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Biomedical subjects

J Michael

Publications and source records attributed to J Michael.

At least 37 records · Page 2Linked to original sources
PubMed1998

The effect of depression on return to drinking: a prospective study.

BACKGROUND: The effect of depression on return to drinking among individuals with alcohol dependence is controversial. From February 1, 1993, to April 15, 1996, we consecutively recruited 40 women and 61 men hospitalized for alcohol dependence and followed them up monthly for 1 year to assess the effect of depression on drinking outcomes. METHODS: We conducted structured interviews during hospitalization and monthly following discharge for 1 year to determine whether depression at treatment entry affected the likelihood of return to drinking and whether this effect differed between sexes. Using survival analysis, we examined the effect of depressive symptoms and a diagnosis of current major depression at treatment entry on times to first drink and relapse during follow-up. RESULTS: A diagnosis of current major depression at the time of hospitalization was associated with shorter times to first drink (hazard ratio, 2.03; 95% confidence interval [CI], 1.28-3.21; P=.003) and relapse (hazard ratio, 2.12; 95% CI, 1.32-3.39; P=.002). There was no significant difference between women and men in this effect. Depressive symptoms as measured by the Beck Depression Inventory did not predict time to first drink or relapse in women or men. CONCLUSIONS: A diagnosis of current major depression at entry into inpatient treatment for alcohol dependence predicted shorter times to first drink and relapse in women and men. Our results differ from earlier reports that men and women differ in the effect of depression on return to drinking.

Adult↗
PubMed1998

Nicardipine for hypertensive emergencies in children with renal disease.

Hypertensive emergencies secondary to renal diseases were treated with nicardipine in three children. Nicardipine is the first intravenously administered dihydropyridine calcium channel blocker. Its physiological actions include vasodilation, with limited effects on the chronotropic and inotropic function of the myocardium. Nicardipine, starting at 5 microg/kg per min and then continued at a maintenance infusion of 1-3 microg/kg per min, effectively controlled the mean arterial pressure in the three patients. Apart from occasional superficial thrombophlebitis in a fourth patient, no adverse effects were noted.

Adolescent↗
PubMed1997

Modulation of chloride secretion in the rat ileum by intracellular bicarbonate.

Increasing intracellular bicarbonate concentration ([HCO3-]i) inhibits calcium-mediated Cl- secretion in rat distal colon and T84 cells. We investigated the effect of [HCO3-]i on Cl- secretion in rat ileum. Segments of intact ileum from Sprague-Dawley rats were studied in Ussing chambers and villus and crypt intracellular pH and [HCO3-]i were determined using BCECF. A range of crypt and villus [HCO3-]i from 0 to 31 mM was obtained by varying Ringer's composition. Basal serosal-to-mucosal Cl- flux (JsmCl) averaged 8.5 +/- 0.2 mu eq.h-1.cm-2 and was unaffected by changing [HCO3-]i or serosal bumetanide. Carbachol increased JsmCl by 3.9 +/- 0.5 mu eq.h-1.cm-2 at [HCO3-]i = 0 mM but only by 1.0 +/- 0.3 mu eq.h-1.cm-2 at high crypt and villus [HCO3-]i. Dibutyryl-cAMP increased JsmCl by 2.5 +/- 0.2 mu eq.h-1.cm-2 at all [HCO3-]i. Carbachol and db-cAMP showed mutual antagonism at low [HCO3-]i and near-additivity at high [HCO3-]i. We conclude that like rat colon and T84 cells, calcium-mediated but not cAMP-mediated Cl- secretion in the ileum is inhibited by increasing [HCO3-]i. Mutual antagonism between carbachol and db-cAMP at low [HCO3-]i was present in ileum and distal colon but not in T84 cells.

Animals↗
PubMed1997

Association of vasculitic glomerulonephritis with membranous nephropathy: a report of 10 cases.

