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A Gunn

Publications and source records attributed to A Gunn.

At least 19 recordsLinked to original sources
PubMed1995

Proliferative compartment deregulation in the non-neoplastic colonic epithelium of familial adenomatous polyposis.

Previous work has shown abnormalities in the proliferative activity of the colorectal mucosa in familial adenomatous polyposis (FAP). Some doubts remain about the validity of these findings because of difficulties in excluding adenomatous crypts, particularly in methods using tritiated thymidine, bromodeoxyuridine, and ornithine decarboxylase. The proliferative activity of the epithelium in colonic resections from 20 FAP patients was compared with that of age, sex, and site matched controls using a new monoclonal antibody MIB1 to assay the expression of Ki-67 antigen in routinely processed tissue. The labelling indices were very similar in the polyposis and control cases (25.5 (1.4)% and 26.7 (1.7)% respectively) but analysis of the distribution of labelled cells showed a significant shift of the proliferative compartment towards the luminal surface in the FAP group. Specifically, the labelling index was lower in the basal fifth of the polyposis crypts and higher in the two fifths at the luminal surface. These results show that analysis of proliferative activity in FAP is now achievable in routine histological material and indicate deregulation of proliferative control in the FAP colonic crypt. This may form a useful diagnostic adjunct to standard clinical and molecular genetic techniques, particularly in view of the current interest in dietary and pharmacological intervention in sporadic colorectal carcinoma.

Adenomatous Polyposis Coli↗
PubMed1993

Primary hyperaldosteronism--evaluation of procedures for diagnosis and localization.

We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.

Adenoma↗
PubMed1992

Bone mineral content in patients with primary hyperparathyroidism: a comparison of conservative management with surgical treatment.

The management of patients with asymptomatic hyperparathyroidism remains controversial. This study examined the extent to which the presence of prospect of bone disease should influence treatment. Bone mineral content (BMC) of the distal forearm was measured by single photon absorptiometry in 67 patients with mild hyperparathyroidism. Twenty-six patients treated surgically and 17 managed conservatively were reviewed regularly for up to 4 years. Eighty per cent of patients had a baseline fat-corrected BMC within the local reference interval for age and sex, but about 75 per cent of values fell below the mean. BMC at the 'distal' site of the surgically treated patients improved or stabilized, but a continuing decline was seen in the patients managed conservatively (P less than 0.01). Differences were small and concern about future osteoporotic fracture should seldom be a major factor in making decisions about surgical correction of mild hyperparathyroidism.

Adult↗
PubMed1992

Re-evaluation of the captopril test for the diagnosis of primary hyperaldosteronism.

OBJECTIVE: We aimed to re-evaluate the captopril test in the diagnosis of primary hyperaldosteronism. DESIGN: Serum aldosterone and plasma renin activity were measured supine prior to and 60, 90, 120 minutes after oral captopril, 25 mg. PATIENTS: We have performed this test in ten patients with primary hyperaldosteronism, two with hypertension and secondary hyperaldosteronism and in ten normokalaemic patients with essential hypertension. MEASUREMENTS: Validity was assessed by mathematical prediction methods. RESULTS: Using a ratio of aldosterone to plasma renin activity greater than or equal to 1400 pmol/l per microgram/ml/h as a predictor of primary hyperaldosteronism, the captopril test had a sensitivity of 100%, a specificity of 83% and a predictive value of 82% with a 60-minute post captopril evaluation being sufficient. Nevertheless, this test was only marginally superior to a careful analysis of the supine values where a similar ratio in the presence of a normal or suppressed plasma renin activity predicted primary hyperaldosteronism with a sensitivity also of 100% but a slightly lower specificity of 75% and predictive value of 77%. CONCLUSION: Application of the captopril test to patients identified as abnormal by screening confirms all cases of primary hyperaldosteronism but false positive or equivocal results, necessitating further investigation, may occur in some patients with essential hypertension.

Adult↗
PubMed1992

An intrachromosomal insertion causing 5q22 deletion and familial adenomatous polyposis coli in two generations.

We report familial adenomatous polyposis coli (FAPC) with epidermoid cysts, osteomata, and areas of congenital hypertrophy of the retinal pigment epithelium (CHRPEs) in a male patient and his maternal aunt, both of whom suffered a mild to moderate degree of mental handicap. Both had an interstitial deletion of the long arm of chromosome 5 (del(5)(q22q23.2)). Two other normal family members had the underlying direct insertion of chromosome 5(dir ins(5)(q31.3q22q23.2)). Molecular genetic and fluorescent hybridisation studies have shown that loci D5S37 and D5S98 are outside the deletion whereas loci detected by probes EF5.44 and YN5.48 are lost. As expected, the molecular analyses indicate loss of one allele at the MCC and APC loci. The APC gene is located within band 5q22. Familial direct insertions should be considered as a cause of recurrent microdeletion syndromes.

