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Objectives Patients starting highly active antiretroviral therapy (HAART) may have a suboptimal CD4 increase despite rapid virological suppression. The frequency and the significance for patient care of this discordant response are uncertain. This study was designed to determine the incidence of a discordant response at two time-points, soon after 6 months and at 12 months, and to determine the relationship with clinical outcomes. Methods Data obtained in the UK Collaborative HIV Cohort Study were analysed. A total of 2584 treatment-naive patients starting HAART with HIV viral load (VL)>1000 HIV-1 RNA copies/mL at baseline and

A small subset of HIV-positive adults have low HIV RNA in the absence of therapy, sometimes for years. Clinical factors associated with low HIV RNA in early infection have not been well defined.We assessed factors associated with low plasma HIV RNA level at study entry in the Strategic Timing of AntiRetroviral Treatment (START) trial. All START participants had a baseline HIV RNA assessment within 60 days prior to randomization. The key covariables considered for this analysis were race, and hepatitis B virus (HBV) and hepatitis C virus (HCV) status. We assessed factors associated with HIV RNA ≤ 50 and ≤ 400 HIV-1 RNA copies/mL using logistic regression. Because of the strong association between region of randomization and baseline low HIV RNA, analyses were stratified by region.We found that, of 4676 eligible participants randomized in START with a baseline HIV RNA assessment, 113 (2.4%) had HIV RNA ≤ 50 copies/mL at baseline, and a further 257 (5.5%) between 51 and 400 copies/mL. We found that HIV exposure routes other than male homosexual contact, higher high-density lipoprotein (HDL) cholesterol levels, higher CD4 cell counts, and higher CD4:CD8 ratio were associated with increased odds of low HIV RNA. HCV antibody positivity was borderline statistically significantly associated with low HIV RNA. Race and HBV surface antigen positivity were not significantly associated with low HIV RNA.In a modern cohort of individuals with early untreated HIV infection, we found that HIV exposure routes other than male homosexual contact and higher HDL cholesterol were associated with increased odds of low HIV RNA.

We compared the use of computational models developed with and without HIV genotype vs. genotyping itself to predict effective regimens for patients experiencing first-line virological failure.Two sets of models predicted virological response for 99 three-drug regimens for patients on a failing regimen of two nucleoside/nucleotide reverse transcriptase inhibitors and one nonnucleoside reverse transcriptase inhibitor in the Second-Line study. One set used viral load, CD4 count, genotype, plus treatment history and time to follow-up to make its predictions; the second set did not include genotype. Genotypic sensitivity scores were derived and the ranking of the alternative regimens compared with those of the models. The accuracy of the models and that of genotyping as predictors of the virological responses to second-line regimens were compared.The rankings of alternative regimens by the two sets of models were significantly correlated in 60-69% of cases, and the rankings by the models that use a genotype and genotyping itself were significantly correlated in 60% of cases. The two sets of models identified alternative regimens that were predicted to be effective in 97% and 100% of cases, respectively. The area under the receiver-operating curve was 0.72 and 0.74 for the two sets of models, respectively, and significantly lower at 0.55 for genotyping.The two sets of models performed comparably well and significantly outperformed genotyping as predictors of response. The models identified alternative regimens predicted to be effective in almost all cases. It is encouraging that models that do not require a genotype were able to predict responses to common second-line therapies in settings where genotyping is unavailable.

We aimed to identify the factors associated with developing AIDS 6 months or more after an HIV diagnosis, and to examine how post-HIV diagnosis AIDS (PHDA) patients differed from true late presenters (HIV diagnosed concurrent with the first AIDS presenting event) in their demographics and comorbidities.A retrospective analysis was undertaken of all inpatients admitted to a large HIV unit presenting with the following AIDS-defining infections: cryptococcal meningitis, cerebral toxoplasmosis or Pneumocystis jirovecii pneumonia between 1 January 2005 and 31 December 2010.114 HIV-positive patients presented with AIDS-defining infections. Compared with late presenters, PHDA patients had a larger proportion of migrants and visitors (53.7% vs. 34.0%, p=0.047), were more likely to inject drugs (9.3% vs 0.0%, p=0.032), had more previous HIV-associated diseases (57.4% vs. 12.8%, p=0.000), psychiatric comorbidities (35.2% vs. 12.8%, p=0.009), rates of alcohol abuse (24.1% vs. 4.3%, p=0.005) and reported social issues (25.9% vs. 0.00%, p=0.000). 88.9% of PHDA patients were lost to follow-up for a period of at least 4 months since diagnosis. Common reasons for clinic non-attendance included travel, social issues, transfer of care and treatment avoidance. Common reasons for antiretroviral treatment breaks included drug side effects, negative beliefs about medication, incompatible lifestyles and social issues.Compared with late presenters, PHDA patients demonstrate clear demographical differences including higher rates of psychiatric comorbidities, social issues, alcohol and substance abuse. Many PHDA patients default follow-up. The retention of HIV patients in care and on treatment must be addressed by clinicians to prevent avoidable morbidity.

