial Scale (AFS) and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), along with clinical psychiatric and rheumatologic assessment, were used to evaluate patients.
RESULTS: No significant correlation between SLEDAI and AFS scores was observed. According to the AFS, the scores of six patients (30%) were suggestive of Personality Disorders, but psychiatric evaluation confirmed this diagnosis in only two (10%) patients. A typical personality pattern or prevalence of a specific Personality Disorder was not observed; however, an important prevalence of Depression (65%) was observed.
CONCLUSIONS: Our findings showed that patients with lupus can develop different types of behavior and psychiatric symptoms without a typical personality trait. No significant correlation between personality changes and disease activity was observed.
Keywords: psychiatric disorders, personality changes, systemic lupus erythematosus.
Systemic Lupus Erythematosus (SLE) is an autoimmune, multi-system, chronic inflammatory disease of unknown origin, characterized by the presence of autoantibodies. It is associated with different clinical manifestations and periods of exacerbation and remission.1 The prevalence of SLE is increased in females of childbearing age and with a family history of autoimmune disease.2,3
The multifactorial origin of the disease, involving hormonal, genetic, environmental, and infectious (viral) factors, and psychological stress, regarded by several authors as a particularly important triggering factor for the development and exacerbation of the disease,2,5 is a consensus in the scientific community.1,3,4
The Central Nervous System (CNS) is frequently affected, giving rise to neurologic and/or psychiatric symptoms.1,3,6
Some studies have correlated those clinical manifestations to the presence of specific antibodies, such as anti-P ribosomal, anti-SSa, anti-DNA, and anti-phospholipid, among others.7,8,9 It has been speculated that the activation of the immune system can result in changes in neurotransmitters and, consequently, in behavior.10
In 1999, a subcommittee of the American College of Rheumatology (ACR) classified 19 neuropsychiatric syndromes related with SLE. Among these, the following were classified as psychiatric syndromes: acute confusional state, cognitive disorders, psychosis, and mood and anxiety disorders.1 However, personality changes were not mentioned.
On a review of the literature on personality changes in SLE patients, Ayache & Costa11 observed that several authors concluded that psychological factors (including personality traits) are important co-determinants, triggers, or intensifiers of the disease. Other authors observed that personality changes can be secondary to the psychological stress imposed by SLE, the disease activity in the CNS, and/or the use of medications like immunosuppressors and corticosteroids.12-28
Vertzman & Pinheiro, apud Lemle,29 are developing, at Universidade Federal do Rio de Janeiro (UFRJ), the Project “Narcissistic Pathologies and Autoimmune Diseases: a Psychoanalytic Comparative Study”. According to those authors, based on clinical experience and some references in the literature, lupus patients would have a narcissistic psychological configuration (they would be selfish, arrogant, self-absorbed). Therefore, they decided to undertake a comparative study to carry on a qualitative assessment (according to the psychoanalytical point of view) of patients with SLE and melancholy. So far, they have reported different types of psychological organization in SLE patients instead of a higher incidence of narcissistic personalities.
Nery et al.30 evaluated 71 SLE patients for the presence and severity of depressive disorder; major depression and a tendency for more severe forms of lupus were diagnosed in 23% of the patients. Depression severity was directly related with disease activity and functional incapacity. Those authors admit the hypothesis that major depression in patients with CNS activity would be a manifestation of the disease mediated by autoimmune mechanisms, which deserves further investigation.
A study to estimate the prevalence of psychiatric disorders in SLE patients and its association with anti-P antibodies was undertook by Nery et al.31 They selected 71 female patients with SLE without neurological manifestations. Psychiatric disorders more prevalent in the last 30 days included mood (26.8%) and anxiety (46.5%) disorders, which were also more prevalent throughout their lives (mood 60%, and anxiety 52.1%). Clinical and laboratorial parameters, including presence or absence of anti-P antibodies, disease activity, and accumulated damage index, did not differ among individuals with and without psychiatric manifestations. The authors concluded that mood and anxiety disorders are the most common psychiatric disorders observed in female SLE patients without neurological manifestations. Mild/moderate types of those psychiatric disorders are not associated with anti-P antibodies in SLE patients.
