Health literacy refers to the capacities and resources that enable individuals to access, understand, appraise and use health information and services. Among people living with type2 diabetes (T2D) in France, the Entred 3 studyshows that certain aspects of health literacy, particularly engagement with healthcare professionnals and understanding of health information, are socially differentiated and associated with health status. Thejointanalysis of these aspects, complemented by active health management and the ability to navigate within the healthcare system, makes it possible to identify distinct profiles associated with contrasting social and clinical characteristics. Health literacy therefore appears to be a relevant lever for reducing T2D-related social inequalities.
Many epidemiological studies conducted in high-income countries have clearly established that type 2 diabetes disproportionately affects socially disadvantaged populations. In France, the latest epidemiological data confirm this trend and reveal that these inequalities are significant and have worsened overtime. Two population groups are particularly at risk: women and people living in overseas departments and regions. More than a phenomenon limited to the most vulnerable populations, these inequalities are part ofa continuous socioeconomic gradient, affecting all social categories. This observation highlights the importance of systematically adopting a strategy of proportionate universalism, combining universal interventions-accessible to all-but with a graduated intensity, adapted to the specific needs of each social category.
Epidemiological studies demonstrate since more than 20 years a clear link between socioeconomic deprivation and the occurrence of complications or death in people living with diabetes, although longitudinal studies remain rare and adjustments limited. In patients with type 2 diabetes, poverty is associated with an increased risk of microangiopathic and macroangiopathic complications (particularly retinopathy, nephropathy, and neuropathy), as well as increased mortality, particularly from cardiovascular disease and cancer. For type 1 diabetes, the relationship is similar: low socioeconomic status increases the likelihood of severe complications and premature mortality, with a gradient that tends to worsen. These inequalities can be explained by unfavorable health behaviors, individual factors, and structural barriers to accessing care. However, certain equitable healthcare teams or systems appear to mitigate this impact, demonstrating the importance of targeted and proactive public health policy in reducing socioeconomic disparities and their consequences on the health of diabetic patients.
French and international data show that social inequalities, low socioeducational level, and psychiatric disorders are associated with disruptions in care pathways, lack of access to healthcare, and an increased risk of severe diabetes-related complications, particularly in the context of diabetic foot disease. Conversely, coordinated, accessible, and territorially adapted multidisciplinary care, especially when based on proactive outreach ("going toward" approaches), is associated with improved prognosis, regardless of the presence of comorbidities. The quality of the relationship between healthcare professionals and the person receiving care appears to be a central lever for continuity of care. Care pathways may therefore act as a form of "medical compensation" for social deprivation and help reduce health inequalities
Calcium nephrolithiasis is common, recurrent, and associated with comorbidities such as hypertension, diabetes, osteoporosis, and chronic kidney disease. Hypercalciuria, hyperoxaluria, and hyperuricosuria are the primary urinary lithogenic factors. Calcium stone disease and hypercalciuria are promoted by high dietary intakes of sodium, animal protein, and oxalate, and by low calcium intake. Evaluation relies on medical history, stone analysis, and standard blood tests with fasting spot and 24-hour urine collections. Recurrence prevention is primarily dietary: urine output >2,5 L/day, NaCl intake < 5-6 g/day, protein <= 1 g/kg/day, and age-and sex-appropriate calcium intake.
The new consensus on primary hyperparathyroidism, jointly drafted by the SFE, the AFCE and the SFMN, provides a comprehensive and up-to-date overview of the medical literature on this common condition. The text addresses changes in epidemiology and clinical profile, with an increase in asymptomatic and normocalcemic forms. It specifies the diagnostic criteria, details the complications, and highlights the contribution of genetics in identifying syndromic forms. The various treatment options, dominated by minimally invasive surgery but also including medical and percutaneous alternatives, are detailed. The consensus also emphasizes the importance of postoperative follow-up and recurrence prevention, offering readers an up-to-date and practical overview of the management of primary hyperparathyroidism.
Primary hyperparathyroidism (PHPT) is a rare condition in children, possibly underdiagnosed in pregnant women-due to the physiological changes in calcium-phosphate balance during pregnancy-and poses a risk in elderly individuals. At each of these specific stages of life, particular diagnostic and therapeutic considerations must be taken into account.
