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Biomedical subjects

J P Mecklin

Publications and source records attributed to J P Mecklin.

At least 19 recordsLinked to original sources
PubMed2006

No evidence for dual role of loss of heterozygosity in hereditary non-polyposis colorectal cancer.

Hereditary non-polyposis colorectal cancer (HNPCC) is caused by germline mutations in mismatch repair (MMR) genes, mostly MLH1 and MSH2. Somatic inactivation of the wild-type allele of the respective MMR gene is required for tumor development. Unexpectedly, a recent study utilizing DNA from paraffin-embedded tissue material detected frequent loss of the mutant MMR gene allele in HNPCC tumors. Dual role for loss of heterozygosity (LOH) was proposed. If somatic loss of the wild-type MMR gene allele had occurred through point mutation or promoter hypermethylation, frequent somatic deletions at the region of the MMR gene locus, perhaps targeting other relevant cancer genes, could quite commonly lead to loss of the mutant allele. To test this hypothesis, we studied a population-based series of 25 fresh-frozen HNPCC tumors with a germline mutation in MLH1 or MSH2 for LOH. Fourteen of the 25 tumors (56%) showed LOH at the respective locus, and all 14 losses targeted the wild-type allele (P=0.00006). These results strongly support the traditional two-hit model of HNPCC gene inactivation.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMed2003

Impact of clinical symptoms and referral volume on endoscopy for detecting peptic ulcer and gastric neoplasms.

BACKGROUND: We investigated the volume of dyspeptic patients referred by general practitioners (GPs) to upper gastrointestinal endoscopy and the impact on endoscopic findings. We also examined the correlation between clinical symptoms and endoscopic findings. METHODS: We collected data on patients sent for upper gastrointestinal endoscopy by GPs of 30 healthcare centres in 1996 in our hospital referral area of 260,000 inhabitants. In addition, national and local cancer registries were used to enumerate the gastric cancer cases detected in 1996. RESULTS: The study population consisted of 3378 patients, mean age 58 years (interquartile range 25 years, male:female 1:1.3). Among the 30 healthcare centres, referral volumes for upper gastrointestinal endoscopy varied from 0.6 to 9.2 per 1000 inhabitants per year (median 3.3/1000/year). In healthcare units with 'high' (> or = 3.3/1000/year, 15 healthcare units, 1297 patients) and 'low' (<3.3/1000/year, 15 healthcare units, 2065 patients) referral volumes, the detection rates were as follows: duodenal ulcer (DU) 3.5% (n = 46) versus 4.0% (n = 83, P = 0.5), gastric ulcer (GU) 4.9% (n = 64) versus 5.3% (n = 110, P = 0.6), gastropathy 43.8% (n = 568) versus 35.6% (n = 736, P < 0.001), gastric cancer 0.5% (n = 6) versus 0.5% (n = 11, P = 0.8), gastric polyps 2.4% (n = 31) versus 1.5% (n = 30, P < 0.05). Independent risk factors for gastric cancer were age (OR 6.5 per decade, 95% CI 2.4-17.9), male sex (OR 5.5, 95% CI 1.8-17.1) and alarming symptoms and/or signs (OR 3.6, 95% CI 1.2-10.7); for GU, Helicobacter pylori (OR 2.6, 95% CI 1.9-3.5) and alarming symptoms (OR 2.0, 95% CI 1.4-2.7); for DU, male sex (OR 1.6, 95% CI 1.1-2.2) and H. pylori (OR 3.9, 95% CI 2.7-5.5); and for gastric polyp(s), age (OR 2.0 per decade, 95% CI 1.1-3.5) and high referral volume (OR 1.7, 95% CI 1.0-2.0). A high referral volume did not associate positively either with the number of peptic ulcers or gastric cancer. CONCLUSIONS: Alarm symptoms associate strongly with significant gastric lesions such as GU and cancer. Increased referral volume results in an increased number of gastropathy and gastric polyp(s), but not of peptic ulcer or cancer.

Dyspepsia↗
PubMed2002

No support for endoscopic surveillance for gastric cancer in hereditary non-polyposis colorectal cancer.