Therefore, a review of the literature on the presence of a personality pattern in lupus patients is inconclusive. The results of studies on personality changes secondary to the disease or medication are controversial. Evaluation of lupus patients is complex due to the variety of factors that can interfere with it. Due to the need of further studies to elucidate this matter, we decided to undertake this study, whose objectives include: a) to evaluate personality traits and possible implications in female patients with lupus, trying to relate changes in disease activity with personality changes; b) to determine whether or not there are one or more characteristic personality patterns in the study group; and c) to determine the presence of behavioral patterns or psychiatric disorders associated with the disease, both during remission and active disease.
PATIENTS AND METHODS
Twenty patients followed-up at the Outpatient Collagenosis Clinic of the Rheumatology Department of the University Hospital (UH) of Universidade Federal de Mato Grosso do Sul (UFMS) participated in this study. The project was submitted to the Ethics Committee of UFMS and approved on 04/27/2004 (protocol # 380/2004).
Female patients, 18 to 50 years old, with a diagnosis of SLE according to ACR32 criteria were included in the study. Illiterate patients, with a score lower than expected for their age and educational background in the Mini-Mental State Exam;33 with severe psychiatric disorders or using psychotropic drugs on the first evaluation; with other associated chronic diseases; and suspected or confirmed pregnancy were excluded.
Patients were consecutively selected, from May to June 2004, for the study after a review of their records. Those that fulfilled the above mentioned criteria were invited to participate in the study. Forty patients were initially selected, but we were not able to locate all of them and some of them did not agree to participate in the study. Therefore, the study population, which can be considered non-probabilistic and by judgment, was composed of 20 patients.
The following scales were used besides the clinical psychiatric and rheumatologic evaluations:
a) Adjustment/Neuroticism Factorial Scale – AFS34
This scale evaluates a dimension of the human personality called Emotional Adjustment/Neuroticism, also known as Factor N. According to Hutz & Nunes,34 factor N has a close correlation with personality disorders catalogued by current psychiatric diagnostic systems, such as the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders, DSM-IV,35 and the International Classification of Mental and Behavioral Disorders, CID-10.36
This tool consists of 82 items distributed in the following sub-scales:34
N1 (Vulnerability – 32 items): High scores suggest Dependent Personality Disorder, while very low scores suggest Avoidant Personality Disorder.
N2 (Psychosocial Disadjustment – 14 items): High scores suggest Personality Disorders, such as Antisocial and Borderline. The significance of low scores is not known.
N3 (Anxiety – 25 items): High scores suggest Anxiety disorder; low scores suggest symptoms such as impulsivity and high risk behavior.
N4 (Depression – 20 items): High scores suggest Depressive Disorders; low scores suggest difficulty to detect and face problems, which might be directly related with strategies to face diseases.
To calculate the general score, the scores of the subscales (N1, N2, N3, and N4) should be added. General scores of 80 to 120 are expected for the majority of the population. Higher or lower scores might suggest a Personality Disorder, requiring further investigation by a psychiatrist or psychologist.34
From the score of each subscale, one can calculate the percentile score for each factor. A score higher than 70 or lower than 30 in any of those subscales may indicate a more specific psychological and/or psychiatric disorder.37
b) SLEDAI – Systemic Lupus Erythematosus Disease Activity Index38
The Systemic Lupus Erythematosus Disease Activity Index is used around the world to evaluate lupus activity based on clinical (rheumatologic) evaluation and standardized laboratorial tests. Total scores can range from 0 to 105 points. We adopted the classification recommended by Cook et al.:39 inactivity (0 pts); mild activity (1 to 3 pts); moderate activity (4 to 7 pts); and severe activity (> 8 pts).