BACKGROUND: The concomitant occurrence of a vasculitic glomerulonephritis and membranous nephropathy in the same patient is unusual. We report data on 10 patients with this unusual combination. METHODS: Ten patients (nine males/one female; median age 63.5 years, range 30-70 years) presented between 1981 and 1995 with: acute renal failure (n = 3), nephrotic syndrome (n = 4), non-nephrotic range proteinuria and renal insufficiency (n = 3). The median serum creatinine at presentation was 296 mumol/l (range 65-1749 mumol/l). One patient had a vasculitic transformation from membranous nephropathy 5 years after the original presentation, coincident with an acute deterioration of renal function requiring dialysis; in all other patients the two glomerular disorders were seen together at presentation. Treatment was with oral prednisolone and cyclophosphamide (eight patients), of whom one also had plasma exchange; and oral prednisolone and azathioprine (one patient). Specific immunosuppressive treatment was withheld in one patient with histological evidence of chronic renal damage. Sera from four patients out of nine tested were positive for ANCA. RESULTS: After a median follow-up of 3.5 years (range 2 months-10 years), renal function had improved in three patients and remained stable in two. Two patients required renal replacement therapy. Three patients had died: one was ANCA-negative and died of a systemic vasculitis, and the other two died of sepsis. CONCLUSION: Membranous nephropathy complicated by a vasculitic glomerulonephritis: (1) has a more aggressive clinical course than membranous nephropathy alone, (2) appears to have an association with ANCA, (3) should be considered in those patients with an accelerated decline in renal function, and (4) may respond to treatment with immunosuppressive drugs.

Adult↗
PubMed1997

Focal segmental necrotizing glomerulonephritis in rheumatoid arthritis.

We report ten patients with rheumatoid arthritis (RA) who developed a focal segmental necrotizing glomerulonephritis (FSNGN) and extracapillary proliferation typical of vasculitic glomerulonephritis. Five patients also had extrarenal vasculitis. Renal presentation was with renal impairment (n = 9) (median creatinine 726 mumol/l, range 230-1592 mumol/l), microscopic haematuria (n = 8) and proteinuria (n = 10). Nine patients were seropositive for rheumatoid factor and nine had bone erosions. Serum from four of five patients tested by indirect immunofluorescence was positive for antineutrophil cytoplasmic antibody (ANCA) with perinuclear staining. Only three patients had penicillamine or gold therapy. Treatment was with prednisolone and cyclophosphamide (six patients, two of whom were also plasma-exchanged), prednisolone and azathioprine (two patients) and prednisolone alone (two patients). There was a marked improvement in renal function in eight patients. Two patients with dialysis-dependent renal failure recovered renal function, although in one patient this was transient and she required further dialysis 4 months later. Two other patients progressed to dialysis at 3 months and 1 year respectively. Four patients died, one remains dialysis-dependent, and four continue to have good renal function at 5 year follow-up (median creatinine 148.5 mumol/l, range 120-193 mumol/l). One patient was lost to follow-up at 5 years. FSNGN should be considered in all patients with RA and renal impairment, proteinuria and/or microscopic haematuria. This diagnosis appears to be more likely in patients with clinical extrarenal vasculitis, bone erosions or who are seropositive. In these cases, an urgent renal biopsy is indicated.

Adult↗
PubMed1997

Controlled trial of pulse versus continuous prednisolone and cyclophosphamide in the treatment of systemic vasculitis.