The views of people with HIV and their professional carers about patients' views on involvement in decision-making and information-seeking were studied, using a standardized self-report instrument. Patients and staff reported high levels of desire for patients' involvement in their care, but there were important differences between groups. Staff had higher preference for patients' involvement in decision-making than the patients themselves, while the opposite was the case for information-seeking. There were differences between professional groups and symptomatic and asymptomatic patients, social workers generally reporting higher preference for patients' autonomy, while doctors reported lower levels. Symptomatic patients tended to have lower preference for autonomy than asymptomatic ones. The significance and practical implications of the findings are discussed.

We studied 124 homosexual men aged 36.7 +/- 7.6 years (range 23-57) using Doppler echocardiography. One hundred and one patients (Group A) had had acquired immunodeficiency syndrome for 1.6 +/- 1.0 years and 23 patients (Group B) had had HIV infection without opportunistic infections for 3.2 +/- 2.3 years. Doppler echocardiography was normal in 31% of Group A patients and in 61% of Group B. Pericardial effusion was found in 44 Group A patients (44%) and two Group B patients (9%). In Group A, left ventricular dilatation and/or dysfunction were found in 20 patients (20%), aortic root dilatation and regurgitation in eight patients (8%) and an intracardiac echogenic mass in seven patients (7%); in Group B one patient (4%) had an intracardiac mass. Forty-four (44%) Group A patients had cardiac presentations, and of these 22 had cardiomegaly with clinical signs of heart failure; 10 patients had tachyarrhythmias compared to only two in Group B. Although the CD4 lymphocyte count (%) was significantly lower in Group A than in Group B (5.4 +/- 6.1 vs 13.3 +/- 7.3, P < 0.001), the presence of pericardial effusion, left ventricular dysfunction, right-sided cardiac enlargement or the duration of HIV infection, did not relate to the CD4 level in either group. Although often not diagnosed clinically, cardiac involvement in patients with AIDS is a clinical reality, with pericardial effusion, cardiomyopathy and left ventricular dysfunction appearing to have a high prevalence in male homosexual patients with AIDS. These clinical and echocardiographic findings are associated with clinically apparent intercurrent opportunistic infections, rather than the HIV virus per se, or the severity of infection as reflected by the CD4 count.

Both Mycobacterium tuberculosis and atypical mycobacteria, particularly Mycobacterium avium-intracellulare. are common in patients infected with the human immunodeficiency virus (HIV). Mycobacterium avium-intracellulare (MAI) is the commonest cause of bacteraemia in patients with the acquired immune deficiency syndrome (AIDS).^'^ Although cutaneous involvement with MAI is not uncommon as part of disseminated disease,*'^ skin disease without bacteraemia is rare.^"'' Miliary tuberculosis of the skin (tuberculosis cutis miliaris disseminata) is an extremely rare manifestation of infection with Mycobacterium tuberculosis, with only 25 cases ever reported in patients over 15 years of age,""^** Two such cases have recently been reported in patients with AIDS.'^-^^