Evaluation and Follow-up Schedules
Clinical evaluations (rheumatologic and psychiatric) and application of the scales were done simultaneously with laboratorial tests, within one week, to compare possible changes in SLE activity with personality changes. Patients were evaluated three and six months after the initial assessment to determine the presence of possible changes in AFS according to disease evolution and/or external factors, such as psychosocial stressors that could emerge in different moments. Therefore, we considered this a prospective cohort study.
Analysis of the Data
Descriptive and analytical statistical analysis were undertaken using the following tests: non-parametric Friedman test with Student-Newman-Keuls post-test; Chi-square test; and Mc-Nemar and Fisher’s exact tests. Results are presented in the form of descriptive statistics, charts, and tables; for such, the SigmaStat software, version 2.0, was used, and relationships and differences were considered significant when P < 0.05.40
AFS and Psychiatric Evaluation Results
Table 1 shows general AFS scores on all three evaluations: on the initial assessment, 15% of the patients presented abnormal scores; on the 2nd evaluation, 26% had abnormal scores; and on the 3rd evaluation, 35% had abnormal scores. A significant relationship between AFS scores and the study moments was observed. This relationship was observed between the 1st and 2nd evaluations (McNemar test, P = 0.019) and between the 1st and 3rd evaluations (P = 0.037). A significant relationship was not observed between the 2nd and 3rd evaluations (P = 0.118). For this test, AFS scores were subdivided in: a) abnormal (lower than 80 or greater than 120 points), and b) normal (between 80 and 120 points). Together, our results indicate a reduction in the incidence of normal cases, according to the AFS, along time, and an increase in abnormal cases, especially for scores lower than 80 points. Among patients with “abnormal” scores, only one patient (5%) received a diagnosis of Personality Disorder after psychiatric evaluation.
On Table 2 we observe a lack of significant relationship between psychiatric evaluation and AFS scores (Chi-square test, P = 0.060). Out of three (15%) patients classified as abnormal by the AFS, only one (5%) had a psychiatric diagnosis on clinical evaluation (Moderate Depressive Episode and Dependent Personality disorder). Besides, 14 patients (70%) with a psychiatric diagnosis had normal general AFS scores.
We also observed that 15 patients (75%) had one or two psychiatric diagnosis in T0. According to the clinical evaluation Moderate Depressive Episode (MDE), the only psychiatric diagnosis in 10 patients (50%), was the most prevalent diagnosis; MDE and Mild Mental Retardation were diagnosed in two patients (10%); and MDE and Dependent Personality disorder in one (5%) patient. One patient (5%) had a diagnosis of Bipolar Disorder and Borderline Personality Disorder; one (5%) patient, Alcohol Abuse and Tobacco Dependency; and only five (25%) patients did not have a psychiatric diagnosis in the initial evaluation.
Table 3 shows the number of patients and percentile scores of the AFS subscales in the initial evaluation: a significant relationship between percentile scores and AFS factors was not observed (Chi-square test, P = 0.243). For those tests, AFS scores were subdivided in: a) abnormal (less than 30 points and greater than 70 points), and b) normal (between 30 and 70 points).
As for factor N1, 40% of the patients had a score above than expected, suggesting possible Dependent Personality Disorder; however, in the psychiatric evaluation, only one (5%) patient had this diagnosis associated with MDE.
Regarding factor N2, only one (5%) patient had a score higher than expected, suggesting Anti-social and Borderline Personality Disorders. However, this was not confirmed in the psychiatric evaluation, although the patient received the diagnosis of MDE and Dependent Personality Disorder.
As for factor N3, the scores of 50% of the patients was higher than expected, indicating the presence of Anxiety Disorder; however, none of the patients was clinically diagnosed with this disorder.
Regarding factor N4, the scores of 30% of the patients were higher than expected, suggesting a depressive state. Among those, 15% had a clinical diagnosis of MDE; 10%, MDE and Mild Mental Retardation; and 5%, Bipolar Disorder and Borderline Personality Disorder.
