IgA Vasculitis in an Adult Linked to Cryptosporidium and Giardia Co-Infection: A Comprehensive Case Study.

BACKGROUND Immunoglobulin A (IgA) vasculitis is a small-vessel vasculitis characterized by the deposition of IgA immune complexes primarily in the skin, kidneys, and gastrointestinal tract. While it predominantly affects children, cases in adults are associated with more severe manifestations. Evidence suggests that infectious triggers play a pivotal role in its etiology. Often, it follows a self-limiting course and doesn't necessitate intervention. CASE REPORT We present the case of a 51-year-old man who presented with a maculopapular rash, arthralgia, and abdominal pain. An examination revealed a purpuric rash on lower extremities and abdomen. A lower extremity duplex ultrasound identified deep vein thrombosis (DVT) in the right leg. Skin biopsy of the rash confirmed the diagnosis of IgA vasculitis, demonstrating perivascular neutrophilic infiltrate and IgA complex deposition. Stool studies revealed co-infection with Cryptosporidium and Giardia. The patient was treated with a prednisone taper with significant improvement in symptoms. CONCLUSIONS This case highlights the potential role of Cryptosporidium as a trigger for IgA vasculitis. The presence of concurrent infections underscores the complex interplay between infections and the development of IgA vasculitis. The co-infection with Giardia suggests that a secondary infection may be involved, further complicating the disease's etiology. The observation of DVT suggests a possible link between IgA vasculitis and a prothrombotic state. This report serves to expand the knowledge of IgA vasculitis triggers and associated complications, guiding clinicians in diagnosing and managing similar cases while emphasizing the importance of vigilance in adults with these symptoms.

Diabetes: Risk factor and translational therapeutic implications for Alzheimer's disease.

Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) commonly co-occur. T2DM increases the risk for AD by approximately twofold. Animal models provide one means of interrogating the relationship of T2DM to AD and investigating brain insulin resistance in the pathophysiology of AD. Animal models show that persistent hyperglycaemia results in chronic low-grade inflammation that may contribute to the development of neuroinflammation and accelerate the pathobiology of AD. Epidemiological studies suggest that patients with T2DM who received treatment with specific anti-diabetic agents have a decreased risk for the occurrence of AD and all-cause dementia. Agents such as metformin ameliorate T2DM and may have other important systemic effects that lower the risk of AD. Glucagon-like peptide 1 (GLP-1) agonists have been associated with a decreased risk for AD in patients with T2DM. Both insulin and non-insulin anti-diabetic treatments have been evaluated for the treatment of AD in clinical trials. In most cases, patients included in the trials have clinical features of AD but do not have T2DM. Many of the trials were conducted prior to the use of diagnostic biomarkers for AD. Trials have had a wide range of durations and population sizes. Many of the agents used to treat T2DM do not cross the blood brain barrier, and the effects are posited to occur via lowering of peripheral hyperglycaemia and reduction of peripheral and central inflammation. Clinical trials of anti-diabetic agents to treat AD are ongoing and will provide insight into the therapeutic utility of these agents.