Current British HIV Association (BHIVA) guidelines recommend that all patients with a CD4 count350 cells/μL are offered highly active antiretroviral therapy (HAART). We identified risk factors for delayed initiation of HAART following a CD4 count350 cells/μL.All adults under follow-up in 2008 who had a first confirmed CD4 count350 cells/μL from 2004 to 2008, who had not initiated treatment and who had6 months of follow-up were included in the study. Characteristics at the time of the low CD4 cell count and over follow-up were compared to identify factors associated with delayed HAART uptake. Analyses used proportional hazards regression with fixed (sex/risk group, age, ethnicity, AIDS, baseline CD4 cell count and calendar year) and time-updated (frequency of CD4 cell count measurement, proportion of CD4 counts350 cells/μL, latest CD4 cell count, CD4 percentage and viral load) covariates.Of 4871 patients with a confirmed low CD4 cell count, 436 (8.9%) remained untreated. In multivariable analyses, those starting HAART were older [adjusted relative hazard (aRH)/10 years 1.15], were more likely to be female heterosexual (aRH 1.13), were more likely to have had AIDS (aRH 1.14), had a greater number of CD4 measurements 350 cells/μL (aRH/additional count 1.18), had a lower CD4 count over follow-up (aRH/50 cells/μL higher 0.57), had a lower CD4 percentage (aRH/5% higher 0.90) and had a higher viral load (aRH/log(10) HIV-1 RNA copies/ml higher 1.06). Injecting drug users (aRH 0.53), women infected with HIV via nonsexual or injecting drug use routes (aRH 0.75) and those of unknown ethnicity (aRH 0.69) were less likely to commence HAART.A substantial minority of patients with a CD4 count 350 cells/μL remain untreated despite its indication.

The findings on the plain abdominal radiographs of 15 patients with cytomegalovirus (CMV) colitis and AIDS were reviewed and compared to an age, sex, CD4 count and symptom-matched control group. The radiographs were examined for mucosal thickening, bowel dilatation, pneumatosis and perforation. Nodular mucosal lesions were the most significant abnormality in those with CMV colitis being present in seven compared to none in the control group (P = 0.006 two tailed). Differences between the CMV colitis group and the control group as regards the other features were not significant. The finding of pneumatosis is the first time this has been described in patients with CMV colitis and AIDS. No evidence of perforation was demonstrated and this is attributed to a high index of suspicion in those with characteristic signs and symptoms in addition to early sigmoidoscopy and prompt treatment.

We investigated whether adverse responses to highly active antiretroviral therapy (HAART) associated with late HIV presentation are secondary to low CD4 cell count per se or other confounding factors.A longitudinal analysis of the UK Collaborative HIV Cohort (CHIC) Study of individuals starting HAART in 1998-2007 was carried out, comparing late presenters (presenting/starting HAART at a CD4 count200 cells/μL) with late starters (presenting at a CD4 count350 cells/μL; starting HAART at a CD4 count200 cells/μL), using 'ideal starters' (presenting at a CD4 count350 cells/μL; starting HAART at a CD4 count of 200-350 cells/μL) as a comparator. Virological, immunological and clinical (new AIDS event/death) outcomes at 48 and 96 weeks were analysed, with the analysis being limited to those remaining on HAART for3 months.A total of 4978 of 9095 individuals starting first-line HAART with HIV RNA500 HIV-1 RNA copies/mL were included in the analysis: 2741 late presenters, 947 late starters and 1290 ideal starters. Late presenters were more commonly female, heterosexual and Black African. Most started nonnucleoside reverse transcriptase inhibitors (NNRTIs); 48-week virological suppression was similar in late presenters and starters (and marginally lower than in ideal starters); by week 96 differences were reduced and nonsignificant. The median CD4 cell count increase in late presenters was significantly lower than that in late starters (weeks 48 and 96). During year 1, new clinical events were more frequent for late presenters [odds ratio (OR) 2.04; 95% confidence interval (CI) 1.19-3.51; P=0.01]; by year 2, event rates were similar in all groups.Amongst patients who initiate, and remain on, HAART, late presentation is associated with lower rates of virological suppression, blunted CD4 cell count increases and more clinical events compared with late starters in year 1, but similar clinical and immunological outcomes by year 2 to those of both late and ideal starters. Differences between late presenters and late starters suggest that factors other than CD4 cell count alone may be driving adverse treatment outcomes in late-presenting individuals.

