| Yunus MB, Khan
MA, Rawlings KK, Green JR, Olson JM, Shah S.
Genetic linkage analysis
of multicase families with fibromyalgia syndrome.
J Rheumatol
1999 Feb;26(2):408-12
"OBJECTIVE: Based on the reports of familial aggregation
of fibromyalgia (FM) syndrome, we investigated its possible genetic linkage to
HLA by studying multicase families. METHODS: Forty Caucasian multicase families
with a diagnosis of FM (American College of Rheumatology criteria) in 2 or more
first degree relatives were investigated. Eighty-five affected and 21 unaffected
members of 41 sibships were studied. Depression symptomology was assessed by Zung
Self-rating Depression Scale (SDS). HLA typing was performed for A, B, and DRB
1 alleles, and haplotypes were determined with no knowledge of the subject's diagnosis.
We investigated genetic linkage to the HLA region by evaluating sibships in multicase
families. RESULTS: Sibship analysis showed significant genetic linkage of FM to
the HLA region (p = 0.028). Subgroup analysis was also performed for 17 families
where the proband was also noted to have depression (with an SDS index value >
or =60). We found that the presence of depression did not influence the observed
results (p = 0.22). CONCLUSION:. Our study of 40 multicase families confirms existence
of a possible gene for FM that is linked with the HLA region. Our results should
be regarded as preliminary and their independent confirmation by other studies
is warranted." [Abstract]
OMIM
- Online Mendelian Inheritance in Man: MAJOR
HISTOCOMPATIBILITY COMPLEX, CLASS I, A; HLA-A Horven
S, Stiles TC, Holst A, Moen T.
HLA antigens in primary fibromyalgia
syndrome.
J Rheumatol 1992 Aug;19(8):1269-70
"HLA
antigens, both class I (A,B,C) and II (DR), were determined in 60 patients with
primary fibromyalgia syndrome and compared to 159 healthy controls. No significant
association between primary fibromyalgia syndrome and alleles of the HLA system
was detected." [Abstract] Burda
CD, Cox FR, Osborne P.
Histocompatability antigens in the fibrositis
(fibromyalgia) syndrome.
Clin Exp Rheumatol 1986 Oct-Dec;4(4):355-8
"HLA
antigen Class I (A, B, C) and II (DR) were determined in a small group of fibrositis
(fibromyalgia) patients and normal controls. Sixty-seven percent of fibrositis
patients had DR4 versus 30% of normal controls. There was also an increased relative
risk (4.5). No statitical significance of other Class I and II antigens in fibrositis
was found." [Abstract] Biasi
G, Fioravanti A, Galeazzi M, Marcolongo R.
[Absence of correlation
between HLA antigens and fibromyalgia syndrome in Italian patients]
Ann
Ital Med Int 1994 Oct-Dec;9(4):228-30
"Fibromyalgia syndrome (FS) is a
frequently seen extra-articular rheumatism of unknown etiology. Some authors have
suggested a direct role of the immune system in the pathogenesis of the disease
while others have found an increased prevalence of some HLA DR and B antigens.
The aim of our study was to verify the possible association between HLA and FS
in Italian patients with no clinical or immunological evidence of chronic rheumatic
inflammatory diseases. Ninety-two consecutive Italian patients were evaluated:
86 were typed for HLA A-B-C antigens and 74 for HLA DR antigens. The study was
performed by standard NIH microlymphocytotoxicity technique and by NIH prolonged
technique on B lymphocyte purified preparations. There was no statistically significant
difference between any HLA A-B-C and DR antigens in the patients compared with
the controls. We conclude that in the pathogenesis of FS there is no clear cut
evidence of immunologic or genetic involvement." [Abstract] Gursoy
S, Erdal E, Herken H, Madenci E, Alasehirli B, Erdal N.
Significance
of catechol-O-methyltransferase gene polymorphism in fibromyalgia syndrome.
Rheumatol
Int 2003 May;23(3):104-7
"Fibromyalgia syndrome (FS) is associated with
a neuroendocrinal disorder characterized by abnormal function of the hypothalamic-pituitary-adrenal
(HPA) axis, including hyperactive adrenocorticotropic hormone (ACTH) release and
adrenal hyporesponsiveness. Catechol-O-methyltransferase (COMT) enzyme inactivates
catecholamines and catecholamine-containing drugs. Polymorphism in the gene encodes
for the COMT enzyme. For this study, the significance of COMT polymorphism was
assessed in FS. There were three polymorphisms of the COMT gene: LL, LH, and HH.
