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Biomedical subjects

E Palazzo

Publications and source records attributed to E Palazzo.

At least 19 recordsLinked to original sources

Effects of (S)-3,4-DCPG, an mGlu8 receptor agonist, on inflammatory and neuropathic pain in mice.

In this study, the effect of (S)-3,4-dicarboxyphenylglycine (DCPG), a selective mGlu8 receptor agonist, has been investigated in inflammatory and neuropathic pain models in order to elucidate the role of mGlu8 receptor in modulating pain perception. Inflammatory pain was induced by the peripheral injection of formalin or carrageenan in awake mice. Systemic administration of (S)-3,4-DCPG, performed 15 min before formalin, decreased both early and delayed nociceptive responses of the formalin test. When this treatment was carried out 15 min after the peripheral injection of formalin it still reduced the late hyperalgesic phase. Similarly, systemic (S)-3,4-DCPG reduced carrageenan-induced thermal hyperalgesia and mechanical allodynia when administered 15 min before carrageenan, but no effect on pain behaviour was observed when (S)-3,4-DCPG was given after the development of carrageenan-induced inflammatory pain. When microinjected into the lateral PAG (RS)-alpha-methylserine-O-phoshate (MSOP), a group III receptor antagonist, antagonised the analgesic effect induced by systemic administration of (S)-3,4-DCPG in both of the inflammatory pain models. Intra-lateral PAG (S)-3,4-DCPG reduced pain behaviour when administered 10 min before formalin or carrageenan; both the effects were blocked by intra-lateral PAG MSOP. (S)-3,4-DCPG was ineffective in alleviating thermal hyperalgesia and mechanical allodynia 7 days after the chronic constriction injury of the sciatic nerve, whereas it proved effective 3 days after surgery. Taken together these results suggest that stimulation of mGlu8 receptors relieve formalin and carrageenan-induced hyperalgesia in inflammatory pain, whereas it would seem less effective in established inflammatory or neuropathic pain.

Analysis of Variance↗

In vitro and in vivo pharmacology of synthetic olivetol- or resorcinol-derived cannabinoid receptor ligands.

BACKGROUND AND PURPOSE: We have previously reported the development of CB-25 and CB-52, two ligands of CB1 and CB2 cannabinoid receptors. We assessed here their functional activity. EXPERIMENTAL APPROACH: The effect of the two compounds on forskolin-induced cAMP formation in intact cells or GTP-gamma-S binding to cell membranes, and their action on nociception in vivo was determined. KEY RESULTS: CB-25 enhanced forskolin-induced cAMP formation in N18TG2 cells (EC50 approximately 20 nM, max. stimulation = 48%), behaving as an inverse CB1 agonist, but it stimulated GTP-gamma-S binding to mouse brain membranes, behaving as a partial CB1 agonist (EC50 =100 nM, max. stimulation = 48%). At human CB1 receptors, CB-25 inhibited cAMP formation in hCB1-CHO cells (EC50 = 1600 nM, max. inhibition = 68% of CP-55,940 effect). CB-52 inhibited forskolin-induced cAMP formation by N18TG2 cells (IC50 = 450 nM, max. inhibition = 40%) and hCB1-CHO cells (EC50 = 2600 nM, max. inhibition = 62% of CP-55,940 effect), and stimulated GTP-gamma-S binding to mouse brain membranes (EC50 = 11 nM, max. stimulation approximately 16%). Both CB-25 and CB-52 showed no activity in all assays of CB2-coupled functional activity and antagonized CP55940-induced stimulation of GTP-gamma-S binding to hCB2-CHO cell membranes. In vivo, both compounds, administered i.p., produced dose-dependent nociception in the plantar test carried out in healthy rats, and antagonised the anti-nociceptive effect of i.p. WIN55,212-2. In the formalin test in mice, however, the compounds counteracted both phases of formalin-induced nociception. CONCLUSIONS AND IMPLICATIONS: CB-25 and CB-52 behave in vitro mostly as CB1 partial agonists and CB2 neutral antagonists, whereas their activity in vivo might depend on the tonic activity of cannabinoid receptors.