BACKGROUND: The DNA mismatch repair gene mutations underlying hereditary non-polyposis colorectal cancer syndrome (HNPCC) also predispose, besides colorectal and endometrial cancer, to gastric cancer. usually of the intestinal type. The carcinogenetic pathway behind the elevated gastric cancer risk is largely unknown. METHODS: The aim of this study was to determine whether there are any premalignant lesions to search for in gastric surveillance in HNPCC by comparing gastric histopathology between mutation-positive and mutation-negative family members. We searched for differences in occurrence of Helicobacter pylori, inflammation, atrophy, intestinal metaplasia and dysplastic changes. Upper gastrointestinal endoscopy was performed for 73 mutation-positive and 32 mutation-negative family members. RESULTS: One case of duodenal cancer was detected in the mutation-positive group, but no gastric neoplastic lesions were seen in either group. There were no differences in the occurrence of polyps, H. pylori, inflammation, activity, atrophy nor intestinal metaplasia tested with binaric, logistic, regression analysis. CONCLUSIONS: We conclude that surveillance gastroscopy may not be beneficial in HNPCC, since neither cases of early cancer nor premalignant lesions could be detected in our series of 73 mutation-positive subjects.

Adult↗
PubMed2001

Germline mutations in BMPR1A/ALK3 cause a subset of cases of juvenile polyposis syndrome and of Cowden and Bannayan-Riley-Ruvalcaba syndromes.

Juvenile polyposis syndrome (JPS) is an inherited hamartomatous-polyposis syndrome with a risk for colon cancer. JPS is a clinical diagnosis by exclusion, and, before susceptibility genes were identified, JPS could easily be confused with other inherited hamartoma syndromes, such as Bannayan-Riley-Ruvalcaba syndrome (BRRS) and Cowden syndrome (CS). Germline mutations of MADH4 (SMAD4) have been described in a variable number of probands with JPS. A series of familial and isolated European probands without MADH4 mutations were analyzed for germline mutations in BMPR1A, a member of the transforming growth-factor beta-receptor superfamily, upstream from the SMAD pathway. Overall, 10 (38%) probands were found to have germline BMPR1A mutations, 8 of which resulted in truncated receptors and 2 of which resulted in missense alterations (C124R and C376Y). Almost all available component tumors from mutation-positive cases showed loss of heterozygosity (LOH) in the BMPR1A region, whereas those from mutation-negative cases did not. One proband with CS/CS-like phenotype was also found to have a germline BMPR1A missense mutation (A338D). Thus, germline BMPR1A mutations cause a significant proportion of cases of JPS and might define a small subset of cases of CS/BRRS with specific colonic phenotype.

Abnormalities, Multiple↗
PubMed2001

Psychological consequences of predictive genetic testing for hereditary non-polyposis colorectal cancer (HNPCC): a prospective follow-up study.

Predictive genetic testing for cancer allows identification of those with the mutation (mutation positive) who should undergo cancer surveillance aiming at early detection of cancer and those without the mutation (mutation negative), whose unnecessary worry can be alleviated and who need not undergo frequent surveillance. However, there is a risk that predictive testing might have a harmful emotional impact on an individual. In the course of a predictive genetic testing protocol, we assessed general anxiety (by the State-Trait Anxiety Inventory [STAI]), fear of cancer and death, satisfaction with life and attitude to the future using a questionnaire survey in 271 individuals tested for hereditary non-polyposis colorectal cancer (HNPCC). Measurements were made before the first counseling (baseline), at the test disclosure session (STAI only) and 1 and 12 months after disclosure. Although at every measurement, the mutation-positive individuals were more afraid of cancer than those who were mutation negative, in both groups fear of cancer decreased significantly from baseline after disclosure. The mutation-positive subjects were more anxious than their counterparts immediately after the test disclosure, but the differences had disappeared at the follow-ups. In other variables, neither differences between the groups defined by mutation status nor changes with time were detected. Our findings suggest that counseling and testing relieve fear of cancer; no harmful emotional impact was detectable at the 1-year follow-up. To confirm these findings, however, the impact of testing should be studied after a longer interval. Furthermore, to evaluate the ultimate interpretation of these results, studies are needed to investigate the impact of fear of cancer on surveillance behavior among the mutation-positive subjects.

Adult↗
PubMed2001

Microsatellite marker analysis in screening for hereditary nonpolyposis colorectal cancer (HNPCC).

Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant cancer predisposition syndrome caused by germ-line mutations in DNA mismatch repair genes. It is relevant to identify HNPCC patients because colonoscopic screening of individuals with HNPCC mutations reduces cancer morbidity and mortality. Microsatellite instability (MSI) is characteristic of HNPCC tumors. A panel of five markers (BAT25, BAT26, D2S123, D5S346, and D17S250, the so-called Bethesda markers) has been proposed for screening for MSI. To test a hypothesis that the use of BAT26 alone is feasible in screening for MLH1/MSH2 mutation-positive HNPCC patients, we compared the MSI results of 494 colorectal cancer patients obtained using BAT26 with results obtained using the Bethesda markers. BAT26 was able to identify all 27 mutation-positive individuals in this series. The marker failed to identify 2 high MSI tumors and 20 low MSI tumors, all of which expressed MLH1, MSH2, and MSH6 when scrutinized by immunohistochemistry.

Adaptor Proteins, Signal Transducing↗
PubMed2001

MSH6 and MSH3 are rarely involved in genetic predisposition to nonpolypotic colon cancer.

A set of 90 nonpolypotic colon cancer families in which germ-line mutations of MSH2 and MLH1 had been excluded were screened for mutations in two additional DNA mismatch repair genes, MSH6 and MSH3. Kindreds fulfilling and not fulfilling the Amsterdam I criteria, showing early and late onset colorectal (and other) cancers, and having microsatellite stable and unstable tumors were included. Two partly parallel approaches were used: genetic linkage analysis (19 large families) and the protein truncation test (85, mostly smaller, families). Whereas MSH3 was not involved in any family, a large Amsterdam-positive, late-onset family showed a novel germ-line mutation in MSH6 (deletion of CT at nucleotide 3052 in exon 4). The mutation was identified through genetic linkage (multipoint lod score 2.4) and subsequent sequencing of MSH6. Furthermore, the entire MSH6 gene was sequenced exon by exon in families with frameshift mutations in the (C)8 tract in tumors, previously suggested as a predictor of MSH6 germ-line mutations; no mutations were found. We conclude that germ-line involvement of MSH6 and MSH3 is rare and that other genes are likely to account for a majority of MSH2-, MLH1-mutation negative families with nonpolypotic colon cancer.

Adult↗
PubMed2001

The clinical features of ovarian cancer in hereditary nonpolyposis colorectal cancer.

OBJECTIVE: Hereditary nonpolyposis colorectal cancer (HNPCC) is a hereditary cancer susceptibility disorder associated with a very high risk for carcinoma of the colon and an elevated risk for certain extracolonic cancers including ovarian cancer. Our aim in this study was to describe the clinicopathologic features of ovarian cancer in HNPCC family members. METHODS: . Members of the International Collaborative Group on HNPCC collected retrospective data on 80 ovarian cancer patients who were members of HNPCC families, including 31 known mutation carriers, 35 presumptive carriers (by colorectal/endometrial cancer status), and 14 at-risk family members. RESULTS: Mean age at diagnosis of ovarian cancer was 42.7. Nonepithelial tumors made up only 6.4% of the cancers, and borderline tumors comprised just 4.1% of the epithelial cancers. Among frankly malignant epithelial cases, most cancers were well or moderately differentiated, and 85% were FIGO stage I or II at diagnosis. Synchronous endometrial cancer was reported in 21.5% of cases. CONCLUSIONS: Ovarian cancer in HNPCC differs from ovarian cancer in the general population in several clinically important respects. It occurs at a markedly earlier age. It is more likely to be epithelial. If it is a frankly invasive epithelial cancer, it is more likely to be well or moderately differentiated. HNPCC patients with ovarian cancer are more likely to have a synchronous endometrial cancer than other ovarian cancer patients and are more likely to be diagnosed at an early stage.

Adult↗
PubMed2001

Genotype and phenotype in hereditary nonpolyposis colon cancer: a study of families with different vs. shared predisposing mutations.