The analysis of COMT polymorphism was performed using polymerase chain reaction
(PCR). Sixty-one patients with FS and 61 healthy volunteers were included in the
study. Although no significant difference was found between LL and LH separately,
the LL and LH genotypes together were more highly represented in patients than
controls ( P=0.024). In addition, HH genotypes in patients were significantly
lower than in the control groups ( P=0.04). There was no significant difference
between COMT polymorphism and psychiatric status of the patients as assessed by
several psychiatric tests ( P>0.05). In conclusion, COMT polymorphism is of
potential pharmacological importance regarding individual differences in the metabolism
of catechol drugs and may also be involved in the pathogenesis and treatment of
FS through adrenergic mechanisms as well as genetic predisposition to FS."
[Abstract] Gursoy
S.
Absence of association of the serotonin transporter gene polymorphism
with the mentally healthy subset of fibromyalgia patients.
Clin
Rheumatol 2002 Jun;21(3):194-7
"The serotonin transporter (5-HTT) gene
is considered to be a promising candidate for genetic involvement in some mood
disorders owing to its role in the regulation of serotoninergic neurotransmission.
In this study, we aimed to assess the significance of the 5-HTT gene in fibromyalgia
syndrome (FS) as well as to find out whether the 5-HTT gene polymorphism is associated
with this disease. Fifty-three mentally healthy fibromyalgia patients and 60 unrelated
healthy volunteer controls were included in the study. Symptom Checklist-90-Revised
(SCL-90-R), Beck Depression Inventory (BDI), and State and Trait Anxiety Inventory
tests (STAI-I and II) were applied to both patients and controls. A PCR analysis
of 5-HTT gene polymorphism was performed, and the results of the patients with
FS and healthy controls were compared. In both FS patients and healthy controls
the S/S, S/L and L/L alleles of the 5-HTTLPR genotype were represented in 24.5
% and 33%, 56.6% and 38.3%, and 18.9% and 28.3%, respectively. Additionally, in
FS patients and healthy controls the 10/10, 10/12 and 12/12 alleles of the VNTR
variant were represented in 5.9% and 11.7, 51% and 36.7%, and 43.1% and 51.7%,
respectively. The 5-HTTLPR and VNTR results of the patients and controls were
not significantly different ( P>0.05). We concluded that neither 5-HTT nor
its polymorphism is associated with FS. Our results also address the frequencies
of 5-HTT gene alleles in our population. Further studies are required to better
understand the genetic basis of FS." [Abstract]
Offenbaecher M, Bondy B, de Jonge S, Glatzeder K,
Kruger M, Schoeps P, Ackenheil M.
Possible association of fibromyalgia
with a polymorphism in the serotonin transporter gene regulatory region.
Arthritis
Rheum 1999 Nov;42(11):2482-8
"OBJECTIVE: To analyze the genotypes of the
promoter region of the serotonin transporter gene (5-HTT) in patients with fibromyalgia
(FM). METHODS: Genomic DNA from 62 patients meeting the American College of Rheumatology
1990 criteria for FM and 110 healthy controls was analyzed by polymerase chain
reaction. Additionally, the psychopathologic state of 52 of the FM patients was
evaluated using the Beck Depression Inventory (BDI) and the Symptom Checklist-90-Revised
(SCL-90-R). RESULTS: The 5-HTTLPR genotypes in FM patients versus controls were
distributed as follows: L/L 27% versus 34%, L/S 42% versus 50%, and S/S 31% versus
16%. FM patients with the S/S genotype had higher mean scores on the BDI and the
SCL-90-R compared with those in the L/L and L/S groups. CONCLUSION: A higher frequency
of the S/S genotype of 5-HTT was found in FM patients compared with healthy controls.
The S/S subgroup exhibited higher mean levels of depression and psychological
distress. These results support the notion of altered serotonin metabolism in
at least a subgroup of patients with FM." [Abstract]
Gursoy S, Erdal E, Herken H, Madenci E, Alasehirli
B.
Association of T102C polymorphism of the 5-HT2A receptor gene
with psychiatric status in fibromyalgia syndrome.