Action Potentials↗

Periaqueductal grey CB1 cannabinoid and metabotropic glutamate subtype 5 receptors modulate changes in rostral ventromedial medulla neuronal activities induced by subcutaneous formalin in the rat.

This study was undertaken to analyze the involvement of periaqueductal gray (PAG) cannabinoid or group I metabotropic glutamate receptors in the formalin-induced changes on the rostral ventromedial medulla (RVM) ON- and OFF-cells activities. S.c. injection of formalin into the hind paw produced a transient decrease (4-6 min) followed by a longer increase (25-35 min) in tail flick latencies. Formalin also increased basal activity in RVM ON-cells (42+/-7%) and decreased it in OFF-cells (35+/-4%). Intra-PAG microinjection of (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl) pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate (WIN 55,212-2) (2 nmol/rat), a cannabinoid receptor agonist, prevented the formalin-induced changes in RVM cell activities. Higher dosages of WIN 55,212-2 (4-8 nmol/rat) increased the tail flick latencies, delayed the tail flick-related onset to ON-cell burst, and decreased the duration of OFF-cell pause. Furthermore, WIN 55,212-2 at a dosage of 8 nmol/rat decreased RVM ON-cell (57+/-7%) and increased OFF-cell ongoing activities (26+/-4%). These effects were prevented by N-piperidino-5-(4-chlorophenyl)-1-(2,4dichlorophenyl)-4-methyl-3-pyrazolecarboxamide SR141716A, (1 pmol/rat), a CB1 cannabinoid receptor antagonist, or by 2-methyl-6-(phenylethynyl)pyridine (MPEP 20 nmol/rat), a selective mGlu5 glutamate receptor antagonist. T7-(hydroxyimino) cyclopropa[b]chromen-1alpha-carboxylate ethyl ester (CPCOOE/50 nmol/rat) and (S)-(+)-alpha-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385, 20 nmol/rat), selective mGlu1 glutamate receptor antagonists, were ineffective in preventing the WIN-induced effects. This study suggests that s.c. injection of formalin modifies RVM neuronal activities and this effect is prevented by PAG cannabinoid receptor stimulation. Moreover, the physiological stimulation of PAG mGlu5, but not mGlu1 glutamate receptors, seems to be required for the cannabinoid-mediated effect.

Action Potentials↗

[Sclerosing cholangitis as a complication of Langerhans'cell histiocytosis].

INTRODUCTION: Langerhans'cell histiocytosis is a rare and mainly pediatric disease. Patients with hepatic involvement usually have a disseminated form of the disease, with poor prognosis. Sclerosing cholangitis can occur in 10 to 15% of multivisceral Langerhans'cell histiocytosis. We report the case of a 56-years-old patient who developed sclerosing cholangitis 12 years after the diagnosis of Langerhans'cell histiocytosis. EXEGESIS: A 56-years-old man was admitted because of rapid general health impairment with epigastric pain. He was diagnosed as having Langerhans'cell histiocytosis 12 years ago because of a diabetes insipidus. Lungs were involved and during follow-up vertebral osteocondensation also developed. However, Langerhans'cell histiocytosis was clinically silent at the time of admission, without any treatment. Biologically, cholestasis and inflammation were noted. Digestive radiological investigations (echo-endoscopy, CT-scan, MRI) showed homogenous hepatomegaly and a diffuse infiltration of intra and extrahepatic bile ducts. Liver biopsy yielded the diagnosis of sclerosing cholangitis. Clinical and biological improvement occurred with oral corticosteroids (at 12 months after sclerosing cholangitis diagnosis). CONCLUSION: Sclerosing cholangitis is a potential complication of Langerhans'cell histiocytosis, mainly in its multivisceral form. It can occur at a median of 2 years after diagnosis in children, but occasionally much later in adults, whereas Langerhans'cell histiocytosis seems quiescent. Diagnosis is supported by radiological investigations and liver biopsy. As no drug therapy appears clearly effective, liver transplantation must frequently be considered in these patients.

Abdominal Pain↗

Effects of docosahexaenoic acid on [Ca(2+)](i) increase induced by doxorubicin in ventricular rat cardiomyocytes.