We examined the prevalence of hepatitis C virus (HCV) infection among HIV-positive individuals in the UK, trends in HCV testing and the impact of HCV on HIV treatment outcomes. Trends over time in HCV prevalence were calculated using each patient's most recent HCV status at the end of each calendar year. Logistic regression was used to identify factors associated with having a HCV antibody test, and Cox regression was used to determine whether HCV status was associated with the time to experiencing an immunological response to highly active antiretroviral treatment (HAART), time to virological response and viral rebound. Of the 31,765 HIV-positive individuals seen for care between January 1996 and September 2007, 20,365 (64.1%) individuals were tested for HCV, and 1807 (8.9%) had detectable HCV antibody. The proportion of patients in follow-up ever tested for HCV increased over time, from 782/8505 (9.2%) in 1996 to 14,280/17,872 (79.9%) in 2007. Nine thousand six hundred and sixty-nine individuals started HAART for the first time in or after January 2000, of whom, 396 (4.1%) were HCV positive. Presence of HCV infection did not affect initial virological response, virological rebound or immunological response. The cumulative prevalence of HCV in the UK CHIC Study is 8.9%. Despite UK guidelines, over 20% of HIV-positive individuals have not had their HCV status determined by 2007. HCV infection had no impact on HIV virological outcomes or immunological response to HIV treatment. The long-term impact on morbidity and mortality remain to be determined.

We describe the patterns of antiretroviral drug use at treatment initiation from 1996 to 2005 in a large UK multicentre cohort.We examined trends over time and across 10 clinical sites in stage of disease and type of antiretroviral therapy (ART). Multivariable regression was used to identify factors associated with the CD4 cell count at ART initiation, and with the choice of a protease inhibitor (PI) over a nonnucleoside reverse transcriptase inhibitor (NNRTI), and use of nevirapine over efavirenz.A total of 14 252 patients initiated ART, of whom 54% had a CD4 count200 cells/microL. The most important predictors of starting ART at a lower CD4 cell count were being male, nonwhite, and heterosexual or an injecting drug user (P0.0001). Among those starting ART, the use of highly active ART increased from 23% in 1996 to96% from 2000 onwards. There were differences over time and across the clinics in the use of PIs vs. NNRTIs, in the choice of specific PIs, NNRTIs and nucleoside reverse transcriptase inhibitor (NRTI) backbone, and in the rate at which prescribing practices changed.Clinic site and calendar year were important determinants of choice of drug at ART initiation, whereas clinical and demographic characteristics were more important in influencing the CD4 cell count at initiation of ART.

Ibuprofen abuse may be more prevalent than generally considered. Although normally benign, serious complications have been documented. We report an unusual presentation of hypokalaemia and its associated symptoms as a result of Nurofen Plus (200 mg ibuprofen + 12.8 mg codeine phosphate) abuse. Ibuprofen is generally not included in a standard toxicology screen, but should be considered as a rare cause of hypokalaemia.

To determine whether systemic or deep fungal infections can be prevented, a double-blind, placebo-controlled, phase III trial of itraconazole prophylaxis was undertaken in HIV-infected patients.HIV-1 infected patients with CD4 counts300 cells/microL were treated with itraconazole (200 mg per day) or matching placebo and followed for 2 years. Development of deep fungal infections, episodes of mucocutaneous candidiasis, change in CD4 count, survival and safety data were collected at each study visit.Three hundred and seventy-four patients received study medication, 187 were given itraconazole and 187 matching placebo. Time to development of deep fungal infection did not differ between groups, in an intention to treat analysis. Low CD4 cell count and prior use of Pneumocystis carinii pneumonia (PCP) prophylaxis were significantly associated with a more rapid development of deep fungal infection (P = 0.044 and 0.017, respectively). Itraconazole treatment significantly reduced the incidence of oral candidosis (25% vs. 48% P0.001) and time to development of oral candidosis (508 vs. 413 days, P0.001) but not the number of deep fungal infections (11 vs. 13). Survival did not differ significantly between groups (nine vs. 14 deaths). CD4 counts decreased significantly over time in both study arms. Adverse events did not differ between groups; 20% vs. 23% stopped study medication due to an adverse experience.Although itraconazole prophylaxis significantly reduced the number and time to development of oral candidosis, too few episodes of deep fungal infection were noted to determine whether itraconazole prophylaxis was effective for this condition. Chronic itraconazole treatment is well tolerated in HIV-infected patients with marked immunodeficiency.

