Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Compared to the now numerous studies on the endocrinology of rheumatic diseases in adults, only a small number of studies has been published on children with rheumatic diseases. Prolactin has been most extensively investigated, showing interesting parallels with the findings in adults with rheumatological diseases. Thus, analogous to adult RA most forms of JRA or JCA (with the exception of ANA-positive JRA with uveitis) appear to show, if anything, low to normal levels of prolactin. Since the prolactin levels in adult RA depend on the inflammatory activity, and the physiological prolactin secretion decreases in chronic stress (especially sleep disorders), these results are most likely to be explained as reactive non-specific mechanisms in the stress of the disease. However, specific mechanisms are also being discussed to explain the low prolactin levels in adult RA. The results of prolactin measurements in juvenile SLE, juvenile ankylosing spondylitis and ANA-positive JRA with a raised incidence of uveitis, contrast with this. These conditions sometimes show significantly higher prolactin levels compared to healthy controls. A correlation of the increase of prolactin concentration with the inflammatory activity has been described for juvenile ankylosing spondylitis. These results correlate well with those of adult forms such as diseases of the seronegative spondyloarthropathies type, SLE and iridocyclitis. Raised prolactin concentrations are also found in these diseases. The inflammation promoting and immunostimulatory effects of prolactin found especially in animal experiments are confirmed clinically in these diseases by reports of successful treatments with the prolactin inhibitor, bromocriptine. The results available up to now for human growth hormone in JRA and JCA tend to be comparable with the results for prolactin in these form of paediatric rheumatological diseases. Besides normal values above, all lowered concentrations are measured for this hormone. Apart from other non-specific factors, its diminished secretion is mainly determined by the inflammatory activity of the disease. Low levels of growth hormone are likely to be a significant factor in the growth retardation in children with inflammatory rheumatological diseases. Up to now, the small number of investigations on gonadotrophins and the sex hormones in juvenile SLE and various forms of JRA published have not as yet yielded unequivocal results. The endocrine aspects of paediatric rheumatological diseases are thus still incompletely elucidated. However, there are many promising avenues for further fruitful research in this field.
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PMID:Endocrine aspects of paediatric rheumatic diseases. 891 53

Prolactin in a pituitary peptide hormone which is immunomodulatory. Increased serum prolactin concentrations accelerate autoimmunity in the NZB x NZW F1 mouse model of SLE. Some patients with SLE are hyperprolactinemic and, in cross-sectional and longitudinal studies, serum prolactin has been associated with or correlated to lupus disease activity. Suppression of physiologic levels of prolactin by bromocriptine administration was associated with improvement in SLE in a preliminary study. While specific mechanisms remain to be elucidated, prolactin appears to be immunostimulatory in patients with SLE. A better understanding of its role and its interactions with other immunoregulatory hormones in SLE may lead to novel therapies for the suppression of this hormonally sensitive autoimmune disease.
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PMID:Prolactin and systemic lupus erythematosus. 895 44

Lupus activity during pregnancy has been the subject of much research and debate recently. Data point to increased SLE activity during pregnancy. SLE may flare during any trimester of pregnancy, as well as in the puerperium; however, flares are usually mild, affecting skin and joints, and, unless affecting the kidney, do not confer any adverse prognosis on pregnancy outcome. Diagnosis of SLE flares can be difficult during pregnancy and must rely on a thorough clinical and laboratory assessment. Recent data link sex hormones, particularly prolactin, to SLE activity, which may be one explanation for the high frequency of SLE flares during pregnancy. No data support the thesis that corticosteroids prevent SLE flares during pregnancy, and therefore, prophylactic prednisone should not be given routinely. HCQ does seem to be safe for the fetus, however. SLE flares can be treated, depending on severity, with NSAIDs or with HCQ, prednisone, or azathioprine.
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PMID:Systemic lupus erythematosus flares during pregnancy. 903 72