The clinical use of doxorubicin (DXR) is limited by cardiotoxicity partially due to interference with intracellular Ca(2+) homeostasis and involving the activation of the sarcoplasmic reticulum (SR) Ca(2+) release channels. It is known that docosahexaenoic acid (DHA) is able to potentiate the sensitivity of cancer cells to DXR. The aim of our study was to further evaluate the effects of DHA on [Ca(2+)](i) overload induced by DXR in adult rat ventricular cardiomyocytes in order to verify if DHA interferes with DXR-induced cardiotoxicity too. [Ca(2+)](i) was measured by microfluorimetry. Our data demonstrated that 100 microM DXR induced a statistically significant [Ca(2+)](i)-increase in cardiomyocytes perfused with CaCl(2) Krebs solution (from 135.7 +/- 15 nM to 560.2 +/- 49 nM, n = 9, p < 0.01) and with Ca(2+)-free Krebs solution (from 89.3 +/- 15 nM to 551.1 +/- 35 nM, n = 9, p < 0.01). Treatment with 10 microM DHA for 20 min significantly suppressed DXR [Ca(2+)](i)- increase in cells perfused with CaCl(2) Krebs solution (142.3 +/- 12 nM, n = 9, p < 0.01) and in Ca(2+)-free procedures (100.4 +/- 12 nM, n = 9, p < 0.01). Caffeine 10 mM significantly increased [Ca(2+)](i) in cardiomyocytes perfused with CaCl(2) Krebs solution (from 135.7 +/- 15 nM to 979.2 +/- 17.8 nM, n = 9, p < 0.01) and with Ca(2+)-free Krebs solution (from 89.3 +/- 15 nM to 891.1 +/- 30 nM, n = 9, p < 0.01). Treatment with 10 microM DHA for 20 min suppressed caffeine [Ca(2+)](i)-increase in cardiomyocytes perfused with CaCl(2) Krebs solution (174.2 +/- 28 nM, n = 9, p < 0.01) and in Ca(2+)-free procedures (161.9 +/- 34 nM, n = 9, p < 0.01). In conclusion, our results suggest that DHA is able to prevent acute modifications of calcium homeostasis induced by DXR probably interfering with SR Ca(2+) release channels.

Animals↗

Type I and II metabotropic glutamate receptors modulate periaqueductal grey glycine release: interaction between mGlu2/3 and A1 adenosine receptors.

In this study we investigated the effects of type I and II mGlu receptors ligands in glycine extracellular concentrations at the periaqueductal gray (PAG) level by using in vivo microdialysis, in conscious rats. An agonist of type I mGlu receptors, (S)-3,5-DHPG (1 and 5 mM), but not a selective agonist for mGlu5 receptors, CHPG (3 and 5 mM), was noticed to increase the dialysate glycine levels in a concentration-dependent manner (60+/-15% and 136+/-13%, respectively). CPCCOEt (1mM), a selective mGlu1 receptor antagonist, perfused in combination with (S)-3,5-DHPG, counteracted the effect induced by (S)-3,5-DHPG, but did not change per se the extracellular PAG glycine values, even at the highest dosage used (2 mM). MPEP (1 and 2 mM), a selective antagonist of mGlu5 receptor, did not modify extracellular glycine level. An agonist of type II mGlu receptors, 2R,4R-APDC (25 and 50 microM), decreased the dialysate glycine in a concentration-dependent manner (-26+/-4% and -54+/-6%, respectively). The 2R,4R-APDC-induced decrease in extracellular glycine was prevented by EGlu (0.5 mM), a selective type II mGlu receptors antagonist. EGlu (0.5 and 1 mM), per se, led to a significant decrease (-56+/-7% and -57+/-2%, respectively) in extracellular PAG glycine too. This effect was prevented by DPCPX (100 microM), a selective antagonist for A1 adenosine receptors, but was not affected by CPA (1 mM), a selective A1 adenosine receptors agonist. Intra-PAG perfusion of CPA (0.1-1 mM) decreased the extracellular PAG glycine values (-47+/-13%) with 1 mM concentration. The CPA-induced effect was prevented by DPCPX (100 microM), and resulted to be additive with the 2R,4R-APDC-induced decrease in glycine values. DPCPX (1 mM) increased per se extracellular glycine (48+/-7%) at the highest dose used. Dipyridamole (100 microM), an inhibitor of both adenosine reuptake and phosphodiesterases, decreased extracellular glycine (-28+/-7%). Extracellular concentrations of glutamine never changed throughout this study. These data show opposing effects of type I and II mGlu receptors in the regulation of PAG glycine values. Moreover, functional interaction between type II mGlu and adenosine A1 receptors, which possibly operate through a common transductional pathway, may be relevant in the physiological control of glycine release in awake, freely moving rats at the periaqueductal gray matter.

