Mpox in people with advanced HIV infection: a global case series.

BACKGROUND: People living with HIV have accounted for 38-50% of those affected in the 2022 multicountry mpox outbreak. Most reported cases were in people who had high CD4 cell counts and similar outcomes to those without HIV. Emerging data suggest worse clinical outcomes and higher mortality in people with more advanced HIV. We describe the clinical characteristics and outcomes of mpox in a cohort of people with HIV and low CD4 cell counts (CD4 <350 cells per mm3). METHODS: A network of clinicians from 19 countries provided data of confirmed mpox cases between May 11, 2022, and Jan 18, 2023, in people with HIV infection. Contributing centres completed deidentified structured case report sheets to include variables of interest relevant to people living with HIV and to capture more severe outcomes. We restricted this series to include only adults older than 18 years living with HIV and with a CD4 cell count of less than 350 cells per mm3 or, in settings where a CD4 count was not always routinely available, an HIV infection clinically classified as US Centers for Disease Control and Prevention stage C. We describe their clinical presentation, complications, and causes of death. Analyses were descriptive. FINDINGS: We included data of 382 cases: 367 cisgender men, four cisgender women, and ten transgender women. The median age of individuals included was 35 (IQR 30-43) years. At mpox diagnosis, 349 (91%) individuals were known to be living with HIV; 228 (65%) of 349 adherent to antiretroviral therapy (ART); 32 (8%) of 382 had a concurrent opportunistic illness. The median CD4 cell count was 211 (IQR 117-291) cells per mm3, with 85 (22%) individuals with CD4 cell counts of less than 100 cells per mm3 and 94 (25%) with 100-200 cells per mm3. Overall, 193 (51%) of 382 had undetectable viral load. Severe complications were more common in people with a CD4 cell count of less than 100 cells per mm3 than in those with more than 300 cells per mm3, including necrotising skin lesions (54% vs 7%), lung involvement (29% vs 0%) occasionally with nodules, and secondary infections and sepsis (44% vs 9%). Overall, 107 (28%) of 382 were hospitalised, of whom 27 (25%) died. All deaths occurred in people with CD4 counts of less than 200 cells per mm3. Among people with CD4 counts of less than 200 cells per mm3, more deaths occurred in those with high HIV viral load. An immune reconstitution inflammatory syndrome to mpox was suspected in 21 (25%) of 85 people initiated or re-initiated on ART, of whom 12 (57%) of 21 died. 62 (16%) of 382 received tecovirimat and seven (2%) received cidofovir or brincidofovir. Three individuals had laboratory confirmation of tecovirimat resistance. INTERPRETATION: A severe necrotising form of mpox in the context of advanced immunosuppression appears to behave like an AIDS-defining condition, with a high prevalence of fulminant dermatological and systemic manifestations and death. FUNDING: None.

Gallstones are associated with carotid atherosclerosis.

BACKGROUND/AIMS: Gallstone disease (GD) and cardiovascular disease (CD) are common diseases worldwide with considerable economical impact and they are strongly associated. Carotid atherosclerosis is an excellent marker of risk for CD like stroke and myocardial infarction. The aim of this study was to assess the association between gallstones and carotid atherosclerosis. METHODS: A cross-sectional study was conducted. We evaluated subjects with ultrasonographical evidence of GD and asymptomatic subjects without such evidence. Anthropometric, clinical and biochemical variables were collected. The Metabolic syndrome was evaluated using adult treatment panel III criteria. Carotid artery intima-media thickness (CIMT) was determined by a standard ultrasound protocol. Insulin-like growth factor-1 (IGF-1) serum levels were measured in all subjects. RESULTS: We studied 191 subjects: 62 subjects with GD (53.2% males) and 129 asymptomatic subjects without GD (65.9% males). Subjects with GD exhibited a higher body mass index, body fat percent, insulin serum levels and CIMT (P<0.05 for all). The prevalence of GD was higher in subjects with a CIMT>0.75 independently of other factors [odds ratio (OR) 2.12, 95% confidence interval (CI) 1.04-4.34; P=0.039], and for every 0.1 mm increase in CIMT the independent probability to be a case of GD increased by a factor of 1.25 (95% CI 1.02-1.53; P=0.027). IGF-1 levels did not differ among groups. CONCLUSIONS: Subjects with GD exhibit greater carotid atherosclerosis, and therefore have a higher risk for stroke and myocardial infarction.

Effect of Helicobacter pylori infection on gastric ghrelin expression and body weight.

BACKGROUND & AIM: Ghrelin is a peptide mainly produced by gastric tissue playing an important role in energy homeostasis. It has been suggested that inflammatory and atrophic events induced by Helicobacter pylori (H. pylori) infection in gastric mucosa compromise the survival of the ghrelin-producing cells. The aim of this study was to investigate the effect of H. pylori infection on gastric ghrelin expression and body weight. METHODS: Consecutive patients referred for upper endoscopy were invited to participate. Patients with H. pylori infection (determined by histology) were defined as cases and patients without infection as controls. The density of colonization was classified in mild, moderate, or severe infection. Body mass index (BMI) was calculated. Ghrelin-immunoreactive cells were quantified in gastric biopsies by immunohistochemical staining. RESULTS: We studied 189 cases (92 males, 97 females) and 94 controls (55 males, 39 females). Cases were older (48.16 +/- 16.44 vs. 42.88 +/- 17.04 years, p < 0.05) and exhibited a lower percentage of ghrelin-immunoreactive cells (2.13% vs. 10.43%, p < 0.05) than controls. The prevalence of obesity was significantly lower than normal-weight among all cases, independently of the severity of infection (mild infection, 17.6% vs. 47.3%, p = 0.001; moderate-severe infection, 10.4% vs. 50%, p = 0.001). Univariate analysis showed a non-significant trend suggesting a protective effect of H. pylori against obesity. Nevertheless, BMI did not differ significantly between cases and controls. CONCLUSION: Chronic H. pylori infection contributes to a lower percentage of gastric ghrelin-immunoreactive cells but has no effect on the body weight of infected patients.