Rheumatol
Int 2001 Oct;21(2):58-61
"Serotonin (5-HT) is a key neurotransmitter in
the central nervous system. It is suggested that serotonergic dysfunction may
be involved in the pathophysiology of fibromyalgia syndrome (FS). In this study,
we aimed to investigate T102C polymorphism of the 5-HT2A receptor gene in FS.
Fifty-eight patients with FS and 58 unrelated healthy volunteer controls were
included in the study. In both groups, the C/C, C/T, and T/T genotypes of the
5-HT gene were represented in 31% (22.4% in controls), 50% (53.4%), and 19% (24.1%),
respectively. The 5-HT2A receptor gene polymorphism results were not significantly
different between patients and controls (chi squared test, P>0.05). There was
a significant correlation between patients with the T/T genotype and the subgroup
according to the SCL-90-R test, (analysis of variance, P<0.05). We also saw
that patients with the T/T genotype had the lowest pain threshold. CONCLUSION.
T102C polymorphism of the 5-HT2A receptor gene is not associated with the etiology
of FS. Our results also indicate that the T/T genotype may be responsible for
psychiatric symptoms of FS." [Abstract] Bondy
B, Spaeth M, Offenbaecher M, Glatzeder K, Stratz T, Schwarz M, de Jonge S, Kruger
M, Engel RR, Farber L, Pongratz DE, Ackenheil M.
The T102C polymorphism
of the 5-HT2A-receptor gene in fibromyalgia.
Neurobiol Dis
1999 Oct;6(5):433-9
"Based on a possible involvement of serotonergic dysfunction
in the pathophysiology of fibromyalgia (FM) and on preliminary reports of a possible
genetically driven vulnerability for this disorder we investigated the silent
T102C polymorphism of the 5-HT2A-receptor gene in 168 FM patients and 115 healthy
controls. Our results showed a significantly different genotype distribution in
FM patients with a decrease in T/T and an increase in both T/C and C/C genotypes
as compared to the control population (Fisher's Exact test, two-sided, P = 0.008).
However, the increase in allele-C102 frequency felt short of significance (P =
0.07). Correlation of genotypes to clinical parameters revealed no influences
on age of onset, duration of disease or psychopathological symptoms, measured
with the Beck Depression Inventory and the symptom checklist SCL-90-R. In contrast
to that the pain score, being a self reported information on pain severity, was
significantly higher in patients of the T/T genotype (Mann-Whitney U test, P =
0.028). This suggests that the T102-allele might be involved in the complex circuits
of nociception. However, the T102C polymorphism is not directly involved in the
aetiology of FM but might be in linkage dysequilibrium with the true functional
variant, which has to be unravelled." [Abstract]
Frank B, Niesler B, Bondy B, Späth M, Pongratz DE, Ackenheil M, Fischer C, Rappold G
Mutational analysis of serotonin receptor genes: HTR3A and HTR3B in fibromyalgia patients.
Clin Rheumatol. 2004 Aug;23(4):338-44.
The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) has been implicated in numerous human disorders. Dysfunction of serotonergic neurotransmission is thought to play a major role in the pathophysiology of the fibromyalgia syndrome (FMS) which is characterised by non-restorative sleep and severe pain. In our study, both serotonin receptor subunit genes, HTR3A and HTR3B, have been investigated for sequence variations in FMS patients in order to reveal a possible involvement in the aetiology of FMS. We examined DNA samples from 48 patients with FMS representing sporadic cases by single-strand conformation polymorphism (SSCP) and denaturing high-performance liquid chromatography (dHPLC) analysis, sequenced samples with conspicuous patterns and performed statistical calculations. HTR3A mutational analysis revealed one novel as well as five known sequence variations. Investigating HTR3B, we detected seven formerly described mutations and one novel sequence variant. Statistical computation rated all variants as probably non-disease-related polymorphisms. Nevertheless, one might speculate about an effect of the respective sequence variants on the severity of the disease. Sequence variants of the serotonin receptor subunit genes HTR3A and HTR3B indicate no obvious significance in the aetiology of fibromyalgia, yet they represent the basis for future studies on their pharmacogenetic relevance. [Abstract]
Su SY, Chen JJ, Lai CC, Chen CM, Tsai FJ
The association between fibromyalgia and polymorphism of monoamine oxidase A and interleukin-4.