Animals↗

Oculomotor palsy in six patients with systemic lupus erythematosus. A possible role of antiphospholipid syndrome.

The objective of this study was to describe clinical, laboratory, and radiological features in systemic lupus erythematosus (SLE) patients with oculomotor palsy (OMP). Among a cohort of 750 SLE patients receiving follow-up at our unit between 1985 and 2000, all patients with OMP were studied. Clinical and laboratory data were recorded, as well as cerebral magnetic resonance imaging (MRI) findings where available. Immunological tests included tests for presence and specificity of antinuclear and antiphospholipid antibodies. Six patients had OMP, which occurred within the first 3 years in two patients and after more than 20 years in two patients. Four patients had focal neuropsychiatric SLE (NPSLE) manifestations and two had diffuse neurological involvement. The four patients with focal NPSLE were either anticardiolipin- or lupus anticoagulant-positive. Cerebral fluid was abnormal in two of four patients who had this test. In four of the six patients, cerebral MRI showed evidence of vasculopathy. The therapeutic regimens varied, although all six patients initially received high-dose corticosteroids. OMP resolved or improved significantly in all six patients. OMP in SLE occurs in a broad spectrum of clinical situations but is an infrequent manifestation of NPSLE. This case series, together with literature review data, suggests various pathophysiological mechanisms in patients with focal or diffuse neurological symptoms. In patients with focal NPSLE, a possible cause of OMP is microthrombosis associated with presence of antiphospholipid antibodies.

Adult↗

Interaction between metabotropic and NMDA glutamate receptors in the periaqueductal grey pain modulatory system.

The formalin test was used to investigate the interactive role of periaqueductal grey (PAG) N-methyl-D-aspartate (NMDA) and metabotropic glutamate (mGlu) receptors in the modulation of persistent noxious stimulation in mice. Intra-PAG microinjections of 1 or 3 nmol NMDA, a selective agonist at NMDA-subtype receptors, decreased the nociceptive response (-94+/-5% with 3 nmol) during the latter phase of the test. This effect was antagonized by MK-801, a selective antagonist at NMDA receptors. No change in the early nociceptive phase was observed after NMDA injection. Pretreatment either with 2-methyl-6-phenylethynylpyridine (MPEP, 25 nmol/mouse), a selective antagonist at mGlu5 receptors, or with (2S)-alpha-ethylglutamic acid [(2S)-alpha-EGlu, 30 nmol/mouse], a selective antagonist at group-II mGluRs, prevented the NMDA-induced antinociceptive effect during the late hyperalgesic phase. Pretreatment with (R,S)-alpha-methylserine-O-phosphate [(R,S)-alpha-MSOP, 70 nmol/mouse], a selective antagonist at group-III mGlu receptors, had no effect on the NMDA-induced antinociception. None of the antagonists changed the formalin-induced nociceptive behaviour per se with the dosages used in combination with NMDA. MPEP at 50 nmol/mouse, however, potentiated the early nociceptive phase whilst 100 nmol/mouse attenuated the late phase. Similarly, at the higher dose of 140 nmol/mouse, (R,S)-alpha-MSOP decreased the late hyperalgesic phase. These results provide additional evidence that NMDA and mGlu receptors participate in modulating the hyperalgesia induced by peripheral noxious stimulation. In particular, mGlu receptors may modulate the NMDA receptors in the PAG since their physiological stimulation seems to be required for the NMDA-induced effect. This suggests that, together with ionotropic glutamate receptors, mGlu receptors also play a role in modulating a type of spinal cord neuroplasticity (i.e. wind-up) that has been proposed to mediate hyperalgesia.

Animals↗

Metabotropic and NMDA glutamate receptors participate in the cannabinoid-induced antinociception.