Hereditary nonpolyposis colorectal cancer (HNPCC) is a multi-organ cancer syndrome associated with heritable mutations in DNA mismatch repair genes, particularly MLH1 (MutL Homologue 1) and MSH2 (MutS Homologue 2). We took advantage of the unique characteristics of the Finnish HNPCC families to assess genotype- phenotype correlations in this disorder. We studied 295 mutation carriers (10 mutations in MLH1 and 3 in MSH2) segregating in 55 families. In addition to the comparison of families with different mutations, the enrichment of two MLH1 mutations, one affecting exon 16 (29 families, 186 individuals) and another one affecting exon 6 (10 families, 45 individuals) allowed the comparison of kindreds with identical predisposing mutations. Extracolonic cancers were more common in MSH2 than MLH1 mutation carriers, with the ratios of 0.48 and 0.64, respectively, of colorectal cancer to all cancers (P = 0.076). Within MLH1, two mutations affecting only the amino terminal portion showed a significant association with late onset of cancer as compared to the remaining mutations. Importantly, families with the MLH1 exon 16 mutation displayed significant variation (P = 0.012) in the age at onset of colon cancer, despite shared predisposition. We conclude that even though characteristics of the inherited mutations may explain part of the observed clinical variation, other factors have a significant impact on HNPCC phenotype determination.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Expression of cyclooxygenase-2 in dysplasia of the stomach and in intestinal-type gastric adenocarcinoma.

PURPOSE: Cyclooxygenase (Cox) is the key enzyme in conversion of arachidonic acid to prostanoids. Two Cox genes have been cloned, and expression of Cox-2 mRNA and protein has been shown to be elevated in several human malignancies and in animal models of carcinogenesis. The purpose of this study was to investigate Cox-2 protein expression in human gastric dysplasias and adenocarcinomas. EXPERIMENTAL DESIGN: Performance of several Cox-2 antibodies was evaluated, after which Cox-2 protein expression was studied in 67 gastric cancer specimens and in eight definitive dysplasias by using immunohistochemistry. RESULTS: Cox-2 positivity was detected in 58% (25/43) of the intestinal-type (well-differentiated) tumors and 6% (1/18) of diffuse-type (poorly differentiated) tumors. Consistent with these data, we detected higher expression of Cox-2 mRNA, protein, and enzymatic activity in well-differentiated gastric cancer cell lines (MKN-28 and MKN-74) when compared with poorly differentiated cell lines (HSC-39 and KATO III). Cox-2 immunoreactivity was localized to the carcinoma cells, but the stroma of the tumors was negative. However, strong Cox-2 positivity was consistently detected in stromal cells at sites of erosions and ulcerations. Furthermore, four of nine (44%) definitive dysplasias of the stomach that showed no evidence of invasion were positive for Cox-2. CONCLUSIONS: Cox-2 is expressed by the neoplastic cells in the intestinal-type gastric adenocarcinoma and by precarcinogenic (dysplastic) lesions leading to this disease.

Adenocarcinoma↗
PubMed2000

Genetic reconstruction of individual colorectal tumor histories.

It is difficult to observe human tumor progression as precursor lesions are systematically removed. Alternatives to direct observations, commonly used to reveal the hidden past of species and populations, are sequence comparisons or molecular clocks. Noncoding microsatellite (MS) loci were employed as molecular tumor clocks in 13 human mutator phenotype (MSI(+)) colorectal tumors. Quantitative analysis revealed that specific patterns of somatic MS mutations accumulate with division after loss of mismatch repair (MMR). Tumors had unique patterns of MS mutation, and, therefore, based on this model, each tumor had its own unique history. Loss of MMR occurred very early relative to terminal clonal expansion, with an estimated average of 2,300 divisions since loss of MMR and 280 divisions since expansion. Contrary to the classical adenoma-cancer sequence, MSI(+) adenomas were nearly as old as cancers (2,000 versus 2,400 divisions since loss of MMR). Negative clinical examinations preceded six tumors, independently documenting an absence of visible precursors during early MSI(+) adenoma or cancer progression. These findings further extend a window beyond visible progression since loss of MMR appears to start a genetic phase involving clone sizes or phenotypes below a threshold of clinical detection. This previously occult prologue before visible neoplasia is longer and therefore likely more important than generally appreciated.

Adenocarcinoma↗
PubMed2000

No evidence of Peutz-Jeghers syndrome gene LKB1 involvement in left-sided colorectal carcinomas.