Cyclo (His-Pro) or CHP is a cyclic dipeptide that is known to elicit many biologic activities including inhibition of pituitary prolactin (PRL) secretion. PRL stimulates humoral and cell mediated immune responses and hyperprolactinemia has been found in a subset of systemic lupus erythematosus (SLE) patients in association with active disease. To explore whether CHP may play a role in SLE patients, we measured, CHP and PRL levels in sera of 21 SLE patients and 11 normal controls. The results of this study show significantly (P < 0.001) high levels of CHP in SLE compared to controls. However, there was no significant correlation between serum PRL and CHP levels in SLE patients (r = 0.027, P = 0.29). The increase in serum levels of CHP may be in an attempt to increase hypothalamic content of dopamine which in turn would decrease pituitary PRL synthesis in hyperprolactinemic SLE patients.
Lupus 1997
PMID:Elevated serum levels of cyclo (His-Pro), an endogenous inhibitor of pituitary prolactin secretion, in systemic lupus erythematosus patients. 910 33

A loss in bone mass was reported in premenopausal systemic lupus erythematosus (SLE) women, but this problem has not been studied in SLE males. We evaluated bone mineral density (BMD) in SLE males and the relationship between prolactin (PRL) and testosterone with BMD. We also studied the controversial effect of steroid therapy on BMD in these patients. We measured BMD in the lumbar spine and at the hip in 20 SLE men (mean age 37 y) and in the controls (n = 40). We measured PRL and testosterone in serum and saliva. The mean dose of prednisone at the time of study was 11.6 mg; and cumulative dose was 17.6 g. No significative decrease in BMD was detected in SLE males vs controls; either in the lumbar spine (1.00 +/- 0.1 vs 1.05 +/- 0.1 g/cm2) or in the femoral neck (0.84 +/- 0.1 vs 0.87 +/- 0.1 g/cm2). No patient or control had osteoporosis or fractures. We did not find any relationship between BMD and cumulative dose and baseline dose of corticosteroids. The mean values of PRL and testosterone (serum and salivary) were in the normal range. We did not find any correlation between BMD, PRL and androgens. This study did not show a loss in bone mass in SLE men on corticosteroid therapy.
Lupus 1996 Dec
PMID:Bone mineral density and hormonal status in men with systemic lupus erythematosus. 911 8

We investigated whether the immunosuppressive effect of bromocriptine in mice is due to its direct effect on lymphocyte functions or through inhibition of prolactin secretion. Incubation of mouse Babl/c splenic lymphocytes with bromocriptine in vitro at a concentration of around 0.5 to 1 microgram/mL causes an inhibition of antigen- or mitogen-induced proliferation. However, bromocriptine in vitro has no effect on lymphokine production (gamma-interferon and interleukin-2), expression of interleukin-2 receptor or lymphocyte cytotoxic function. Furthermore, treatment of Babl/c mice with bromocriptine inhibits the mixed lymphocyte reaction and mitogen stimulation, as well as primary and secondary antibody production. However, we postulated that the inhibition of ex vivo functional activity could not account for a direct cytostatic or cytotoxic effect of bromocriptine. This is supported by the in vitro data, which shows that bromocriptine has no effect on proliferating P-815 mastocytoma tumor cells. Finally, (NZB/NZW) F1 mice spontaneously develop a disease similar to systemic lupus erythematosus. In both non-autoimmune Babl/c mice and (NZB/NZW) F1 lupus-mice, the serum level of bromocriptine achieved by a treatment with 5 mg/kg on average is 2-6 ng/mL. On the one hand, this dose is sufficient to significantly alter the ex vivo functional tests in Babl/c mice and to show a beneficial effect in the in vivo model of female lupus-mice. On the other hand, the lowest concentration which could have an inhibitory effect on antigen- and mitogen-induced proliferation in vitro is 200 ng/mL, ie 50 times more than that required in vivo to obtain significant reductions of proteinurea, glomerular membrane proliferation and immune deposits in lupus-mice. The serum levels of gamma-interferon and interleukin-2 are reduced in lupus-mice when compared with Babl/c mice. The treatment with bromocriptine does not influence these parameters. In conclusion, our data demonstrate that the major immunosuppressive activity of bromocriptine is probably dependent on its hypoprolactinemic effect.
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PMID:Bromocriptine has little direct effect on murine lymphocytes, the immunomodulatory effect being mediated by the suppression of prolactin secretion. 918 Oct 47