The purpose of this study was to evaluate the possible contribution of metabotropic glutamate receptors (mGluRs) to cannabinoid-induced antinociception in the periaqueductal grey (PAG) matter of rats. Intra-PAG microinjection of WIN 55,212-2, a cannabinoid receptor agonist, increased the latency of the nociceptive reaction (NR) in a dose-dependent fashion in the plantar test. This effect was prevented by pretreatment with SR141716A, a selective antagonist of CB1 receptors. When injected alone, SR141716A produced, with the highest dosage used, a significant reduction in the latency of the NR. CPCCOEt, a selective mGlu1 receptor antagonist, was unable to prevent the analgesia produced by WIN 55,212-2. On the contrary, MPEP, a selective mGlu5 receptor antagonist, completely antagonized the effect of WIN 55,212-2. However, the analgesia induced by CHPG, a selective mGlu5 receptor agonist, was blocked by MPEP but not by SR141716A. When injected alone, CPCOOEt produced no effect, whereas MPEP produced, with the highest dosage used, a significant reduction in the latency of the NR. These data emphasize that mGlu5 receptors, but not mGluR1, may modulate nociception in the PAG. Similarly, a pretreatment with either 2-(S)-alpha-EGlu or (RS)-alpha-MSOP, selective antagonists for group II and III mGluRs, respectively, prevented the WIN 55,212-2-induced analgesia. When the higher dosage of (RS)-alpha-MSOP was used a decrease in the latency of the NR was observed. This was not the case for 2-(S)-alpha-EGlu. Pretreatment with DL-AP5, a selective antagonist of N-methyl-D-aspartate (NMDA) receptors, blocked the effect of WIN 55,212-2, and by increasing the dosage strongly reduced per se the latency of the NR. This study suggests that endogenous glutamate could tonically modulate nociception through mGlu and NMDA receptors in the PAG matter. In particular, the physiological stimulation of these receptors seems to be required for the cannabinoid-induced analgesia in this midbrain area.

Analgesics↗

Coexisting pseudo-xanthoma elasticum and rheumatoid arthritis. three cases and review of the literature.

Pseudo-xanthoma elasticum (PXE) is an inherited disorder of the connective tissue characterized by cutaneous, ocular and vascular lesions. Coexisting PXE and rheumatoid arthritis (RA) is rare because three cases have only been described. We report three new cases of this association. Analysis of these six cases failed to show any particular biological or clinical features of rheumatoid arthritis associated PXE. The possible association of PXE and RA is discussed.

Adult↗

Anti-oxidized low-density-lipoprotein (OxLDL) antibodies in systemic lupus erythematosus with and without antiphospholipid syndrome.

The aim of this study was to examine potential links between antiOxLDL antibodies and the clinical and biological features of secondary antiphospholipid syndrome (II APLS) associated with systemic lupus erythematosus (SLE). A cohort study was done of 98 SLE patients followed-up for 1 y, including 18 with definite II APLS and 13 patients with definite primary APLS (I APLS). IgG anticardiolipin, IgG anti beta2 GPI, lupus anticoagulant, VDRL and IgG antiOxLDL were measured in all 98 study subjects. High antiOxLDL titers were found in seven (39%) of the 18 patients with II APLS vs 10 (12.5%) of the 80 patients without APLS (P < 0.01; OR = 4.45; 95% CI = 1.4-14.1) and none of the 13 patients with I APLS (P < 0.02). The mean antiOxLDL titer was not significantly higher in the SLE patients with than without II APLS (P > 0.05). A high antiOxLDL titer was correlated with deep venous thrombosis (P < 0.01; OR = 5.77; 95% CI = 0.54-61) but not with arterial thrombosis (P > 0.05; OR = 1; 95% CI = 0.29-3.09), thrombocytopenia, central nervous system involvement, livedo reticularis, or a positive Coombs test. The antiOxLDL antibody titer was correlated with the IgG anticardiolipin antibody titer (r = 0.235; P = 0.02) and with the IgG anti-beta2 GPI antibody titer (r = 0.224; P = 0.026). AntiOxLDL elevation was found in 17% of SLE patients and was significantly associated with II APLS and venous thrombosis. We found no evidence suggesting that antiOxLDL may be associated with atherosclerosis.