Clin Rheumatol. 2006 Mar 18;
Because fibromyalgia (FM) is often comorbid with anxiety, and monoamine oxidase A (MAOA) was reported to be associated with anxiety, we determine if there is MAOA gene polymorphism associated with FM patients. Moreover, interleukin 4 (IL-4) was found to be an important cytokine participating in the immunologic pathway of T-helper 2 (Th-2) cells, in this study, we search if the genetic polymorphism of IL-4 intron3 could be demonstrated in FM patients. The genotype of sixty-two FM patients was compared with that of control subjects. The polymorphism of IL-4 intron3 variable number of tandem repeats (VNTR) was demonstrated by performing the genomic polymerase chain reaction (PCR) and analyzing the length of PCR product. Furthermore, the MAOA 941 G to T polymorphism was also determined by PCR-RFLP (restriction fragment length polymorphism) analysis. The MAOA 941 position genotype polymorphism between FM and control subjects was found neither statistically different in male (p=0.60) or female (p=0.52), nor total allelic frequency (p=0.52). Similarly, the difference of IL-4 intron3 polymorphism between FM and control was neither existing in genotype (p=0.06), nor allele frequency (p=0.07). The result suggests either the genetic linkage between FM and anxiety or that between FM and immunologic diseases are weak. Accordingly, the MAOA 941 position and IL-4 intron3 polymorphisms are not susceptible markers to predict FM. [Abstract]
Blanco LE, de Serres FJ, Ferna?dez-Bustillo E, Kassam DA, Arbesú D, Rodríguez C, Torre JC
alpha1-Antitrypsin and fibromyalgia: new data in favour of the inflammatory hypothesis of fibromyalgia.
Med Hypotheses. 2005;64(4):759-69.
alpha1-Antitrypsin (AAT) circulates in high serum concentrations, and impregnates most body tissues. AAT has a broad anti-inflammatory spectrum, and modulates most inflammatory reactions occurring in human body. Recently, a possible relationship between AAT deficiency (AAT-D) and fibromyalgia (FM) has been raised, with the finding that intravenous infusions of purified human AAT efficiently controlled FM symptoms in two patients with severe hereditary AAT-D. On the other hand, functional magnetic resonance imaging has detected a significant greater activity in pain sensitive areas of the brain in patients with FM, in response to cutaneous stimuli, providing further evidence for a physiological explanation for FM pain. In recent studies abnormal profiles of inflammation markers in serum and biopsies have been found in FM patients. Since most of these inflammation mediators can be inhibited by AAT, these observations would suggest that at least a subset of the FM syndrome could be related to an inflammatory process, possibly due to an imbalance between inflammatory and anti-inflammatory substances, in the soft body tissues. Future directions of research would be: (1) to develop epidemiological studies to determine the gene frequency of AAT deficiency alleles in FM patients; (2) implementation of a double-blind placebo-controlled clinical trial to determine the specific role of AAT augmentation therapy in AAT-D patients with FM; (3) identification of specific laboratory markers for diagnostic and clinical evaluation purposes in FM; (4) application of the newest medical imaging techniques for diagnosis; and (5) identification of genetic, familial, and environmental risk factors suspected to participate in the FM syndrome development. [Abstract] | |
Buskila D, Neumann L
Genetics of fibromyalgia.
Curr Pain Headache Rep. 2005 Oct;9(5):313-5.
The pathogenesis of fibromyalgia (FM) and related conditions is not entirely understood. Recent evidence suggests that these syndromes may share heritable pathophysiologic features. Familial studies suggest that genetic and familial factors may play a role in the etiopathogenesis of these conditions. There is evidence that polymorphisms of genes in the serotoninergic and catecholaminergic systems are linked to the pathophysiology of FM and related conditions and are associated with personality traits. The precise role of genetic factors in the etiopathology of FM remains unknown, but it is likely that several genes are operating together to initiate this syndrome. Larger longitudinal studies are needed to better clarify the role of genetics in the development of FM. [Abstract]
Buskila D, Neumann L.
Fibromyalgia
syndrome (FM) and nonarticular tenderness in relatives of patients with FM.