Although cyclophosphamide and prednisolone are effective in treating systemic vasculitis, the optimum treatment regimes and duration of treatment are unknown. We randomized 54 patients aged 15-70 years (median 57.5 years) with systemic vasculitis (classical polyarteritis n = 8, microscopic polyarteritis n = 17, Wegener's granulomatosis n = 29) to treatment with either pulse cyclophosphamide and prednisolone (PCYP) (n = 24) or continuous oral and prednisolone and cyclophosphamide, with the latter followed after a median of 3 months (range 1.5-10 months) by azathioprine (CCAZP) (n = 30). Patients on CCAZP were more likely to develop leucopenia (13/30) than patients on PCYP, (7/24) although the difference was not significant. The numbers of infective episodes during follow up were comparable in the two groups at 1.7/patient for PCYP and 1.66/patient for CCAZP. Overall, 26/30 patients (87%) treated with CCAZP developed treatment-related toxicity, as did 17/24 patients (71%) treated with PCYP. After a median follow-up of 40.4 months (range 0.7-64.8), there was no difference in the frequency of deaths (PCYP 5, CCAZP 4), relapses (PCCYP 7, CCAZP 8), treatment failures (PCYP 4, CCAZP 4), improvement in disease activity scores or renal function. Survival at three years was 77% in patients treated with PCYP, and 90% in patients on CCAZP (p = 0.38). There was a tendency towards increased toxicity in patients treated with the continuous regimen.

Adolescent↗
PubMed1997

Spatial analysis of the distribution of LaCrosse encephalitis in Illinois, using a geographic information system and local and global spatial statistics.

The spatial and temporal distribution of LaCrosse encephalitis cases in Illinois was analyzed using a geographic information system (GIS) and spatial statistics. Case data were obtained from the Illinois Department of Public Health and mapped on the county, town, and address level. Human cases were concentrated in and around the city of Peoria in central Illinois. Local spatial statistics were used to identify hot spots where cases appear to be concentrated in the Peoria region. Several small towns surrounding the city of Peoria appeared as foci where cases were most common. Second-order spatial analysis of the case distribution was conducted on the address level. Cases were clustered within a range of 3.0 km in the city of Peoria. Since most cases appear to be associated with residential (peridomestic) exposure, and since several cases have been reported from neighboring addresses, transmission may be concentrated around specific sites (hardwood ravines, tire piles). The GIS and spatial analysis may be useful in identifying and targeting for intervention potential sites of enzootic transmission.

Adolescent↗
PubMed1996

Glomerular vascular cell adhesion molecule-1 expression in renal vasculitis.

AIMS: To study the expression of cell adhesion molecules in the renal biopsy specimens of patients with systemic vasculitis and Henoch-Schönlein purpura (HSP); to correlate this with the severity of glomerular inflammation. METHODS: Renal biopsy specimens obtained from eight patients with untreated systemic vasculitis (four with Wegener's granulomatosis and four with microscopic polyarteritis), eight with HSP and nine controls (four with normal histopathology and five with thin glomerular basement membrane disease) were stained using the alkaline phosphatase anti-alkaline phosphatase method with monoclonal antibodies directed against intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. RESULTS: Biopsy specimens of normal kidneys expressed ICAM-1 in glomerular endocapillary cells, Bowman's capsule epithelium, interstitial cells and interstitial vascular endothelium, and VCAM-1 in Bowman's capsule epithelium, proximal tubular epithelium and interstitial vascular endothelium. No staining with antibody directed against E-selectin was seen in any of the biopsy specimens. Biopsy specimens of patients with a vasculitic glomerulonephritis (segmental necrotising glomerulonephritis) expressed VCAM-1 in glomerular endocapillary cells (four of eight patients with systemic vasculitis; two of eight patients with HSP). In patients with a systemic vasculitis glomerular VCAM-1 expression was associated with a more severe renal lesoin (44, 50, 60, and 65% of glomeruli involved) than in those not showing glomerular VCAM-1 expression (3, 3, 11, and 39% of glomeruli involved). CONCLUSION: Expression of VCAM-1 by glomerular endocapillary cells in renal biopsy specimens raises the possibility that recruitment of VLA-4 bearing leucocytes may contribute to glomerular injury in Wegener's granulomatosis and microscopic polyarteritis.

Adolescent↗
PubMed1996

Low calcium dialysate and hyperparathyroidism.