Systemic lupus erythematosus is a difficult disease to study with a variable disease course characterized by exacerbations and remissions. A variety of biologic agents are under investigation as potential treatments for systemic lupus erythematosus, either in murine disease models or in clinical trials. These products are designed to specifically interfere with the following immunologic processes: T-cell activation and T-cell-B-cell collaboration, production of anti-dsDNA antibodies, deposition of anti-dsDNA antibody complexes, complement activation, and deposition, and cytokine activation and modulation. More aggressive interventions include gene therapy and stem-cell transplantation. Recently developed immunomodulators have been studied in patients with systemic lupus erythematosus 2'-Chlorodeoxyadenosine, mycophenolate mofetil, and leflunomide. Additional innovative pharmaceutical treatments include the mild androgen dehydroepiandrosterone, estrogen antagonists, including tamoxifen and selective estrogen receptor modulators, and the prolactin inhibitor bromocriptine. Other promising pharmaceutical interventions include products designed to inhibit synthesis of the proinflammatory mediators: prostaglandins, leukotrienes, and nitric oxide. Although previously regarded as an indication to be avoided in the development of new therapeutics, enthusiasm for studying systemic lupus erythematosus in clinical trials now exists. A variety of biologic and pharmaceutical agents offer promise as potential therapies. As with rheumatoid arthritis, development of these products will benefit from active involvement of rheumatologists and efforts to develop international consensus regarding trial methodology and outcome measures.
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PMID:Approaches to the management of systemic lupus erythematosus. 930 96

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
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PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

The aim of this revision is to explore the possible role of the prolactin in the immune response. The prolactin is a hormone secreted by the pituitary. However, it has a trophic function in the proliferation of the lymphocytes. The cell of the immune system show outer membrane receptor for the prolactin. Moreover, the lymphocytes are capable to produce and secret prolactin. In cell culture, different levels of prolactin show different immune responses- low levels of prolactin awake a weak immune response. In contrast, high levels of prolactin show a strong immune response. Alteration in the sera levels of prolactin has been describes in severe autoimmune disease like systemic lupus erythematosus. Reiter syndrome, adjuvant arthritis, uveitis etc. Until now many evidences has been reported about the roles of the prolactin in the immune response acting like an immunomodulator, but the relevance of this phenomena in the clinical practice is still unclear.
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PMID:[Prolactin as an immunomodulator]. 943 72

In recent years prolactin (PRL) has emerged as an important immunomodulator in various autoimmune disorders. Bromocriptine (BRC) is a dopamine agonist that suppresses secretion of PRL. Good clinical response to BRC has been reported in patients with psoriatic arthritis, Reiter's syndrome, and systemic lupus erythematosus. 5 mg of BRC at bedtime were given to 5 patients (aged 35-50) with refractory rheumatic arthritis (RA) who had failed to respond to previous treatment with at least 2 disease-modifying antirheumatic drugs. Patients were assessed at 4-6 week intervals for 6 months, 3 showed more than 25% improvement in the number of tender and swollen joints at 12 weeks of treatment. However, in only 2 of them was improvement maintained till the end of the 6 months. There were no changes in other measures of disease activity, 1 patient dropped out of the study due to acute exacerbation of her disease 4 weeks after initiation of BRC and required intra-articular injections of corticosteroid. The remaining patient did not show any significant clinical changes. No correlation was found between serum PRL levels and disease activity over time. It is suggested that some patients with refractory RA might improve with BRC. Its use in larger doses in larger groups of patients may help elucidate its role in the treatment of RA.
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PMID:[Bromocriptine for refractory rheumatoid arthritis]. 945 92


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