J
Rheumatol 1997 May;24(5):941-4
"OBJECTIVE: To determine the prevalence
of fibromyalgia (FM) and to assess nonarticular tenderness in relatives of patients
with FM. METHODS: Thirty female patients with FM randomly chosen from 117 of their
close relatives (parents, brothers, sisters, children, husbands) were assessed
for nonarticular tenderness. A count of 18 tender points was conducted by thumb
palpation, and tenderness thresholds were assessed by dolorimetry at 9 tender
sites. FM was diagnosed according to the 1990 American College of Rheumatology
criteria. RESULTS: The prevalence of FM among blood relatives of patients with
FM was 26%, and among their husbands 19%. FM prevalence in male relatives was
14%, and in female relatives 41%. The mean tender point counts of male and female
young relatives was significantly higher than that of controls: 6.1 vs 0.2 (p
< 0.01), and 4.4 vs 0.4 (p < 0.01) respectively. Similarly, adult relatives
had considerably higher mean tender point counts than controls: 4.0 vs 0.04 (p
< 0.01) and 10.3 vs 0.28 (p < 0.01) respectively, for males and females.
CONCLUSION: Relatives of patients with FM have a higher prevalence of FM and are
more tender than the general population, as recently reported and shown in a healthy
control group. This finding can be attributed to genetic and environmental factors."
[Abstract]
Buskila
D, Neumann L, Hazanov I, Carmi R.
Familial aggregation in the fibromyalgia
syndrome.
Semin Arthritis Rheum 1996 Dec;26(3):605-11
"The
authors studied the familial occurrence of fibromyalgia (FMS) to determine a possible
role of genetic and familial factors in this syndrome. Fifty-eight offspring aged
5 to 46 years (35 males and 23 females) from 20 complete nuclear families ascertained
through affected mothers with FMS were clinically evaluated for FMS according
to the ACR 1990 diagnostic criteria. FMS symptoms, quality of life, physical functioning,
and dolorimetry thresholds were assessed in all subjects. Sixteen offspring (28%)
were found to have FMS. The M/F ratio among the affected was 0.8 compared with
1.5 in the whole study group. Offspring with and without FMS did not differ on
anxiety, depression, global well-being, quality of life, and physical functioning.
A high prevalence of FMS was observed among offspring of FMS mothers. Because
psychological and familial factors were not different in children with and without
FMS, the high familial occurrence of this syndrome may be attributable to genetic
factors." [Abstract] Pellegrino
MJ, Waylonis GW, Sommer A.
Familial occurrence of primary fibromyalgia.
Arch
Phys Med Rehabil 1989 Jan;70(1):61-3
"Seventeen families of patients with
primary fibromyalgia were studied for evidence of inherited primary fibromyalgia.
Fifty parents and siblings were included in the analysis. Twenty-six (52%, mean
age 33.5 years) had characteristic symptoms and findings of primary fibromyalgia.
Eleven (22%, mean age 28 years) were asymptomatic but had clinical evidence of
abnormal muscle consistency to palpation without tender or trigger points. One
person had clinical evidence of lupus. Thirteen (26%) had no evidence of fibromyalgia
or abnormal muscle consistency. The mode of inheritance was autosomal dominant.
Identical twins are described who developed symptoms of primary fibromyalgia within
six months of each other, as are two brothers who developed abnormal palpable
muscle consistency years before acquiring the characteristic findings of the fibromyalgia
syndrome. Primary fibromyalgia may be an inherited condition with a variable latent
stage before clinical expression of the disease." [Abstract] Hudson
JI, Goldenberg DL, Pope HG Jr, Keck PE Jr, Schlesinger L.
Comorbidity
of fibromyalgia with medical and psychiatric disorders.
Am
J Med 1992 Apr;92(4):363-7
"PURPOSE: Patients with fibromyalgia have been
reported to display high rates of several concomitant medical and psychiatric
disorders, including migraine, irritable bowel syndrome, chronic fatigue syndrome,
major depression, and panic disorder. To test further these and other possible
associations, we assessed the personal and family histories of a broad range of
medical and psychiatric disorders in patients with fibromyalgia. PATIENTS AND
METHODS: Subjects were 33 women (mean age 42.1 years) who each met American College
of Rheumatology criteria for fibromyalgia and presented to a rheumatologist at
a tertiary referral center. They received the Structured Clinical Interview for
DSM-III-R (SCID); a supplemental interview, in SCID format, for other medical
and psychiatric disorders, including migraine, irritable bowel syndrome, and chronic
fatigue syndrome; and an interview for family history of medical and psychiatric
disorders. RESULTS: Patients with fibromyalgia displayed high lifetime rates of
migraine, irritable bowel syndrome, chronic fatigue syndrome, major depression,
and panic disorder. They also exhibited high rates of familial major mood disorder.