LKB1 serine/threonine kinase is a gene for Peutz-Jeghers cancer predisposition syndrome. Most studies have detected a low frequency of LKB1 defects in sporadic cancer. A notable exception is a recent report describing frequent, mostly missense type, LKB1 mutations in Korean distal colorectal tumors. To clarify the role of LKB1 in colon cancer, we scrutinized 50 left-sided Korean and Finnish specimens. No somatic mutations were found. The seven Korean somatic missense mutations reported previously were functionally analyzed, and five were found not to alter LKB1 kinase activity. One of these changes was found to be a germ-line polymorphism. LKB1 involvement in distal colorectal cancer is not common.

AMP-Activated Protein Kinase Kinases↗
PubMed2000

Predictive genetic testing for hereditary non-polyposis colorectal cancer: uptake and long-term satisfaction.

The aim of this prospective study was to assess the uptake of predictive genetic testing for hereditary non-polyposis colorectal cancer (HNPCC) and its associations with sociodemographic and other factors, and long-term satisfaction with taking the test. The test was offered to all high-risk members (n = 446) of 36 Finnish HNPCC families in which the mutation was known. The procedure comprised an educational counselling session, a period for reflection, and a test disclosure session. Data were collected by questionnaires sent before the educational counselling and 1 month and 1 year after the test disclosure. Of those eligible, 85% (n = 381) completed the first questionnaire study. Non-participation was more common among men living alone who had not participated in the clinical cancer surveillance programme. Of the 347 subjects who attended counselling, 334 (75% of all subjects) were actually tested. After logistic-regression analysis, the only significant factor predicting test acceptance proved to be employment status: those employed were more likely than others to accept the test (odds ratio = 2.25; 95% confidence intervals, 1.09 to 4.6 1). At follow-up, over 90% of the subjects were fully satisfied with the decision to take the test. In conclusion, acceptance of the test was considerably higher than in previously reported studies. We attribute this to our careful face-to-face individualized counselling, our health care system, and to attitudes of the Finnish population, which are generally favourable towards health care and disease prevention.

Adult↗
PubMed2000

Controlled 15-year trial on screening for colorectal cancer in families with hereditary nonpolyposis colorectal cancer.

BACKGROUND & AIMS: Identification of the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome enables prevention of colorectal cancer (CRC) by means of colonoscopy and polypectomies. We evaluated the efficacy of screening in a controlled trial over 15 years. METHODS: Incidence of CRC and survival were compared in 2 cohorts of at-risk members of 22 families with HNPCC. Colonic screening at 3-year intervals was arranged for 133 subjects; 119 control subjects had no screening. Genetic testing was offered to subjects in whose families the causative mutation was known. RESULTS: CRC developed in 8 screened subjects (6%) compared with 19 control subjects (16 %; P = 0.014). The CRC rate was reduced by 62%. In mutation-positive subjects alone, the CRC rates were 18% in screened subjects and 41% in controls (P = 0.02). The decrease resulted from the removal of adenomas in 13 mutation-positive individuals (30%) and in 6 subjects with unknown mutation status (40%). All CRCs in the study group were local, causing no deaths, compared with 9 deaths caused by CRC in the controls. The overall death rates were 10 vs. 26 subjects in the study and control groups (P = 0.003), 4 vs. 12 in mutation-positive subjects (P = 0.05). CONCLUSIONS: Colonoscopic screening at 3-year intervals more than halves the risk of CRC, prevents CRC deaths, and decreases overall mortality by about 65% in HNPCC families.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Microsatellite instability is a favorable prognostic indicator in patients with colorectal cancer receiving chemotherapy.

BACKGROUND & AIMS: Adjuvant 5-fluorouracil (5-FU)-based chemotherapy is standard treatment for stage C colorectal cancer (CRC). Approximately 12% of CRCs are characterized by microsatellite instability (MSI), a hallmark of a DNA mismatch repair defect. We investigated the safety of adjuvant 5-FU-based chemotherapy for MSI(+) CRC and compared the prognosis of MSI(+) and MSI(-) CRC patients receiving adjuvant therapy. METHODS: Previously, a prospective series consisting of 1044 consecutive CRCs has been collected and the MSI status of each sample determined. Patients with stage C cancer who had received adjuvant chemotherapy (n = 95) were followed up for 7-63 months (median, 31 months) after surgery. RESULTS: No unexpected or serious adverse effects were observed when 5-FU-based chemotherapy was used as adjuvant treatment for MSI(+) CRC. Three- year recurrence-free survival was 90% and 43% in the MSI(+) (n = 11) and MSI(-) (n = 84) groups, respectively (P = 0.020). CONCLUSIONS: Adjuvant 5-FU-based chemotherapy is feasible for both MSI(+) and MSI(-) CRCs, and patients with MSI(+) CRC who receive adjuvant therapy have an excellent prognosis.

