Biomedical subjects
Publications and source records attributed to A C Gordon.
A case is reported of absent testis in a boy of 7 months who was noted to have a cystic intra-abdominal mass at 18-19-week prenatal ultrasound scan. This is the second report of prenatally detected testicular torsion, the previous case being noted much later in pregnancy. On both occasions, the diagnosis was only established after birth.
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Static isotope imaging with 99mtechnetium-dimercaptosuccinic acid was performed at a mean age of 34 days in 32 children (50 kidneys) whose vesicoureteral reflux had been identified as a result of prenatal ultrasound scanning. Three patterns of isotope uptake were observed: 1) noninfected primary vesicoureteral reflux (15 children, 24 kidneys), 2) noninfected secondary (obstructed) vesicoureteral reflux (9 patients, 11 kidneys) and 3) infected primary reflux (8 infants, 15 kidneys). In 20 pattern 1 kidneys (83%) renal morphology and differential isotope were normal. In the 4 kidneys (17%) that showed evidence of impaired function this took the form of global parenchymal loss, that is small kidneys rather than focal scarring. In pattern 2 the combination of fetal vesicoureteral reflux and obstruction was a potent cause of renal damage with total or near total loss of function in 7 of 9 refluxing units associated with posterior urethral valves and in 2 kidneys with secondary ureteropelvic junction obstruction. Appearances of focal scarring were confined in pattern 3 and were found in 4 kidneys (27%). This overall incidence of detectable renal damage was lower than expected. Even when infection occurs, prenatal diagnosis may lessen the risk of scarring by enabling treatment to be instituted promptly. The findings suggest that uncomplicated primary vesicoureteral reflux is a relatively benign insult to the fetal kidney and that reflux nephropathy found in children presenting clinically is the result of infected vesicoureteral reflux in postnatal life. Any comparison of published studies will prove difficult until there is a more standardized approach to imaging technique and patient selection.
The Fowler Stephens operation and microvascular procedures were compared for the management of 23 intra-abdominal testes in 15 boys, 7 of whom had the prune belly syndrome. The Fowler Stephens operation was used for 15 testes (4 single-stage and 11 two-stage) and microvascular transfer was used for 8 testes. Eleven testes treated by the Fowler Stephens procedure (73%) and 7 treated by microvascular procedures (88%) were viable and intrascrotal after an average follow-up of 3.0 years, giving an overall success rate of 78%. Eight of 9 post-pubertal testes were biopsied. Severe maturational arrest was evident in all and carcinoma in situ was present in one.
We report follow-up data (minimum of 1 year) on 63 kidneys with antenatally detected pelviureteric junction obstruction, as defined by renographic criteria. The condition was bilateral in 10 patients (i.e. 20 kidneys), 2 patients had unilateral obstruction with contralateral multicystic dysplastic kidneys, and 41 patients had unilateral obstruction with a normal contralateral kidney. In the latter group, 29 (71%) had good function (greater than 40%) at initial assessment. Of the 63 kidneys, 24 (38%) were operated upon following initial assessment, mainly for impaired function. Of 39 patients, initially managed non-operatively, 8 (21%) were operated upon subsequently: 3 for deteriorating function (2 of whom have been reassessed and both have regained their lost function) and 5 for other renographic or ultrasonic indications). Of the original 63 kidneys, 31 (49%) continue to be managed non-operatively; 16 of these (52%) show improving ultrasound appearances, 8 of 17 studied show improved drainage, and all unilateral cases have stable good function. It is concluded that non-operative management of selected cases of antenatally detected pelviureteric junction obstruction is safe.
This report analyses the characteristics and outcome of 25 infants with vesicoureteric reflux detected prenatally on the basis of dilatation of the fetal urinary tract. Sixteen infants had bilateral reflux--a total of 41 refluxing units. The high proportion of males (84%) contrasts with clinically presenting reflux, which is dominated by females. Prenatally diagnosed reflux is generally of a higher grade--usually grade IV. Eight children (32%) had coexistent congenital abnormalities. Chemoprophylaxis was completely effective in 17 children (68%), who remained infection-free; 3 children (12%) had a single urinary infection and were managed conservatively whilst 5 (20%) experienced 2 or more infections and required reimplantation or vesicostomy. Spontaneous cessation of reflux was observed in 6 (35%) of 17 refluxing ureters reassessed after a mean interval of 2.1 years. The significance of isotope findings was sometimes difficult to assess but results in 30 refluxing units support the concept that focal renal scarring is usually a consequence of infected reflux in postnatal life.