CONCLUSIONS: The finding that migraine, irritable bowel syndrome, chronic fatigue
syndrome, major depression, and panic disorder are frequently comorbid with fibromyalgia
is consistent with the hypothesis that these various disorders may share a common
physiologic abnormality." [Abstract]
Offenbaecher M, Glatzeder K, Ackenheil M.
Self-reported
depression, familial history of depression and fibromyalgia (FM), and psychological
distress in patients with FM.
Z Rheumatol 1998;57 Suppl
2:94-6
"The prevalence of FM in the general population is estimated at
2%. FM is among the three most common diagnoses in ambulatory adult rheumatology
practice. To study the degree of depression, the familial history of depression
and FM, as well as the psychological distress in our FM population, we mailed
a standardized questionnaire to 304 FM patients. The response rate was 33%. We
found BDI scores higher than 21 in 27% of the patients indicating clinical relevant
depression. The patients had high levels of global distress measured with the
SCL-90-R as well as elevated scores in the subscales. Twenty three percent had
a familial history of depression, 46% a familial history of FM, and 46% had been
diagnosed with depression in the past." [Abstract] Aaron
LA, Herrell R, Ashton S, Belcourt M, Schmaling K, Goldberg J, Buchwald D.
Comorbid
clinical conditions in chronic fatigue: a co-twin control study.
J
Gen Intern Med 2001 Jan;16(1):24-31
"OBJECTIVES: Chronically fatiguing
illness, defined as fatigue for at least 6 months, has been associated with various
physical health conditions. Our objective was to determine whether there is a
significant relationship between chronically fatiguing illness and 10 clinical
conditions that frequently appear to be associated with fatigue, adjusting for
the potentially confounding effects of psychiatric illness. DESIGN: A co-twin
control study controlling for genetic and many environmental factors by comparing
chronically fatigued twins with their nonfatigued co-twins. SETTING: A nationally
distributed volunteer twin registry. PARTICIPANTS: The study included 127 twin
pairs in which one member of the pair experienced fatigue of at least 6 months'
duration and the co-twin was healthy and denied chronic fatigue. Fatigued twins
were classified into 3 levels using increasingly stringent diagnostic criteria.
MEASUREMENTS AND MAIN RESULTS: Twins reported on a history of fibromyalgia, irritable
bowel syndrome, multiple chemical sensitivities, temporomandibular disorder, interstitial
cystitis, postconcussion syndrome, tension headache, chronic low back pain, chronic
pelvic pain (women), and chronic nonbacterial prostatitis (men). The prevalence
of these comorbid clinical conditions was significantly higher in the fatigued
twins compared to their nonfatigued co-twins. Most notably, compared to their
nonfatigued co-twins, the chronically fatigued twins had higher rates of fibromyalgia
(> 70% vs < 10%) and irritable bowel syndrome (> 50% vs < 5%). The
strongest associations were observed between chronic fatigue and fibromyalgia
(odds ratios > 20), irritable bowel syndrome, chronic pelvic pain, multiple
chemical sensitivities, and temporomandibular disorder (all with odds ratios >
or = 4). Regression analysis suggested that the number of comorbid clinical conditions
associated with chronic fatigue could not be attributed solely to psychiatric
illness. CONCLUSIONS: Chronically fatiguing illnesses were associated with high
rates of many other clinical conditions. Thus, patients with chronic fatigue may
present a complex clinical picture that poses diagnostic and management challenges.
Nonetheless, clinicians should assess such patients for the presence of comorbid
clinical conditions. Future research should provide a better understanding of
the temporal relationship of the onset of fatigue and these conditions, and develop
strategies for early intervention." [Abstract] Sinaii
N, Cleary SD, Ballweg ML, Nieman LK, Stratton P.
High rates of autoimmune
and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases
among women with endometriosis: a survey analysis.
Hum Reprod
2002 Oct;17(10):2715-24
"BACKGROUND: Women with endometriosis may also
have associated disorders related to autoimmune dysregulation or pain. This study
examined whether the prevalence of autoimmune, chronic pain and fatigue and atopic
disorders is higher in women with endometriosis than in the general female population.