On Table 4 one can observe that factor N1 scores in the first evaluation were significantly higher than in the 2nd and 3rd evaluations (Friedman test, P = 0.007; with Student-Newman-Keuls post-test, P < 0.05). Significant differences in AFS scores for factors N2, N3, and N4 were not observed among the different evaluations. Total standardized scores were significantly higher in the initial evaluation than in subsequent evaluations (Friedman test, P = 0.005; with Student-Newman-Keuls post-test, P < 0.05).
Table 5 shows that percentile and general AFS scores had a trend to decrease along the study, although a statistically significant difference was not observed.
RELATIONSHIP BETWEEN AFS AND SLEDAI RESULTS IN DIFFERENT EVALUATIONS
A significant relationship was observed between disease activity, according to SLEDAI scores, and the duration of the treatment. A reduction in the incidence of moderate/severe disease and an increase in the incidence of remission/mild disease were observed during the study.
A significant relationship between SLEDAI and AFS cores was not observed (Chi-square test, 1st evaluation: P = 0.088; 2nd evaluation: P = 0.348; 3rd evaluation: P = 0.371) (Table 5). Therefore, we did not observe a relationship between personality disorders and SLE activity.
The majority of the patients were of African descent, similar to the results of several studies reported in the literature.14-17 The mean age of the patients was similar to that of the majority of the studies;14-17 however, the mean age of the patients in other studies41,23 was higher. Most patients were married, similar to the studies of Segui et al.18 and Dobkin et al.23
The school level of the study patients (10.1 ± 2 years) was lower than that reported by international studies.41,24 Approximately 55% of our patients were housewives; this data also differs from that of most international studies like Segui et al.,18 in which 25% of the patients were housewives.
We observed a reduction in the incidence of cases classified as normal by the AFS and an increase in those classified as abnormal along the study. We believe that this can be partially explained by the fact that, in the 2nd evaluation, six (46.1%) patients, initially diagnosed with depression, were treated with antidepressants, while 4 (30.7%) the same diagnosis in the 3rd evaluation. The medication could have reduced the scores of the depression and anxiety subscales. However, a normalization of the scores is expected with the use of the appropriate medication and not a reduction to levels below normal.
We also did not observe a significant relationship between psychiatric evaluation and AFS scores. Therefore, the present study did not confirm the correlation between AFS scores, according to the literature,34 and the current nosology.
The prevalence of psychiatric disorders was very high (75%) in our study population. Our incidence was higher than those reported by Waterloo et al.41 (50%) and Hutchinson et al.42 (44%). The small number of patients in the present study might explain this difference.
According to the literature, Depression is significantly related with SLE. In the present study, the prevalence of Depression in the 1st evaluation was 65%, which is higher than that reported by Waterloo et al.41 (28%), Hutchinson et al.42 (27%), and Nery et al.30 (23%). Once more, we believe that the small number of patients in our study could explain this difference.
One patient (5%) had a diagnosis of Dependent Personality Disorder. We did not find in the literature any references to this diagnosis in SLE patients. However, some studies41,23 detected psychological aspects consistent with this disorder in SLE patients; but in those studies, the authors did not report this diagnosis.
Bipolar Disorder and Borderline Personality Disorder were diagnosed in one (5%) patient. Once more, the literature does not have any references to this disorder in SLE patients; however, some studies also reported symptoms typical of Borderline Personality Disorder41,23,43 in SLE patients, but the authors did not report this diagnosis in their evaluations.
Mean percentile and general AFS scores showed a tendency to decrease during the study, although a statistically significant difference was not observed. As mentioned previously, we believe that this reduction could be related to the use of antidepressants by some patients on the 2nd and 3rd evaluations. However, not all patients followed the treatment prescribed by the psychiatrist.
Therefore, as the authors have stated,34 we observed that AFS scores are only indicative of Personality Disorders. Only one patient (5%) had a clinical diagnosis of Dependent Personality Disorder confirmed by general and specific (N1) scores. However, despite the diagnosis of depression (MDE), her percentile score for this factor (N4) was within normal parameters. The other patient who also had a clinical diagnosis of Personality Disorder (Borderline) had normal AFS scores and, paradoxically, a low score (5 pts) in the subscale related with this factor (N2).