Adenomatous Polyposis Coli↗
PubMed1992

Parathyroidectomy in uraemic hyperparathyroidism: a clinical study.

Osteodystrophy is a common and sometimes debilitating complication of renal failure. Hyperparathyroidism plays a crucial role in the development of this condition. Significant morbidity is also incurred by the effects of calcium deposition in other tissues. We report a series of 27 patients undergoing parathyroidectomy between May 1988 and November 1989. All had biochemical, radiological and clinical evidence of hyperparathyroidism. Surgery was well tolerated leading to an improved quality of life and avoidance of the need for aluminium containing phosphate binders.

Adolescent↗
PubMed1991

Role of a regional register for familial adenomatous polyposis: experience in the northern region.

Within 36 months of its formation the Northern Region Polyposis Registry had increased the number of identified gene carriers of familial adenomatous polyposis from 56 to 65 in a population of 3.1 million and had achieved a 15-fold increase in the number of at-risk relatives being regularly screened. Review of the surgical records at the outset of the registry revealed that the mean age at diagnosis of those patients detected by screening was 24.7 years, whereas it was 36.6 years for those detected by symptoms. Ten of the 31 in the latter group had colorectal carcinomas whilst only one of those detected by screening had a cancer and a significantly higher proportion had sphincter-saving surgery. A regional registry can provide an effective screening and counselling service to surgeons treating patients with familial adenomatous polyposis. At-risk relatives are best assessed by combining results of the different screening procedures now available but the prime requirement of a successful registry is dedicated domiciliary counselling.

Adenomatous Polyposis Coli↗
PubMed1991

The UK Northern region genetic register for familial adenomatous polyposis coli: use of age of onset, congenital hypertrophy of the retinal pigment epithelium, and DNA markers in risk calculations.

A polyposis register has been established in the Northern Region of England. A total of 48 families with 71 living affected subjects has been identified during the first three years of operation, a prevalence of 2.29 x 10(-5). Indirect ophthalmoscopy identifies the majority of gene carriers by showing multiple areas of congenital hypertrophy of the retinal pigment epithelium (CHRPE). The absence of this sign in families limits its value where a relative with CHRPE has not been identified. Combining eye examination with data on age of onset and linked DNA markers is highly effective in carrier exclusion; 38% of 528 first, second, and third degree relatives had their carrier risk reduced to less than 1 in 1000. Even with such assurance many subjects will request continued bowel screening at a reduced frequency. Little interest has been shown in prenatal diagnosis. The principal value of a genetic register with domiciliary nurse visiting is the reduction in early mortality among unrecognised gene carriers.

Adenomatous Polyposis Coli↗
PubMed1991

Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep.

The role of edema in the pathogenesis of hypoxic-ischemic injury in the immature brain is controversial. We studied 15 chronically instrumented fetal sheep following transient cerebral ischemia, to estimate changes in extracellular space using an impedance technique, to quantify the electroencephalogram with real-time spectral analysis, and to assess histologic outcome 3 days after the insult. These measurements were made in the parasagittal cortex. There was a rapid loss of extracellular space from 5 +/- 2 minutes after the onset of ischemia. Following 10 minutes of ischemia (n = 7) the intracellular edema peaked but then quickly resolved (6 +/- 4 minutes), and mild selective neuronal loss was seen. In contrast, the swelling was biphasic after 30-40 minutes of ischemia (n = 8). The early edema resolved slowly (28 +/- 12 minutes) but incompletely, and secondary swelling began at 7 +/- 2 hours and peaked at 28 +/- 6 hours. The early swelling was the more severe. Postinsult epileptiform activity began at 8 +/- 2 hours and peaked at 10 +/- 3 hours; later there was laminar necrosis of the underlying cortex. The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity. The increased metabolic load of the epileptiform activity may have worsened this delayed deterioration.

Animals↗
PubMed1991

Yersiniosis in free-ranging muskoxen on Banks Island, Northwest Territories, Canada.

Sixty-seven muskox (Ovibos moschatus) carcasses, 53 skeletal remains and two sick muskoxen were seen during an aerial survey of the Thomsen River region, northern Banks Island, Northwest Territories, Canada in late July 1986. Complete necropsies were performed on 29 muskoxen estimated to have died within the previous 3 to 5 days. Twenty were diagnosed with acute yersiniosis due to Yersinia pseudotuberculosis serotype 1B and were in excellent body condition. A diagnosis could not be made on seven animals due to marked autolysis; however, these muskoxen also were in excellent body condition. The remaining two were aged, emaciated muskoxen. This report describes the first occurrence of yersiniosis in free-ranging muskoxen and the first documentation of large scale mortality due to this disease in a free-ranging population of wild ungulates.

Acute Disease↗