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The daily plasma progesterone (P) concentrations achieved during insertion of P (750 mg) sponges into two groups of ewes were examined. Group I received prostaglandin (PG) treatment, which was required to suppress the P production (to levels of < 0.3 ng hormone/ml plasma) from the corpora lutea (CL) of a previous superovulation treatment, following which these Group I ewes and the anestrous Group II ewes were sponge treated. Radioimmunoassay (RIA) and enzymeimmunoassay (EIA) were used to measure the P levels in both groups. Progesterone (750 mg) sponges with and without citric acid impregnation were inserted into all the ewes for 12 days (d). Citric acid lowered the P levels reaching the plasma from the sponges, but it did not mask the characteristic profile (during the treatments) determined by the states of the ewes (single PG and double PG injected, Group I or in the anestrous Group II). The plasma P levels in Group I and II ewes rose to at least 7.0 ng/ml at intervals during treatment. The duration and magnitude of the P concentrations in the plasma were higher in the single PG compared with the double PG ewes during sponge insertion in Group I. The anestrous Group II ewes showed two major peaks (Day 1, P<0.01 and Days 11 to 12, P<0.05) during sponge treatment. A P level > 2.0 ng/ml was maintained over the entire treatment in the single PG and in the anestrous hormone-treated ewes, and was of shorter duration (7 d) in the double PG-treated animals. These endogenous patterns in P profiles of the ewes indicate that the hormone level during sponge insertion varies in magnitude and duration, parameters determined by the physiological/endocrinological state of the ewes at the start of the treatment. The EIA correlated significantly (P<0.001) with the RIA for the measurement of P concentration, when analyzed daily on an individual animal basis.
We analyzed 25 cases of multicystic kidney to assess the impact of prenatal diagnosis on the management of this condition. The incidence of unilateral multicystic kidney was 1 in 4,300 live births. Of the 23 children with unilateral multicystic kidneys only 3 (13 per cent) had a readily palpable lesion. These findings suggest that multicystic kidney is a more common renal anomaly than was previously recognized and that the majority of cases remained undiagnosed before the advent of prenatal diagnosis. Ultrasound re-evaluation in 11 children suggests that the natural history of multicystic kidneys is towards spontaneous involution. Two kidneys were not identifiable by followup ultrasound. Hypertension and malignancy complicating multicystic kidney are reported infrequently. The literature on hypertension does not generally support the view that multicystic kidney poses a significant risk of hypertension in later childhood or adult life. We believe that the routine removal of multicystic kidneys in infancy is no longer appropriate.
Following a four-day control period during which an elevated serum calcium level either stabilized or continued to rise despite maximally tolerated saline diuresis, 12 patients with neoplastic hypercalcemia were treated with intravenous etidronate disodium (etidronate) 7.5 mg/kg/day for up to seven days. Serum calcium reverted to normal levels in all patients, with the mean pretreatment serum calcium level of 12.5 +/- 0.4 mg/dl dropping to 9.2 +/- 0.2 mg/dl (p less than 0.01) by Day 7. Elevated urinary calcium (1,107 +/- 134 mg/g creatinine) and hydroxyproline levels (154 +/- 16 mg/g creatinine) declined to 245 +/- 52 mg/g creatinine and 75 +/- 14 mg/g creatinine, respectively, suggesting a marked reduction in bone resorption following treatment. Serum phosphorus levels were unchanged, but urinary phosphorus levels dropped rapidly from 1,181 +/- 125 mg/g creatinine before treatment to 723 +/- 94 mg/g creatinine after two days. Serum parathyroid hormone levels (mid-molecule assay) were suppressed before treatment (64 +/- 16 pg/ml), but rose rapidly to 223 +/- 68 pg/ml by Day 7 of treatment. The value of serum 1,25-dihydroxyvitamin D was initially below normal (16 +/- 3 pg/ml), but rose rapidly with treatment to 42 +/- 12 pg/ml by Day 7. Symptoms of hypercalcemia and bone pain improved with treatment, and no serious adverse reactions to treatment were encountered. Intravenous etidronate is apparently an effective and safe treatment for neoplastic hypercalcemia.
