Significance: Cancer-associated tissue-specific lactic acidosis stimulates and mediates tumor invasion and metastasis and is druggable. Rarely, malignancy causes systemic lactic acidosis, the role of which is poorly understood. Recent Advances: The understanding of the role of lactate has shifted dramatically since its discovery. Long recognized as only a waste product, lactate has become known as an alternative metabolism substrate and a secreted nutrient that is exchanged between the tumor and the microenvironment. Tissue-specific lactic acidosis is targeted to improve the host body's anticancer defense and serves as a tool that allows the targeting of anticancer compounds. Systemic lactic acidosis is associated with poor survival. In patients with solid cancer, systemic lactic acidosis is associated with an extremely poor prognosis, as revealed by the analysis of 57 published cases in this study. Although it is considered a pathology worth treating, targeting systemic lactic acidosis in patients with solid cancer is usually inefficient. Critical Issues: Research gaps include simple questions, such as the unknown nuclear pH of the cancer cells and its effects on chemotherapy outcomes, pH sensitivity of glycosylation in cancer cells, in vivo mechanisms of response to acidosis in the absence of lactate, and overinterpretation of in vitro results that were obtained by using cells that were not preadapted to acidic environments. Future Directions: Numerous metabolism-targeting anticancer compounds induce lactatemia, lactic acidosis, or other types of acidosis. Their potential to induce acidic environments is largely overlooked, although the acidosis might contribute to a substantial portion of the observed clinical effects. Antioxid. Redox Signal. 37, 1130-1152.

• Klíčová slova
• drug delivery, drug targeting, lactate, lactic acidosis, sodium bicarbonate, solid cancer,
• MeSH
• acidóza laktátová * MeSH
• kyselina mléčná MeSH
• lidé MeSH
• mezery v důkazech MeSH
• nádorové mikroprostředí MeSH
• nádory * komplikace   farmakoterapie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• kyselina mléčná MeSH

INTRODUCTION: The aim of this study is to present a case of 44 years old woman with topiramate induced metabolic acidosis and kidney stones. MATERIALS AND METHODS: The laboratory features of topiramate caused renal tubular acidosis in blood and urine during topiramate treatment, with correction of metabolic acidosis by potassium citrate, and after topiramate withdrawal are presented. Differential diagnosis of all possible causes of metabolic acidosis is discussed. RESULTS: The results revealed negative base excess in extracellular fluid of - 9.2 mmol/L, low serum HCO3- concentration (18.6 mmol/L), trend to alkaline urine (pH 6.39) and low urine citrate concentration (0.3 mmol/24h). After topiramate withdrawal, all parameters of the internal environment normalized. CONCLUSIONS: This study has shown that long-term topiramate administration could induce metabolic acidosis and consequently urholithiasis. Thus, we could recommend testing blood acid base balance, urinary pH and citrates in patients taking topiramate and suffering from kidney stones.

• Klíčová slova
• acidosis, glomerular filtration rate, renal tubular acidosis, topiramate, urolithiasis,
• MeSH
• acidóza chemicky indukované   MeSH
• antikonvulziva škodlivé účinky   MeSH
• dospělí MeSH
• fruktosa škodlivé účinky   analogy a deriváty   MeSH
• ledvinové kameny chemicky indukované   MeSH
• lidé MeSH
• migréna prevence a kontrola   MeSH
• nenasazení léčby MeSH
• topiramat MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• antikonvulziva MeSH
• fruktosa MeSH
• topiramat MeSH

BACKGROUND: Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis with normal or only moderately elevated glycemia. The mechanisms are not fully understood but involve increased ketogenesis and complex renal metabolic dysfunction, resulting in both ketoacidosis and hyperchloremic acidosis. We report a rare case of fatal empagliflozin-associated acidosis with profound hyperchloremia and review its pathogenesis. CASE PRESENTATION: A patient with type 2 diabetes mellitus treated with empagliflozin underwent an elective hip replacement surgery. Since day 4 after surgery, he felt generally unwell, leading to cardiac arrest on the day 5. Empagliflozin-associated euglycemic diabetic ketoacidosis with severe hyperchloremic acidosis was identified as the cause of the cardiac arrest. CONCLUSIONS: This unique case documents the possibility of severe SGLT2 inhibitor-associated mixed metabolic acidosis with a predominant hyperchloremic component. Awareness of this possibility and a high index of suspicion are crucial for correct and early diagnosis.