Adult↗
PubMed2000

Classical Barrett esophagus contrasted with Barrett-type epithelium at normal-appearing esophagogastric junction. Central Finland Endoscopy Study Group.

BACKGROUND: Incomplete intestinal metaplasia or specialized columnar epithelium (SCE) is the histologic hallmark of Barrett esophagus (BE), but it may also occur at a normal-appearing gastroesophageal junction without BE. We studied whether differences occur between BE patients and those with SCE at the squamocolumnar junction but without BE (abbreviated JSCE), in terms of endoscopic and histologic signs of gastroesophageal reflux disease (GERD) and Helicobacter pylori gastritis. METHODS: A total of 1059 consecutive patients referred for endoscopy in one hospital district in Finland were enrolled in the study. Biopsy specimens (at least two from each site) were obtained from the gastric antrum and the corpus of the stomach and from the esophagogastric junction and distal esophagus. RESULTS: Classical BE was detected in 25 (2%) and JSCE in 99 (9%) patients. Dysplasia in the metaplastic mucosa was observed in six BE patients but in none of the JSCE patients (P < 0.001). In multivariate analysis the independent risk factors for BE were endoscopic erosive esophagitis (odds ratio (OR), 6.08; 95% confidence interval (CI), 2.50-14.82), male sex (OR, 3.02; 95% CI, 1.20-7.65), and age (OR, 1.02 per year; 95% CI, 1.00-1.06). The independent risk factors for JSCE were endoscopic erosive esophagitis (OR, 1.88; 95% CI, 1.08-3.29) and age (OR, 1.03; 95% CI, 1.02-1.05) but not H. pylori infection (OR, 1.57; 95% CI, 0.83-2.97) or chronic gastritis (OR, 0.88; 95% CI, 0.44-1.75). In univariate analysis, however, JSCE was associated with antral-predominant atrophic gastritis (77% H. pylori-positive). Unlike in JSCE patients, male sex strongly predominated among BE patients (P = 0.01). The mean ages of BE and JSCE patients did not differ. CONCLUSIONS: Both BE and JSCE without BE increase in prevalence with age, and both associate with endoscopic erosive esophagitis but not with H. pylori gastritis. However, because of the marked sex disparity, JSCE cannot be a direct precursor of BE, and some factors other than GERD alone also play a role in the pathogenesis of BE. Compared with BE, dysplasia is a rare finding in JSCE, and endoscopic surveillance with biopsy specimens from JSCE patients without dysplasia is not recommended.

Barrett Esophagus↗
PubMed2000

Evaluation of a counselling protocol for predictive genetic testing for hereditary non-polyposis colorectal cancer.

OBJECTIVES: To evaluate the feasibility of a reduced counselling programme for predictive genetic testing for hereditary non-polyposis colorectal cancer (HNPCC) in terms of counsellees' opinions on the extent and significance of genetic counselling and need for psychological support at different phases of the testing procedure. DESIGN: Prospective follow up study with pre-test questionnaire assessment of background sociodemographic variables. The protocol comprised a pre-test counselling session, a period for reflection, and a test disclosure session. The outcome variables were studied by post-test questionnaires at one month and one year follow up. SUBJECTS: Two hundred and seventy one high risk members of 36 families with HNPCC who attended both counselling sessions and completed the questionnaires. RESULTS: The pre-test counselling was considered fairly or very useful by 89% of respondents and one post-test session was considered sufficient by over 80% of respondents at follow up. Fifty three percent would have used extra psychological support had it been offered with the counselling. On enquiry one year after receiving the test result, only 2% stated that the need for support was at its greatest at that time, while the majority (46%) reported that the need for support had been greatest at the moment of test disclosure. CONCLUSIONS: A protocol that includes one comprehensive pre-test counselling session and a test disclosure session, supplemented with the option of professional psychological support, seems to be sufficient for both the educational and supportive needs of counsellees. Only a minority expressed a need for post-test follow up sessions, which suggests that, in this disorder, resources can be directed to the beneficial surveillance programmes rather than to extensive psychological support.

Adult↗