Adolescent↗

Somatostatin receptor scintigraphy and gallium scintigraphy in patients with sarcoidosis.

UNLABELLED: Somatostatin receptor scintigraphy (SRS) has been shown to reveal sarcoidosis sites. The aim of this study was to prospectively compare SRS and gallium scintigraphy in the evaluation of pulmonary and extrapulmonary involvement in patients with proven sarcoidosis. METHODS: Eighteen patients with biopsy-proven sarcoidosis were included. Nine were or recently had been receiving steroid therapy at the time of the examination. Planar gallium scintigraphy (head, chest, abdomen, and pelvis) and thoracic SPECT were performed at 48-72 h after injection of a mean dose of 138 +/- 21 MBq 67Ga. Planar SRS and thoracic SPECT were performed at 4 and 24 h after injection of a mean dose of 148 +/- 17 MBq 111n-pentetreotide. RESULTS: Gallium scintigraphy found abnormalities in 16 of 18 patients (89%) and detected 64 of 99 clinically involved sites (65%). SRS found abnormalities in 18 of 18 patients and detected 82 of 99 clinically involved sites (83%). Of the 9 treated patients, gallium scintigraphy found abnormalities in 7 (78%), detecting 23 of 39 clinically involved sites (59%), whereas SRS found abnormalities in 9, detecting 32 of 39 clinically involved sites (82%). CONCLUSION: This study suggests that, compared with gallium scintigraphy, SRS appears to be accurate and contributes to a better evaluation of organ involvement in sarcoidosis patients, especially those treated with corticosteroids.

Adrenal Cortex Hormones↗

Periaqueductal gray matter metabotropic glutamate receptors modulate formalin-induced nociception.

The role played by periaqueductal gray (PAG) matter metabotropic glutamate receptors (mGluRs) in the modulation of persistent noxious stimulation was investigated in mice. The formalin test was used as a model of persistent pain. Intra-PAG microinjections of (S)-3, 5-DHPG (25 and 50 nmol/mouse) and L-CCG-I (30 and 60 nmol/mouse), agonists of group I and group II mGluRs, respectively, decreased the nociceptive response (-92+/-6% and -89+/-8%, respectively) during the late phase. No change of the early nociceptive phase was observed after (S)-3,5-DHPG or L-CCG-I treatments. These effects were antagonized by a pretreatment with CPCCOEt (40 nmol/mouse) and (2S)-alpha-EGlu (30 nmol/mouse). CPCCOEt is a selective antagonist of group I mGlu receptors, while (2S)-alpha-EGlu is an antagonist of group II. Intra-PAG microinjections of L-SOP (60 and 120 nmol/mouse), a selective agonist of group III mGluRs, induced an increase of the nociceptive response (+95+/-7%) during the late hyperalgesic phase. (R,S)-alpha-M-SOP (70 nmol/mouse), a selective antagonist of group III mGluRs, completely antagonized the L-SOP-induced effect. These results show that PAG mGluRs participate in modulating the late hyperalgesic behaviours induced by formalin. It seems, therefore, possible that group I and group II mGluRs positively modulate PAG antinociceptive descending pathway following a persistent noxious stimulation, while group III mGluRs modulate it negatively.

Animals↗

Effects of persistent nociception on periaqueductal gray glycine release.

Glycine is a candidate nociception inhibitory transmitter in specific brain regions, like for example the spinal cord, the thalamic nuclei and the periaqueductal gray matter. However, quantitative changes in glycine released in these brain regions during peripheral inflammation episodes have not been characterized in awake animals. To address this issue, an in vivo microdialysis study was carried out in freely moving rats in order to analyse periaqueductal gray matter extracellular glycine concentration following unilateral formalin injection into the dorsal skin of the right hind-paw. The extracellular concentration of glutamine was also evaluated in order to analyse whether or not a non-neurotransmitter amino acid was equally modified. Intra-periaqueductal gray matter tetrodotoxin perfusion reduced extracellular glycine concentration (-44+/-5%), but did not change the glutamine dialysate values. Peripheral injection of formalin reduced the glycine release during the early phase (-62+/-8%) and the late phase (-36+/-6%) of hyperalgesia, although not during the analgesic period. Perfusion with naloxone (300microM) neither prevented the formalin-induced decreases in extacellular glycine concentration, nor modified the perfusate basal values of glycine and glutamine. These results show that, contrary to what has been recognized on the interactive role of opioids and GABA into the periaqueductal gray matter (i.e. opioid disinhibition), endogenous opioids seem not to modulate the activity of glycinergic neurons in the same midbrain area. In the light of these preliminary data, it is reasonable to suppose that GABA and glycine are probably not co-released at the level of periaqueductal gray matter of the rat.