• Klíčová slova
• Case report, Empagliflozin, Euglycemic ketoacidosis, Hyperchloremic acidosis, SGLT2 inhibitor,
• MeSH
• acidóza * chemicky indukované   komplikace   MeSH
• diabetes mellitus 2. typu * komplikace   farmakoterapie   MeSH
• diabetická ketoacidóza * diagnóza   MeSH
• glifloziny * škodlivé účinky   MeSH
• lidé MeSH
• srdeční zástava * MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• empagliflozin MeSH Prohlížeč
• glifloziny * MeSH

A 4-year-old boy suffering from hypocitraturic and hypercalciuric renal tubular acidosis with nephrolithiasis and nephrocalcinosis is reported. Renal function tests indicated that the patient had type 1 renal tubular acidosis. Potassium citrate rather than potassium bicarbonate, sodium citrate or bicarbonate is the preferred treatment for stones in RTA-I.

• MeSH
• antacida terapeutické užití   MeSH
• citráty metabolismus   terapeutické užití   MeSH
• kyselina citronová MeSH
• lidé MeSH
• nefrokalcinóza komplikace   farmakoterapie   moč   MeSH
• oxid uhličitý metabolismus   MeSH
• poruchy metabolismu vápníku komplikace   moč   MeSH
• předškolní dítě MeSH
• renální tubulární acidóza komplikace   farmakoterapie   moč   MeSH
• vyšetření funkce ledvin MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• předškolní dítě MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• antacida MeSH
• citráty MeSH
• kyselina citronová MeSH
• oxid uhličitý MeSH

• MeSH
• acidóza enzymologie   veterinární   MeSH
• bachor enzymologie   MeSH
• kolorimetrie MeSH
• koncentrace vodíkových iontů MeSH
• nemoci skotu enzymologie   MeSH
• oxidace-redukce MeSH
• oxidoreduktasy analýza   metabolismus   MeSH
• skot MeSH
• spektrofotometrie MeSH
• trávení MeSH
• zvířata MeSH
• Check Tag
• skot MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• oxidoreduktasy MeSH

• Klíčová slova
• ACIDOSIS/complications *, HYPERTENSION/complications *, PULMONARY EMPHYSEMA/complications *, PULMONARY HEART DISEASE/complications *,
• MeSH
• acidóza komplikace   MeSH
• cor pulmonale komplikace   MeSH
• emfyzém * MeSH
• hypertenze komplikace   MeSH
• lidé MeSH
• nemoci cév * MeSH
• plicní emfyzém komplikace   MeSH
• plicní hypertenze * MeSH
• respirační acidóza * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Topical carbonic anhydrase inhibitors (CAI), used for treatment of glaucoma, are generally regarded as safe and unconnected with systemic side effects. We report an unusual case of fatigue, metabolic acidosis, and normocytic anaemia associated with ocular administration of the CAI, dorzolamide, in a patient with impaired renal function. In chronic kidney disease, where CAI elimination may be decreased, and patients prone to develop metabolic acidosis, systemic absorption of ocular administered CAI could lead to rare, but potentially serious adverse reaction, that are a consequence of inhibition of extraocular carbonic anhydrase isoenzymes.