To evaluate whether successful, long-term immune reconstitution in vivo can be achieved in end-stage AIDS patients following antiretroviral therapy (ART).A 1-year prospective study of changes of CD4+ and CD8+ T-cell surface phenotypes, T-cell receptor (TCR) repertoires and capacity to control in vivo replication of cytomegalovirus (CMV) was performed in five treatment-naive end-stage AIDS patients (median CD4+ T-cell counts of 19 cells/microL) following therapy. Proportions of CD45RA+, CD45RO+ and CD28+ cells within the CD4+ and CD8+ subsets, were determined by flow cytometry. Changes in TCR Vbeta repertoires within the CD4+ and CD8+ T-cell compartments were evaluated using CDR3 spectratyping. CMV replication was determined by a sensitive polymerase chain reaction (PCR) assay using whole blood.Following ART, proportionate increases in 'naive' (CD45RA+) and 'memory' (CD45RO+) T cells were observed within both CD4+ and CD8+ T-cell subsets, while increased numbers of CD28+ T cells were mainly observed within the CD4+ subset. Diversification of CD4+ and CD8+ TCR repertoires was established concomitantly with renewed in vivo control of CMV replication.An important degree of molecular and functional immune recovery is possible in end-stage AIDS patients introduced to therapy. Diversification of TCR repertoires and the in vivo restoration of immunocompetence to control opportunistic infections clearly show that an important degree of molecular immune reconstitution is established following the initiation of ART even in late-stage AIDS.

HIV-infected patients presenting with oral or oesophageal candidosis were randomised to four weeks treatment with itraconazole 200 mg, followed by itraconazole or matching placebo for a prophylaxis phase of 24 weeks. Clinical and mycological evidence of candidosis infection was assessed on a four-weekly basis. Seventy patients were enrolled, of whom 50 completed 28 days of itraconazole therapy; 74% (37 patients) were clinically cured and 40% were also mycologically cured. Fifteen patients were withdrawn for a variety of reasons including non-compliance, adverse events and the use of excluded medications. Forty-four patients were enrolled in the prophylactic phase. There were significantly more relapses of candidosis, and time to candidosis was significantly shorter in the placebo group than in the itraconazole treated group (p = 0.0001). Itraconazole 200 mg daily is effective and well tolerated for the treatment and prevention of oral and oesophageal candidosis in HIV-infected patients.

An interactive voting session at the end of the European symposium on evolving therapies provided an opportunity for panel discussion on various therapeutic options based on a series of case studies. The interactive voting and subsequent discussion focused on the preferred options for first-line, second-line and salvage therapy. In addition, issues of compliance and drug resistance were addressed. All case studies were entirely hypothetical and were projected into the future when it is anticipated that today's investigational drugs are likely to be available for general use.

Acquired immunodeficiency syndrome (AIDS)-defining illnesses are known to occur at different levels of immunosuppression, and the incidence of diagnoses may also vary according to the CD4 lymphocyte count strata. Information about the incidence of disease at different levels of immunosuppression would help clinicians monitoring patients and would allow prophylaxis to be targeted at the most appropriate population.Between 1982 and July 1995, 4883 patients testing positive for the human immunodeficiency virus were seen at either the Royal Free or Chelsea and Westminster Hospitals in London, England. The incidence of each diagnosis, both overall and stratified by CD4 lymphocyte count, was calculated using a person-years analysis. Patients who had no CD4 lymphocyte counts measured during follow-up were excluded from the analysis.During a median follow-up period of 27.6 months, 3875 AIDS-defining illnesses were reported in 1713 patients. The incidence of AIDS-defining illnesses ranged from 6.22 per 100 person-years of follow-up for Pneumocystis carinii pneumonia (95% confidence interval, 5.74-6.70) to 0.37 for extrapulmonary tuberculosis (95% confidence interval, 0.26-0.48). The incidence of each AIDS-defining illness increased as the CD4 lymphocyte count declined; diagnoses such as cytomegalovirus and Mycobacterium avium-intracellulare complex infection had a low incidence at CD4 lymphocyte counts above 0.05x10(9)/L (50/mm3), while Kaposi sarcoma, P carinii pneumonia, and esophageal candidiasis had a high incidence throughout all CD4 lymphocyte count strata.This study provides important information about the risk of AIDS-defining illnesses at lower CD4 lymphocyte counts, enabling disease-specific prophylaxis to be targeted at the most appropriate population. In the future, as more prophylactic therapies are developed, this study will provide historical data of the incidence of diseases before specific prophylaxis was introduced.

We report the first case of aquagenic urticaria in a patient with human immunodeficiency virus (HIV) infection. This is a rare physical urticaria not previously described in this context. The disorder proved unamenable to conventional treatment with antihistamines, but did respond dramatically to stanozolol, suggesting a novel indication for this anabolic steroid.