Animals↗

The family history of patients with primary or secondary antiphospholipid syndrome (APS).

OBJECTIVE: To evaluate familial history for evidence of antiphospholipid syndrome (APS) and autoimmune disease in rheumatology department patients with primary or secondary APS. METHODS: We retrospectively studied patients with APS and systemic lupus erythematosus (SLE) managed at the Rheumatology Department of the Bichat University Hospital, Paris, between 1987 and 1996. Data were collected by chart review and by a 1997 standardized telephone interview. RESULTS: We identified 108 patients with APS managed during the ten-year study period. According to classical classification criteria, 39 patients had primary antiphospholipid syndrome (PAPS) and 69 secondary antiphospholipid syndrome (SAPS). Family history data were obtained for 29 (74%) and 55 (80%) PAPS and SAPS patients. respectively (78% of the 108 patients). Twelve PAPS (41% and 19 SAPS (35%) patients had one or more relatives with evidence of at least one clinical feature of APS such as thrombosis or recurrent fetal loss; of these patients, seven in the PAPS (24%) and 11 in the SAPS (20%) group had two or more relatives with evidence of a clinical feature of APS. Three PAPS (10%) and 14 SAPS (25%) patients had one or more family members with an autoimmune disease. CONCLUSION: A positive family history for autoimmune disease and/or antiphospholipid syndrome is common in patients with PAPS or SAPS. This finding supports a genetic contribution to APS. The percentage of a positive family history for autoimmune disease tend to be higher in patients with SAPS than in those with PAPS.

Abortion, Habitual↗

IgG anti-beta2-glycoprotein I antibodies in adult patients with systemic lupus erythematosus: prevalence and diagnostic value for the antiphospholipid syndrome.

OBJECTIVE: To investigate the prevalence of serum anti-beta2-glycoprotein I (anti-beta2-GPI) antibodies and other antiphospholipid antibodies (aPL) in patients with systemic lupus erythematosus (SLE). To study their diagnostic value for the antiphospholipid syndrome (APS). METHODS: Anti-beta2-GPI and IgG anticardiolipin (aCL) were determined in sera from 102 consecutive patients with SLE using ELISA. Serum and plasma tests were also done for lupus anticoagulant (LAC), syphilis, and antibodies to dsDNA. Clinical and laboratory features of APS were observed. RESULTS: Prevalences were 23.5% for aCL and 18.6% for anti-beta2-GPI. Correlations between the presence of aCL and anti-beta2-GPI and between their titers were statistically significant (p<0.0001). No associations were found between anti-beta2-GPI and disease activity criteria (SLEDAI, ECLAM, dsDNA). Anti-beta2-GPI were significantly associated with LAC (p = 0.005), APS (p = 0.005), and a high aCL titer (aCL > 5 SD; p< or =0.001). LAC was the best diagnostic criterion for APS. CONCLUSION: These data suggest that determination of anti-beta2-GPI in addition to aCL and LAC is unlikely to improve the diagnosis of APS in patients with SLE.

Adolescent↗

[Outcome of pregnancies in lupus: experience at one center].