Increasing dose of budesonide, each dose given for a minimum of 1 month, were administered via a Nebuhaler to 14 patients. Two consecutive abnormally low fasting morning plasma cortisol values, taken 2 weeks apart, were accepted as evidence of hypothalamo-pituitary-adrenal (HPA) hypofunction. Data from nine of the 14 patients entering the study were available for analysis. One patient developed HPA hypofunction while inhaling 2.4 mg budesonide per day and another retained normal HPA function on a dose of 12 mg. In the remaining patients, intermediate doses resulted in suppression, or the patients were withdrawn unsuppressed for other reasons (n = 3). The results in this small patient sample suggest that budesonide administered via the Nebuhaler in doses up to 1.6 mg daily does not significantly affect plasma cortisol.
Exposure to organic solvents was compared by interview and questionnaire in 50 patients with biopsy-proven proliferative glomerulonephritis in whom there was no evidence of systemic disease or preceding infection with that of 100 control subjects matched for age, sex and social class. The interview was conducted by a lay person who did not know whether the interviewee was a patient with glomerulonephritis or a control subject. The exposure scores derived from the results of the questionnaires were significantly greater in the patients with glomerulonephritis than the control subjects (13,186 +/- 3,716 vs. 3,030 +/- 1,152, p less than 0.01). The degree of exposure was higher in those patients with the more severe diffuse endocapillary proliferative glomerulonephritis than in those with mesangial proliferative glomerulonephritis. In the glomerulonephritis patients solvent exposure was mainly occupational in origin and involved fuels, paints and degreasing agents in most cases. This occupational exposure was significantly greater than in the control subjects (13,061 +/- 3,858 vs. 2,878 +/- 1,146, p less than 0.01). It is suggested that exposure to organic solvents may participate in the pathogenesis of non-systemic proliferative glomerulonephritis.
Peripheral blood mononuclear cells from asthmatic patients were cultured in soft agar with or without the synthetic glucocorticoid methylprednisolone (MP). The resulting colonies consisted mostly of T lymphocytes but included monocytes, often in a central position. Colony growth from patients whose asthma had responded satisfactorily to glucocorticoid medication was inhibited by MP in vitro at concentrations as low as 10(-9) M, and the ratio of helper to suppressor/cytotoxic T cells was reduced relative to untreated cultures. In contrast, patients shown to be resistant to the therapeutic effects of glucocorticoids yield colonies which differed little in number, size or constituent phenotype, whether untreated or exposed to MP at concentrations as high as 10(-8) M. Higher concentrations inhibited colony growth from both types of patient. Hybrid colonies were generated from partially purified cells from pairs of patients: monocytes from one member and lymphocytes from the other. The steroid sensitivity of these colonies was found to be dependent upon the source of the monocytes and not the lymphocytes. The results support the view that, in glucocorticoid resistant asthma, there is a defect in monocyte responsiveness to the hormone. This defect could explain the poor therapeutic effect of glucocorticoids in these patients. The results suggest that monocyte factors may be of importance in the pathogenesis of asthma in general.
In order to investigate the cellular mechanism of glucocorticoid resistance in chronic asthma, peripheral blood mononuclear cells (MNC) from asthmatic patients were cultured in soft agar. Cells from patients known to be clinically sensitive to glucocorticoid therapy did not differ significantly from those of clinically resistant patients in terms of their immunophenotype or the number of colonies generated by culture in the presence of phytohaemagglutinin. The glucocorticoid methylprednisolone (MP) at low concentration (10 nmol/l) inhibited colony growth from cells of glucocorticoid-sensitive patients, whereas there was much less inhibition of colony growth from resistant patients' cells. In a small prospective study inhibition of colony growth by methylprednisolone in vitro correlated with the subsequently determined sensitivity of the patients' asthma to glucocorticoid therapy. Assessment in vitro of glucocorticoid sensitivity may help to predict which patients may be spared ineffectual glucocorticoid medication. The results raise the possibility that peripheral blood mononuclear cells may respond to glucocorticoid in a similar manner to cells involved in the pathogenesis of asthma.
The relationship between epilepsy and psychiatric disorder in general and the relationship between epilepsy and psychosis in particular remain controversial issues of long standing. In order to reexamine these central issues concerned with epilepsy/psychopathology relationships, we utilized a Minnesota Multiphasic Personality Inventory (MMPI) sequential diagnostic system to reanalyze 87 published MMPI profiles of patients with epilepsy, other neurological disorders, and chronic physical illnesses encompassing a total of 2786 patients. We found that overall rates of psychopathology were not increased in epilepsy. However, when psychopathology was present, the level of psychosis was greatest in patients with epilepsy. The results are related to the larger literature concerned with the relationship between epilepsy and psychopathology.
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