Electrolyte, acid-base, and mineral metabolism disorders are among the most common and clinically significant problems experienced in internal medicine patients. Their development reflects disturbances in regulated homeostatic mechanisms involving the kidneys, bones, endocrine systems, and cellular ion transport. Disorders such as hyponatremia, hypernatremia, hypokalemia, hyperkalemia, metabolic acidosis, metabolic alkalosis, and abnormalities of calcium and phosphorus metabolism are associated with substantial morbidity and mortality when not promptly recognized and appropriately treated. Accurate diagnosis requires a deep understanding of the underlying pathophysiology, assessment of volume status, interpretation of laboratory findings, and identification of contributing kidney, endocrine, medications, and systemic factors. This review describes the physiological mechanisms governing electrolyte and acid-base homeostasis and discusses the clinical presentation, diagnostic evaluation, and evidence-based management of common electrolyte disorders encountered by Internists. We place emphasis on distinguishing etiologies and applying practical diagnostic algorithms to guide treatment decisions. In addition, the review highlights the interconnected regulation of calcium and phosphorus by parathyroid hormone, vitamin D, and fibroblast growth factor 23 and its relevance in kidney disease and other disorders. By integrating foundational physiology with current clinical practice guidelines, this review provides internists with a practical framework to solve electrolyte issues they face with confidence.

Progressive multiple sclerosis (PMS) represents a severe and disabling form of MS characterized by a gradual accumulation of neurological impairment and limited responsiveness to conventional disease-modifying therapies. Unlike the relapsing forms of the disease, progressive MS is driven not only by peripheral immune dysregulation but also by persistent neuroinflammation, microglial activation, mitochondrial dysfunction, and progressive neurodegeneration within the central nervous system. These complex and overlapping pathogenic mechanisms contribute to irreversible axonal loss and pose significant challenges for therapeutic intervention. Although recent advances in immunomodulatory treatments have improved outcomes for some patients, currently available therapies provide only limited benefits in slowing disease progression. Consequently, the identification of novel molecular pathways and therapeutic targets has become a major focus in the development of more effective strategies for progressive MS. Rapid progress in understanding the cellular and molecular basis of disease progression has facilitated the exploration of innovative therapeutic approaches, including targeted immunotherapies, neuroprotective agents, remyelination-promoting strategies, and emerging cell-based interventions. Here, in this review, we summarize current advances in the therapeutic landscape of progressive MS, highlighting recently approved treatments as well as promising agents under clinical investigation. Particular emphasis is placed on the underlying mechanisms of action of these therapies and their potential to modify disease progression, restore neural function, and support the development of personalized treatment strategies for patients with PMS.

Hypothermia is classically defined as a reduction in the body's core temperature below 95.0°F (35.0 °C). Most reported cases of hypothermia are due to environmental exposure to low ambient temperatures (accidental hypothermia). Other causes of hypothermia include sepsis, severe hypothyroidism (myxedema coma), acute spinal cord injury, diabetic ketoacidosis, multisystem trauma, and prolonged cardiac arrest. Frostbite, chillblain and trench foot all have specific therapies to prevent limb loss. There have been significant advances in these therapeutic options over the past decade which are detailed in this issue.