Inherited Metabolic Diseases (IMDs) are rare genetic disorders with an enzyme and/or transport system dysfunction of a metabolic pathway. Infections frequently induce Acute Metabolic Decompensation (AMD) in patient with IMDs, and may also compromise the outcome of disorders not primarily recognized as crisis prone. On the other hand, immunocompromise resulting from metabolic defects can render the host more vulnerable to recurrent or severe infections. Metabolic syndrome (MetS) is a cluster of metabolic symptoms, including visceral obesity, insulin resistance, glucose intolerance, dyslipidemia, and hypertension that are interlinked to cause increased population risk of chronic disease and impaired immune defences. The worldwide prevalence of obesity, a main contributor for MetS, nearly tripled between 1975 and 2018 and over half of all adults are predicted to be obese by 2050. In addition to NCDs, MetS modulates host-pathogen interactions, rendering the host more susceptible to severe viral infections including flu and coronaviruses. Here, we review recent findings that challenge this dogma and demonstrate a new concept in the regulation of host defense: early metabolic reprogramming of both immune and nonimmune cells powerfully determines infection outcome, severity of disease, and long term health. This review discusses the relationships between IMDs and infections in a bidirectional manner examining mechanisms, impact of diet, immune metabolic disturbances, and novel treatments.

Background: Malaria remains a major public health concern in Sudan, predominantly caused by Plasmodium falciparum, while Plasmodium vivax continues to emerge in several regions. Thrombocytopenia is frequently associated with malaria infection, yet its pattern and severity vary between species. This study investigated the occurrence of thrombocytopenia among malaria infected individuals in Sinnar and Khartoum States.

Methods: A cross sectional, hospital-based study was conducted between November and March 2020. A total of 160 EDTA blood samples were collected from malaria suspected patients. Malaria diagnosis was performed using Rapid Diagnostic Tests (RDTs) and Giemsa stained blood films. Platelet counts were measured using an automated hematology analyzer (SYSMEX KX 21). Data were analyzed using SPSS version 22.

Results: Of the 160 malaria positive participants, P. falciparum accounted for 77.5% (n=124), while P. vivax represented 22.5% (n=36). Thrombocytopenia was more prevalent among P. falciparum cases, with 56.2% exhibiting abnormal platelet counts, compared to 8.8% in P. vivax cases. Males represented 60.6% of infected individuals. The highest infection rate occurred in the age group 1–25 years (47.5%). A statistically significant association was found between malaria species and platelet count abnormalities (p = 0.000).

Conclusion: Thrombocytopenia is a common hematological abnormality in malaria, particularly in P. falciparum infections. Its presence may assist clinicians in supporting malaria diagnosis, monitoring disease severity, and guiding management decisions.