A functionnal digestive tract is essential to ensure a good nutritional status. Each digestive organ has a specific function, which finally transforms food into nutrients. Therefore, a digestive disease leads to a risk of malnutrition, that may concern up to 75% patients. Management of malnutrition in these situations requires a dietetic approach, based on digestive pathophysiology, and often requires artificial nutrition. Thus, assessing the digestive function, especially absorption, is fundamental to choose an appropriate nutritionnal support (enteral or parenteral).
Age-related changes and the presence ofcognitive disorders, if any, can impact food intake or digestive system function, and contribute to an increased risk of undernutrition. Undernutrition at any age is the result of an imbalance between protein and energy intake and expenditure. The diagnosis of thinness is not based on the same BMI thresholds in subjects aged 70 and over. The threshold for these patients is BMI <22 kg/m2, which is associated with an increased risk of mortality. The consequences of undernutrition can be very serious in an elderly patient, with the onset of other geriatric syndromes such as gait disorders or functional dependence, as well as an increased risk of hospitalization and infection. In the case of neurodegenerative disease, the patient is exposed to several risk factors for undernutrition due to lack of intake and hypercatabolism, which requires appropriate care at every stage of the disease.
In France, in 2023, 433,136 new cases of cancer were diagnosed, with a predominance of men (57%). The median age at diagnosis is 70 for men and 68 for women. The number of cancer cases has doubled during the period 1990-2023. Without appropriate nutritional care, the number of people living with cancer and suffering from malnutrition is likely to increase. Thinness is defined as a BMI below the norm (18,5 kg/m(2 )for people under70, 22 kg/m(2 )for people over 70). What does thinness mean in oncology? How many people suffer from it? What are the consequences? How can we combat cancer-related weight loss?
Thinness is a state of underweight defined by a body mass index < 18,4 kg/m(2). A weight loss is considered significant if it is higher than 5% or5 kg of body weight overa period of6 months. So-called endocrine thinness is linked to an excess or an insufficient hormonal secretion, an appetite loss of central origin, or a lack of development of adipose tissue (lipoatrophy). The 2 most common causes are type 1 diabetes when it is discovered and hyperthyroidism. Other causes are rare: adrenal insuffi ciency, pheochromocytoma, certain forms of diarrhea of endocrine origin or hydro-electrolyte disorders, the exceptional diencephalic cachexia. Finally, generalized lipoatrophies are a cause of apparent thinness.
Diabetes is a complex metabolic disease, with two main forms: type 1 and type 2 diabetes. The hereditary nature depending on the type of diabetes, and their origin is often polygenic. In particular, multiple variants of the genes involved have been identified. Due to this heterogeneity, it is difficult to model these pathologies. However, there are certain other forms of diabetes, including neonatal diabetes and MODY (Maturity Onset Diabetes of the Young), which involve only a single gene. Over the past few decades, the dogma has been to study these monogenic diseases using genetically modified (transgenic) mice. These models have provided fundamental foundations for defining the hierarchy of transcription factors involved in pancreatic development and beta-cell pathophysiology. However, recent studies have shown that there are significant differences between the human and mouse pancreas. In this update, we will examine how the use of stem cells, but also of the generation of human pancreas organoids, allows us to progress in understanding the fundamental biology of these monogenic diabetes and to glimpse the 1(st) therapeutic possibilities emerging from these technological innovations.
Constitutional thinness is a condition characterised bylow body weight, observed from early childhood and persisting into adulthood, with no established organic or functional cause. It is often confused with certain acquired forms of thinness, such as anorexia nervosa. This type of thinness is genetically inheritable. The differential diagnosis is based on the evaluation of weight curves as well as biological and psychometric markers. In terms of diet, affected individuals have a normal energy intake but feel full more quickly. Paradoxically, although they have a positive energy balance, they struggle to gain weight, suggesting anabolic resistance. Constitutional thinness is also associated with osteo-muscular fragility, with reduced bone density and decreased muscle capacity. Therapeutic strategies focus on muscle strengthening and nutritional adjustment, although weight gain is difficult.