We determined the outcome of all pregnancies in SLE patients in our lupus cohort between 1991 and 1997. The women were advised that pregnancy was acceptable if the disease had been inactive for 6 months (SLEDAI < or = (4 at 2 serial examinations) and daily prednisone dose was below 10 mg. Patients were advised against pregnancy in case of active nephritis or neurolupus. In case of antiphospholipid antibodies, patients were treated with aspirin or heparin if previous fetal losses were documented. In case of anti-SSA ab, patients were monitored with ultrasound and given dexamethasone in case of atrioventricular block. Fifty-nine pregnancies were registered among 31 women: mean age at diagnosis of SLE was 25.3 +/- 3.7 years (range: 17-31); mean disease duration before pregnancy 4.4 +/- 3 years (0-14); mean ACR score 5.4 +/- 1.5 (4-9). Seven patients had ACL ab, 8 had anti-SSA ab. Pregnancies ended in: 13 early spontaneous abortions (9 not related to disease flare up, 4 related to SAPL); 7 elective abortions (patient decision in 5 cases, severe lupus flare up in 2); one in utero death; 19 full term births (> 38 weeks); and 19 preterm births. Cesarean section was performed in 11 cases (6 for fetal distress, dystocia and previous ceasarian; 5 for active lupus). Severe sepsis occurred in one premature infant who died at the age of 1 week. Intrauterine growth retardation was observed in 11 cases, mean APGAR score was 8.9 +/- 1.43. Child development was normal in all cases except one child with mild mental retardation. Severe lupus flare ups occurred in 6 cases, of which 4 were pregnancies in unadvised situations. Six mild flare ups were documented in the post partum. One fatal case of neonatal lupus with AVB was observed. In conclusion, in our experience, the live birth rate is similar to the general population and the risk of lupus flare up is low when the above mentioned criteria are applied. Systematic increase of steroid dose at pregnancy onset does not seem to be necessary. The high rate of prematurity remains a problem to be solved.

Adult↗

SAPHO syndrome: a long-term follow-up study of 120 cases.

OBJECTIVE: To assess the long-term outcome of the synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome. METHODS: All patients with the SAPHO syndrome seen at our unit between 1974 and 1997 were identified. Follow-up was prospective from 1992 to 1997. Data before 1992 were analyzed retrospectively. Clinical symptoms, treatments and biological data, including erythrocyte sedimentation rate and C-reactive protein, were recorded at least yearly. When available, radiological data, HLA B27 status, and findings from bone or skin biopsy specimens were recorded. For each drug, an efficacy index (El) was determined as follows: "0" for less than 30% improvement, as judged by the patient, on horizontal visual analog scale, "0.5" for partial efficacy, and "1" for more than 60% improvement. RESULTS: We identified 120 patients with the SAPHO syndrome (50 men, 70 women), of whom 102 patients were followed-up prospectively after 1992; 3 of these 102 patients were lost to follow-up. Six patients also had Crohn's disease, and three had ulcerative colitis. Except for a significant association of palmoplantar pustulosis (PPP) or psoriasis vulgaris (PV) with axial osteitis (P = .007), the dermatologic presentation had no significant influence on rheumatic symptoms (ie, osteitis or arthritis, peripheral or axial). The HLA B27 antigen was not significantly associated with a particular pattern of distribution of arthritis or osteitis. No severe or disabling complications were noted. In the 47 patients followed-up for more than 5 years (mean, 9.5; range, 5 to 23), the mean number of osteitis or arthritis foci increased during follow-up from 1.57 to 1.91 and from 2.68 to 3.11, respectively. Nonsteroidal antiinflammatory drugs (NSAIDs) were prescribed in 113 of 120 (94%) patients, with a mean El of 0.67 (+/-0.39). Corticosteroid (CS) therapy was used in 23 patients, with a mean El of 0.67 (+/-0.42). Colchicine and sulfasalazine had a mean El of 0.36 (+/-0.44) and 0.16 (+/-0.30), in 28 and 18 patients, respectively. Methotrexate was given to 10 patients (6 with peripheral arthritis), with a mean El of 0.64 (+/-0.48). Doxycyclin (100 mg twice daily) was used in 20 patients, usually to treat osteitis, with a mean El of 0.26 (+/-0.42). Intraarticular injections of a CS or osmic acid were used in 27 patients, with a mean El of 0.77 (+/-0.35). CONCLUSIONS: SAPHO syndrome is a relevant and stable entity, with a good long-term prognosis. NSAIDs and intraarticular injections (CS or osmic acid) most often alleviate rheumatic symptoms, but prednisone or methotrexate are sometimes necessary and appear globally helpful.

Acquired Hyperostosis Syndrome↗