As can be seen in Table 3, the percentile scores of the subscales of a substantial proportion of the study population indicated changes compatible with Personality Disorders. However, only two (10%) patients received this diagnosis, according to the clinical psychiatric evaluation, which is still considered the diagnostic gold standard. According to Bernick,43 even before the advent of evaluation scales, careful observation has always been the most invaluable source of information on psychiatric phenomena. However, it should be emphasized that, although our psychiatric evaluation was based on IDC-10 criteria,36 it is still extremely subjective, and the scale is a more objective evaluation method.
Our findings are similar to those of Vertzman & Pinheiro, apud Lemle (2005),29 who, even using a different referential (psychoanalytical), reported that SLE patients have their own, homogenous, and specific psychological model.
Due to the reduced number of patients in the present study, we cannot extrapolate our results to all SLE patients; however, we observed, when analyzing their medical records, that the majority of patients with more benign evolution during the study period did not show strict adherence to rheumatologic and psychiatric treatments. According to Fráguas Jr.,44 effective Depression treatment improves the baseline medical condition and quality of life of patients, reducing the inadequate use of medical services.
The present study did not detect a relationship between personality changes and SLE activity. This data is similar to that reported by Ishikura et al.,22 who also did not observe a relationship between the psychological characteristics of their patients and SLE activity. However, it differs from the results reported by Segui et al.,18 Ward et al.,24 and Yuko et al.,25 who observed a relationship between psychiatric symptoms (including personality disorders) and disease activity.
To conclude, we observed, in the present study, an important prevalence of psychiatric disorders (75%), but not Personality Disorders (only 10%). Moderate Depressive Episode (MDE) was the most common diagnosis, affecting approximately 65% of the patients. But a typical personality pattern or prevalence of a specific Personality Disorder was not observed.
A significant relationship between the psychiatric diagnosis (ICD-10 criteria) on the 1st evaluation and AFS scores and percentiles was not observed. A significant relationship between SLEDAI and AFS scores was also not observed during the study period; therefore, the association between personality changes and disease activity was not confirmed. According to statistical probabilities, it is possible that, if we had a larger study population, several associations among SLE aspects and psychiatric disorders, which were not confirmed here, would be statistically significant. Therefore, further studies with a larger number of patients are necessary to accurately assess those hypotheses.
We would like to acknowledge the trust deposited on us by the patients with Systemic Lupus Erythematosus who agreed to participate in this study, as well as to all the colleagues who collaborated voluntarily with all the phases of this study, for their extreme generosity.
5. Araújo GRB. De “lupus” et homine: contribuições a um espaço de atuação do psiquiatra em Hospital Geral. (Dissertação de Mestrado). Rio de Janeiro: Universidade Federal do Rio de Janeiro, 1989.
6. Miguel Filho EC. Alterações Psicopatológicas no Lúpus Eritematoso Sistêmico. (Tese de Doutorado). São Paulo: Universidade de São Paulo, 1992.
8. Leritz E, Brandt J, Minor M, Reis-Jensen F, Petri, M. Neuropsychological functioning and its relationship to antiphospolipid antibodies in patients with Systemic Lupus Erythematosus. J Clin Exp Neurops 2002; 24:527-33.
10. Maes MBE, Bonaccorso S, Hunsel FV et al. Increased 24-hour urinary cortisol excretion in patients with post-traumatic stress disorder and patients with major depression, but not in patients with fibromyalgia. Acta Psych Scand 1998; 98:328-35.
12. Liang MH, Rogers M, Larson M et al. The psychosocial impact of Systemic Lupus Erythematosus and Rheumatoid Arthritis. Arthritis Rheum 1984; 27:13-9.
13. Cabral MA, Giglio JS, Stangehaus G. Características de personalidade de pacientes artríticos reumatóides, tratados no ambulatório de um Hospital-Escola. Revista ABP-APAL 1986; 8:102-106.
14. Liang MH, Socher SA, Larson MG, Schur PH. Reliability and validity of six systems for the clinical assesment activity in Systemic Lupus Erithematosus. Arthritis Rheum, 1989; 32(9):1107-18.