METHODS AND RESULTS: A cross-sectional survey was conducted in 1998 by the Endometriosis
Association of 3680 USA members with surgically diagnosed endometriosis. Almost
all responders had pain (99%), and many reported infertility (41%). Compared with
published rates in the general USA female population, women with endometriosis
had higher rates of hypothyroidism (9.6 versus 1.5%, P < 0.0001), fibromyalgia
(5.9 versus 3.4%, P < 0.0001), chronic fatigue syndrome (4.6 versus 0.03%,
P < 0.0001), rheumatoid arthritis (1.8 versus 1.2%, P = 0.001), systemic lupus
erythematosus (0.8 versus 0.04%, P < 0.0001), Sjogren's syndrome (0.6 versus
0.03%, P < 0.0001) and multiple sclerosis (0.5 versus 0.07%, P < 0.0001),
but not hyperthyroidism or diabetes. Allergies and asthma were more common among
women with endometriosis alone (61%, P < 0.001 and 12%, P < 0.001 respectively)
and highest in those with fibromyalgia or chronic fatigue syndrome (88%, P <
0.001 and 25%, P < 0.001 respectively) than in the USA female population (18%,
P < 0.001 and 5%, P < 0.001 respectively). CONCLUSIONS: Hypothyroidism,
fibromyalgia, chronic fatigue syndrome, autoimmune diseases, allergies and asthma
are all significantly more common in women with endometriosis than in women in
the general USA population." [Abstract]
Berg AM, Naides SJ, Simms RW.
Established
fibromyalgia syndrome and parvovirus B19 infection.
J Rheumatol
1993 Nov;20(11):1941-3
"OBJECTIVE. To determine the seroprevalence of
prior and persistent parvovirus B19 (B19) infection in a group of patients with
fibromyalgia (FS) compared with controls. METHODS. Fifteen female patients with
FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and
eleven patients with FS who did not recall any such illness (-VP) were selected
from a referral practice. We excluded patients with FS who described a history
of trauma prior to the onset of FS symptoms. Twenty-six female medical workers
served as controls. Serum IgM and IgG anti-B19 antibodies were measured by ELISA.
Polymerase chain reaction (PCR) products from serum were analyzed by dot blot
hybridization for B19 DNA. Fisher's 2-tailed exact test was used to compare the
proportion of positive serologies in each group. RESULTS. No patient or control
had positive IgM levels. For all patients with FS, the prevalence of prior B19
infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00)
and that of the general population. No significant difference was found in the
prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11,
p = 0.25). None of the patients or controls showed evidence for persistent B19
viremia, as determined by PCR analysis. CONCLUSION. Our data do not suggest that
B19 plays a pathogenic role in this population of patients with FS. Testing for
IgM against B19 within 2-3 months of symptom onset may prove more helpful in further
defining the role of B19 in FS." [Abstract]
Kato K, Sullivan PF, Evengård B, Pedersen NL
Importance of genetic influences on chronic widespread pain.
Arthritis Rheum. 2006 May;54(5):1682-6.
OBJECTIVE: To estimate the relative importance of genetic and environmental factors in chronic widespread pain, and to assess whether there are sex differences in the type or magnitude of these influences. METHODS: Data were collected from a national sample of twins > or = 42 years of age, all of whom were participants in the Swedish Twin Registry. The presence of chronic widespread pain was assessed via computer-assisted telephone interviews, which were conducted between 1998 and 2002, using the American College of Rheumatology criteria for fibromyalgia. No clinical examinations were performed. In preliminary analyses, probandwise concordance rates and tetrachoric correlations were calculated. Structural equation modeling was then performed to estimate additive genetic, shared environmental, and nonshared environmental sources of variability in susceptibility for the development of chronic widespread pain. RESULTS: Of 61,355 eligible twins, 44,897 individuals (73.2%) responded to the interview. Both members of 15,950 pairs responded to the items regarding pain symptoms; of these pairs, 4,170 were monozygotic, 5,881 were same-sex dizygotic, and 5,755 were opposite-sex dizygotic. The prevalence of chronic widespread pain was 4.1%, and the ratio of women to men was 3.3 to 1. Probandwise concordance rates and tetrachoric correlations suggested modest genetic influences for both women and men. Genetic and shared environmental influences explained approximately half of the total variance, with no indication of sex differences in either the type or magnitude of these influences. CONCLUSION: Individual differences in the likelihood of developing chronic widespread pain reflect modest genetic influences. There are no significant sex differences in the type or expression of the genes responsible for chronic widespread pain or in the magnitude of the relative importance of these influences on chronic widespread pain. [Abstract]
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