• Klíčová slova
• carbonic anhydrase inhibitor, dorzolamide, drug-induced anaemia, drug-induced metabolic acidosis,
• MeSH
• acidóza chemicky indukované   MeSH
• anemie chemicky indukované   MeSH
• aplikace oční MeSH
• glaukom farmakoterapie   MeSH
• inhibitory karboanhydras aplikace a dávkování   škodlivé účinky   MeSH
• lidé středního věku MeSH
• lidé MeSH
• renální insuficience komplikace   MeSH
• sulfonamidy aplikace a dávkování   škodlivé účinky   MeSH
• thiofeny aplikace a dávkování   škodlivé účinky   MeSH
• únava chemicky indukované   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• dorzolamide MeSH Prohlížeč
• inhibitory karboanhydras MeSH
• sulfonamidy MeSH
• thiofeny MeSH

Metabolic acidosis is a major risk factor of kidney disease progression as a consequence of impaired H+ urinary excretion by the decreased kidney NH3 synthesis. Two key enzymes participate: a) Phosphate-dependent glutaminase under the genomic control of metabolic acidosis and b) Phosphate independent glutaminase localized on proximal tubule microvili under the nongenomic control. Two types of kidney disease metabolic acidoses are dominant: a) Hyperchloremic metabolic acidosis usually on the basis of hereditary or toxic alterations, isolated or as a part of Fanconi syndrome. b) Hyperphosphatemic metabolic acidosis of renal insufficiency. Metabolic acidosis shares serious consequences: metabolic acidosis increases protein catabolism of amino acids, inhibits proteosynthesis (albumin!), accelerates renal osteodystrophy development, modulates calcidiol and parathormone plasma levels and evokes insulin resistance. The present therapy requires full correction of metabolic acidosis!

• MeSH
• glutamin fyziologie   MeSH
• ledviny patofyziologie   MeSH
• lidé MeSH
• renální tubulární acidóza komplikace   patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• glutamin MeSH

D-lactic acidosis represents a rare form of metabolic acidosis that occurs most commonly in patients with short bowel syndrome. This is a serious, sometimes life-threatening complication. The cause is the accumulation of D-lactate in the body, which is formed in excessive amounts by fermentation of unabsorbed carbohydrates by the intestinal microbiota. The nervous system is predominantly affected, which also results in clinical manifestations. The clinical picture is dominated by a wide range of non-specific neurological symptoms. The disease can sometimes manifest as somnolence to coma. From the aspect of laboratory diagnostics, the disease is characterized by severe metabolic acidosis with an increased anion gap. In this case report, we present a unique case of a 54-year-old woman with Crohns disease and short bowel syndrome who in a short time was repeatedly hospitalized for recurrence of severe metabolic acidosis with severe impaired consciousness. Based on the evaluation of anamnestic data, clinical picture and laboratory tests, the patient was diagnosed with D-lactic acidosis. In the discussion we discuss the individual steps that led to this diagnosis and compare our experience with data in the world literature.

• Klíčová slova
• D-lactic acidosis, encephalopathy, short bowel syndrome,
• MeSH
• acidóza laktátová * komplikace   diagnóza   MeSH
• acidóza * MeSH
• kyselina mléčná MeSH
• lidé středního věku MeSH
• lidé MeSH
• syndrom krátkého střeva * komplikace   diagnóza   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• kyselina mléčná MeSH

Pseudohypoaldosteronism type 2 (PHA2) is a rare inherited condition of altered tubular salt handling. It is characterized by the specific constellation of hyperkalaemic hyporeninemic hypertension, hyperchloremic metabolic acidosis and hypercalciuria. Molecular genetic testing confirms the diagnosis in the majority of cases. Thiazides constitute effective treatment. Due to its rarity, the diagnosis is often delayed. We here present two children with PHA2, who were initially treated with fludrocortisone and bicarbonate complicated mainly by exacerbation of their hypertension. Discontinuation of their previous therapy and commencement of thiazide diuretics led to normalisation of their blood pressure and electrolyte and acid-base status.

• Klíčová slova
• Gordon syndrome, Hyporeninemic hypertension, Pseudohypoaldosteronism type 2, Thiazides,
• MeSH
• acidóza * diagnóza   etiologie   MeSH
• dítě MeSH
• fludrokortison terapeutické užití   MeSH
• hyperkalemie * diagnóza   etiologie   MeSH
• hypertenze * etiologie   farmakoterapie   diagnóza   MeSH
• krevní tlak * účinky léků   MeSH
• lidé MeSH
• pseudohypoaldosteronismus * diagnóza   komplikace   farmakoterapie   genetika   patofyziologie   MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• fludrokortison MeSH