With the recent identification of a new herpesvirus in patients with Kaposi's sarcoma (human herpesvirus-8 or Kaposi's sarcoma-associated herpesvirus), there have been several reports on the use of anti-herpesvirus therapy (foscarnet, ganciclovir and aciclovir) and risk of developing Kaposi's sarcoma. We therefore investigated the association between use of anti-herpesvirus drugs and Kaposi's sarcoma in a large unselected group of patients with AIDS.We studied a group of HIV-positive patients at the Chelsea and Westminster Hospital, for whom details on all AIDS-defining diagnoses made during follow-up, treatment and regular CD4 counts were available. Cox proportional hazards models with time-dependant covariates were used to assess the association between treatment with aciclovir, foscarnet and ganciclovir and risk of Kaposi's sarcoma.A total of 3688 patients have been followed up for a median period of 4.2 years, during which time 598 patients (16.2%) developed Kaposi's sarcoma. After adjustments for sex, exposure category, age, treatment with antiretrovirals or Pneumocystis carinii pneumonia prophylaxis, the development of AIDS-defining conditions (including separate adjustment for the development of cytomegalovirus and herpes simplex virus) and CD4 count, there was a decreased risk of developing Kaposi's sarcoma with foscarnet [relative hazard (RH), 0.38; 95% confidence interval (CI), 0.15-0.95; P = 0.038] and with ganciclovir (RH, 0.39; 95% CI, 0.19-0.84; P = 0.015), but not with aciclovir (RH, 1.10; 95% CI, 0.88-1.38; P = 0.40).These results suggest that both foscarnet and ganciclovir may have some activity in preventing the occurrence of Kaposi's sarcoma, but that aciclovir has no benefit. Further studies of the effect of these drugs on the risk of Kaposi's sarcoma is warranted.

An HIV-1 p17 subunit vaccine, HGP-30, was evaluated in 38 HIV-1 seronegative individuals in phase I clinical trials in U.K. and U.S.A. The vaccine preparation induced cytotoxic T-cell (CTL) (11/25) and lymphocyte proliferation responses to KLH (19/20) and HGP-30/p17 (24/29) as well as antibody responses to HGP-30 (29/38) and KLH (38/38). The CTL activity was observed in a higher number of vaccine recipients (9/18) in the lower dose groups (10 and 25 micrograms/kg) than the vaccine recipients (2/7) in the 50 and 100 micrograms/kg dose group. These observations suggest that the 10-25 micrograms/kg vaccine dose may preferentially induce TH1 cell responses. TH1 cell responses have been suggested as important in inducing protective cell mediated immunity. The CTL response has been shown to be CD8+. In a pilot study in SCID mice, HIV-1 virus challenge studies in mice reconstituted with cells from an HGP-30 immunized individual showed protection against virus challenge as compared to SCID mice reconstituted with cells from a non-immunized subject. These studies suggest that HGP-30 is capable of inducing protective cellular immunity.

Three hundred and ninety eight serum samples from 270 human immunodeficiency virus (HIV) antibody positive asymptomatic homosexual men were tested in the Abbott and Dupont HIV antigen ELISA tests. In the Abbott test 62 (16%) of the sera were positive, according to the manufacturer's instructions, compared with 55 (14%) in the Dupont test. Twenty six sera were positive with the Abbott test but negative with the Dupont test and 19 sera were positive only by the Dupont test. Only 36 (9%) of the sera were positive in both tests. The Abbott confirmatory neutralisation test gave excellent agreement with the initial Abbott HIV antigen ELISA test; the Dupont confirmatory test was only in agreement with the initial positive Dupont antigen ELISA test in one third of the sera tested. Although the overall sensitivity of each of the two commercial assays tested was similar, the Abbott method may be preferable for clinical purposes if confirmation of an initial ELISA positive test result by neutralisation assay is required.

We report a case of pneumatosis intestinalis (PI) occurring in association with cryptosporidiosis in a patient documented as being HIV-seropositive. Chest and abdominal radiographs taken 2 months previously were normal and the patient did not have any evidence of gastrointestinal infection at that time. The case was complicated by cyst rupture resulting in a pneumoretroperitoneum and pneumomediastinum. The association of pneumatosis and cryptosporidiosis has not been previously reported.