Type 2 diabetes mellitus-related neuropathy does not respond, or only poorly, to intensive glycemia control, unlike type 1 diabetes mellitus. This neuropathy, particularly its pain component, is associated with many metabolic factors independent from glycemia, especially obesity and dyslipidemia. It may also be worsened by iatrogenic factors: hypoglycemia, abrupt diabetic decompensation, vitamin B12 deficiencydue to metformin.
The neurological disorders are rare complications with an estimated incidence of between 0,08 and 16% ofbariatric procedures. They occur between 4 months to more than 10 years after surgery. The common presentations are mostly subacute sensory polyneuropathy due to micronutrient deficiencies (especially vitamin B1 and B12, copper, and multiple deficiencies), and mononeuropathy due to entrapmentfollowing majorand rapid weight loss. Inflammatory and immunologic mechanisms may also play a role in these complications. Rare but serious encephalopathies are also possible, including Gayet-Wernicke encephalopathy. Their prognosis can be extremely serious, and resolution of symptoms appears to depend on prompt treatment. Risk factors include gastrointestinal symptoms and lack of nutritional management. Even if procedures with malabsorption are more at risk, no surgery, even purely restrictive types, seems to be immune. Routine monitoring of micronutrient levels, along with patient education to recognize warning signs such as paresthesias, neurogenic pain, and balance disorders.
Many epidemiological, pathophysiological and experimental data suggest a role of metabolic syndrome, particularly excess weight and dys lipidemia, in idiopathic axonal polyneuropathies. Searching for metabolic syndrome and cardiovascular risk factors might therefore be interesting in these neuropathies. However, physical exercise, dietary changes or even anti-obesity drugs have not yet shown to improve these neuro-
Adult-onset hereditary metabolic diseases (AOHMDs) are rarer and less well-known than those in children. However, they are often less severe and, in some cases, treatable. AOHMDs can present with neurological symptoms, particularly peripheral neuropathy. Peripheral neuropathy in AOHMDs may be subclinical, so systematic screening for it in suspected cases can aid in the diagnostic process.
The contexts suggestive of vitamin B1 deficiency are manifold: bariatric surgery, hyperemesis gravidarum, psychiatric disorders, chronic ethylism, etc. The clinicoelectrical phenotype of neuropathy is traditionally motor rather than sensory, painful and generally length-dependent, buta variety of presentations have been described. Differential diagnosis with Guillain-Barre syndrome is crucial and sometimes difficult, relying on the general context (primarily weight loss) and the presence of an insidious onset with secondary acute decompensation. The association with an incomplete Wernicke's triad, or cardiac failure with increased output, is stronglysuggestive of vitamin B1 deficiency. Dosing for vitamin B1 should become a reflex prior to supplementation as soon as a deficiency is suggested as a cause of neuropathy.
The association of diabetes and chronic kidney disease (CKD) is a major public health issue due to its prevalence and to enhanced risk of severe renal and cardiovascular outcomes. The JACARDI program (Joint Action on CARdiovascular diseases and DIabetes), funded by the European Union, aims to promote public health initiatives related to the health of residents of the European partner countries, including France, in the field of cardiovascular diseases and diabetes. In this context, the ambition of the ITINERANCE project is to improve the dissemination and application of preventive measures, according to recent guidelines, in order to reduce the risk of major cardiovascular events and the progression of CKD in people living with diabetes. This initiative is based on an original collaboration between public health stakeholders (4 university hospitals and Sant & eacute; Publique France) and medical biology laboratories, local stakeholders, essential in the care of people with diabetes and CKD.
A better understanding of the molecular causes of rare genetic obesities and their associated phenotypes involving the hypothalamus now allows the consideration of innovative treatments focused on appetite control. These conditions, which combine severe obesity from early childhood, eating disorders, and endocrine and neurodevelopmental comorbidities, are complex to manage because lifestyle changes are more difficult to implement, and bariatric surgery is often less effective and not recommended. New therapies target anomalies in weight regulation, particularly the leptin-melanocor tin pathway, to improve satiety and reduce hyper phagia. This review describes the currently available pharmacological treatments, as well as those under clinical evaluation. The positioning of these treatments in the management of these patients needs to be well defined to develop precision medicine for genetic forms of obesity.