A low calcium dialysate reduces hypercalcemia from calcium-containing phosphate binders and makes phosphate control possible without the use of aluminum salts. We asked whether this might, however, lead to hyperparathyroidism. We prospectively studied serum concentrations of parathyroid hormone levels (by an immunoreactive intact molecule assay) in 173 patients on continuous ambulatory peritoneal dialysis (CAPD) who were started on a low calcium dialysate (Ca2+ 1.25 or 1.00 mmol/L) because of hypercalcemia. Median follow-up was 13.2 months (range 1-28). Initial serum parathyroid hormone was [median(range)]: 70(5-1043) ng/L pre low calcium dialysate, and this rose to 130(5-914) ng/L at 0-6 months; 130(5-1030) ng/L at 6-12 months; 170(170-1400) ng/L at 12-18 months; and 130(5-1200) ng/L at 18-24 months (p = 0.0006). Twenty-two patients required a parathyroidectomy because of a sustained rise in parathyroid hormone that was not responsive to alfacalcidol and hypercalcemia. Initial serum parathyroid hormone was significantly higher in these patients at 359 (5-1073) ng/L as compared to a level of 69.5 (6-1147) ng/L in patients who did not have a parathyroidectomy (p = 0.0009). There was a significant sustained fall in mean serum corrected calcium from 2.77 (2.37-3.51) mmol/L to 2.53 (1.39-3.20) mmol/L at three months (p = 0.0006), a nonsignificant rise in mean serum alkaline phosphate from 179 (47-1858) mmol/L to 191 (55-1821) mmol/L (p = 0.15), and a fall in mean serum phosphate levels from 1.87 (0.59-3.18) mmol/L to 1.68 (0.45-3.6) mmol/L (p = 0.76). Our data suggest that the benefits of a low calcium dialysate in CAPD patients are balanced by an increased risk of hyperparathyroidism, and that this risk is higher in patients with an initially high serum parathyroid hormone level.

Adult↗
PubMed1994

Anti-idiotypic activity against anti-myeloperoxidase antibodies in pooled human immunoglobulin.

We investigated the ability of six different pooled human immunoglobulin (PHIG) preparations to inhibit the binding of anti-myeloperoxidase (MPO) antibodies to MPO. All six PHIG preparations inhibited the binding of anti-MPO antibodies from six sera to MPO in a concentration-dependent manner in the concentration range 0.016-10 mg/ml. There was considerable variation in the ability of each PHIG preparation to inhibit the binding of anti-MPO antibody in a given serum. Further differences were seen in the ability of a given PHIG to inhibit anti-MPO binding in different sera. F(ab')2 fragments from two PHIG preparations also inhibited in a concentration-dependent manner anti-MPO binding to MPO in all six sera in the concentration range 0.002-2.65 mg/ml, with a maximum inhibition of 42%. Little inhibition was seen with F(ab')2 of normal human IgG from individual donors (1.8-12.2% at the maximum concentration of 2 mg/ml). F(ab')2 fragments from three anti-MPO containing sera and two affinity-purified anti-MPO antibodies were eluted by affinity chromatography from Sepharose-bound PHIG F(ab')2 and showed anti-MPO antibody activity. We have shown that PHIG and F(ab')2 fragments of PHIG inhibit anti-MPO binding to MPO, and further that F(ab')2 fragments of PHIG bind to F(ab')2 fragments of anti-MPO antibodies. These observations indicate binding between the variable regions of PHIG and the antigen binding site of anti-MPO antibodies, and are consistent with an anti-idiotypic reaction. The variability seen in the inhibitory effect of the different PHIG preparations in anti-MPO-positive sera implies differences in their anti-idiotype content, while the variability of the inhibitory effect of a particular PHIG preparation between different sera suggests heterogeneity in the idiotypic repertoire of anti-MPO antibodies. Such variations in the inhibitory effect of different PHIG preparations on antibody binding may be an important determinant of their therapeutic effect.

Animals↗