The findings of 27 lymph node biopsies performed on 24 homosexual patients with lymphadenopathy are presented. Six had acquired immune deficiency syndrome (AIDS) and 18 lymphadenopathy only, of whom one subsequently developed AIDS. All these patients had antibodies to the human T-cell lymphotropic virus type III (HTLV-III) suggesting that HTLV-III is currently the commonest cause of lymphadenopathy in homosexual men. The histopathological findings of six of seven nodes from AIDS patients showed either follicular depletion alone or follicular and paracortical lymphocyte depletion. Nodes from four patients showed Kaposi's sarcoma, three of which also showed follicular hyperplasia. In two of these patients there were no cutaneous manifestations of this condition. One lymph node from a patient with persistent generalized lymphadenopathy (PGL) showed Mycobacterium tuberculosis. Six nodes from six other patients have had features oftoxoplasmosis although there was no serological or clinical evidence of recent toxoplasma infection. The remaining 11 lymph nodes from patients with PGL and one node from a patient with transient lymphadenopathy, showed reactive follicular hyperplasia only. We conclude that homosexuals with lymphadenopathy who are HTLV-III antibody positive do not need a routine node biopsy unless an alternative diagnosis is strongly suspected.

The effect of oral secoverine hydrochloride on neostigmine-stimulated sigmoid motility in 12 patients with irritable bowel syndrome was studied in a double-blind placebo-controlled cross-over study. Both spontaneous and stimulated motor activity were significantly reduced by the compound in comparison with placebo. The most sensitive indices were the frequency of wave activity, maximum amplitude and motility index. Two patients reported mild dizziness after secoverine.

Nine of 122 patients dead from AIDS in central London presented with neurological disease, confirmed pathologically in seven. Seven had no other major systemic manifestations. AIDS needs to be considered in the differential diagnosis of meningitis, dementia, diffuse and focal encephalopathies, brainstem syndromes, myelopathy, visual failure and peripheral nerve syndromes. As AIDS becomes more widespread there will be an increasing need for diagnostic HIV testing in many neurological syndromes.

Summary Clinical neurological involvement at various times throughout the illness was recorded in 52% of 122 patients seen in central London who died from acquired immunodeficiency syndrome (AIDS). Various metabolic encephalopathies, dementias, focal encephalopathies, retinopathies and peripheral nerve pathology were the most frequent manifestations. Seven of 9 patients with a neurological presentation had no other major systemic illness. The median time from diagnosis of AIDS to death was 9 months and from onset of neurological symptoms to death 4 months. Human immunodeficiency virus dementia, central nervous system opportunistic infections, presence of Kaposi sarcoma, neurological presentations and minor symptoms were not associated with major change in survival time.

A joint prospective long term study of gastric biopsies has been undertaken to survey intestinal metaplasia Types I, II, and III in terms of their incidence, distribution and value in the selection of high risk cancer patients. This study is based on protocols agreed between three centres for endoscopy, histological interpretation, and mucin histochemistry. The results on the first 1350 gastric biopsies examined during 1981-1982 are presented. Intestinal metaplasia was found in 267 biopsies (20%), being common in association with carcinoma (71%), less so in benign conditions such as gastric ulcer (39%), and chronic gastritis (24%), but rare in 'normal' (3%). Type I intestinal metaplasia was predominant (73%) in all the biopsies with intestinal metaplasia and was most common in benign conditions, 70% in gastric ulcer and 76% in chronic gastritis. Type III intestinal metaplasia (incomplete sulphomucin-secreting intestinal metaplasia) was recorded in only 9.8% of all the biopsies with intestinal metaplasia and had a higher incidence in carcinoma (35%), than in benign conditions (7%) (p less than 0.0001). These results suggest that intestinal metaplasia types may have different malignant potential and their identification may be useful in screening patients for early detection of cancer.

A patient with HIV infection presented with multiple cutaneous Kaposi's sarcomata. Biopsy of one of these showed the presence of amastigotes within an otherwise typical Kaposi's sarcoma. Further investigations proved the patient to have visceral leishmaniasis (kala azar). Visceral leishmaniasis has been reported in HIV infection but it is rare and this presentation is unique. The patient made a good response to a prolonged course of treatment with sodium stibogluconate and allopurinol.