15. Lim LC, Lee T, Boey, M. Psychiatric manifestation of Systemic Lupus Erythematosus in Singapore: A cross – culture comparison. Br J Psychiatry 1991; 159:520-3.
16. Braden CJ. Patterns of change over time in learned response to chronic illness among participants in a Systemic Lupus Erythematosus self-help course. Arthritis Care Res 1991; 4(4):158-67.
17. Onda K, Kato SA. Clinical study psychopathology in Systemic Lupus Erythematosus. Seishin Shinkeigaku Zasshi 2000; 102(7):616-39.
18. Segui J, Ramos-Casals M, Garcia-Carrasco et al. Psychiatric and psychosocial disorders in patients with Systemic Lupus Erythematosus: a longitudinal study of active and inactive stages of the disease. Lupus 2000; 9(8):584-8.
20. Santoantonio J. Estudo de características da personalidade de adolescentes com Lúpus Eritematoso Sistêmico por meio do método de Rorschach. (Tese de Doutorado). São Paulo, Universidade Federal de São Paulo (UNIFESP), 2001.
22. Ishikura R, Morimoto N, Tanaka K et al. Factors associated with anxiety, depression and suicide ideation in female outpatients whit SLE in Japan. Clin Rheumatol 2001; 20(6):394-400.
25. Yuko M, Takeshi S, Yumiko A, Toru H, Shigeru H. Psychological profiles and health status in Japanese female patients with Systemic Lupus Erythematosus: the Miyagi Lupus Collaborative Study. J Epidemiol 2002; 2(2):55-3.
26. Martins JM, Alves J, Trinca A et al. Personality, brain asymmetry, and neuroendocrine reactivity in two immune-mediate disorders: a preliminary report. Brain Behav Immun 2002;16:383-97.
27. Trysberg T, Tarkowsky A. Cerebral inflammation and degeneration in Systemic Lupus Erythemathosus. Curr Opin Rheumatol 2004; 16:527-33.
31. Nery FG, Borba EF, Viana VS et al. Prevalence of depressive and anxiety disorders in Systemic Lupus Erythematosus and their association with anti-ribosomal P antibodies. Prog Neuropsychopharmacol Biol Psychiatry. 2008; 32(3):695-700.
32. Tan EM, Cohen AS, Fries JF et al. Special article: The 1982 revised criteria for the classification of Systemic Lupus Erythematosus. Arthritis Rheum 1982; 25:1271-7.
33. Almeida OP. Instrumentos para avaliação de pacientes com demência. In: Gorenstein C, Andrade LHSG, Zuardi AW, eds. Escalas de Avaliação Clínica em Psiquiatria e Psicofarmacologia. São Paulo: Lemos, 2000. pp. 331-5.
35. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed). Washington, DC: APA, 1994.
36. Organização Mundial de Saúde – OMS: Classificação de Transtornos Mentais e de Comportamento. Porto Alegre: Artes Médicas, 1993. pp. 194-206.
38. Bombardier C, Gladman, D D, Urowitz M B, Caron D, Chang, C H & Committee on Prognosis Studies in SLE. Derivation of the SLEDAI – A disease activity index for lupus patients. Arthritis Rheum 1992; 35:630-640.
39. Cook RJ, Gladman DD, Pericak D, Urowitz MB. Prediction of short-term mortality in Systemic Lupus Erythematosus with time dependent measures of disease activity. J Rheumatol 2000; 27(8):1892-5.
40. Shott S. Statistics for health professionals. London: W.B. Saunders Company, 1990.
42. Hutchinson GA, Nehall FRC, Simeon DT. Psychiatric Disorders in Systemic Lupus Erythematosus. W I Med J 1996; 45:48.
Danusa Céspedes Guizzo Ayache
Rua Rio Grande do Sul, 1590. Vila Célia
Campo Grande, MS, Brazil
E-mail: [email protected]
Received on 11/02/2008.
Approved on 09/01/2009.
We declare no conflict os interest.