Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using medical manuscripts and texts from the Byzantine period (330-1453), this article describes various, to date little discussed, aspects of Byzantine nosology, public health and therapeutics. Many diseases in the Byzantine era were widespread and had a high morbidity such as respiratory disease, various kinds of anaemia, pestilential diseases (e.g. quartan fever, plague, dysentery and cholera), parasitic diseases, orthopaedic, rheumatic and psychiatric disorders, trachoma and alcoholism. Other very serious and relatively frequent conditions included leprosy, mania, gout, cancerous tumours and ulcers. Important elements of nephrology and various renal diseases were described and investigated, such as acute and chronic renal failure, acute and chronic nephritis, pyelonephritis, necrotic renal diseases, crush syndrome, and ulcers of the kidneys, i.e. tuberculosis or renal tumours. The microhistology and physiology of the kidneys were first studied by Oribasius, who discerned the existence of the capillaries--tau rho iota chi omicron epsilon iota delta eta--some centuries before Malpighi. He also correctly described the blood circulation, general and pulmonary, as a precursor to Harvey. The first hospitals were organised during the Byzantine period, and the practice of Byzantine medical science and its social applications were regulated by a special medical legislation and deontology. Byzantine medicine was fruitfully connected with the Christian faith and developed the supreme model of the saints unmercenary--alpha nu alpha rho gamma epsilon rho omicron iota--physicians such as Cosmas and Damian (3rd century), Panteleemon (3rd-4th centuries) and the women physicians and miracle-worker saints, Zenais and Philonilla (1st century), the 'friends of peace', and Hermione (1st-2nd centuries).
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PMID:Diseases in the Byzantine world with special emphasis on the nephropathies. 918 37

The clinical history of lithium began in mid-19th century when it was used to treat gout. It was subsequently administered as a substitute for sodium chloride and towards the end of 1940 its effects for the control of mania were discovered. At present it is used effectively for treatment of mania and for the prophylaxis of bipolar disorder. Though its effect on affective illnesses is evident, the same cannot be said of its mechanism of action, since in spite of the numerous studies performed to date it is still not known exactly how this ion acts. Many theories have been proposed, the most important of which are: normalisation of possible ionic alterations; interactions with the adenylyl cyclase cAMP system; effects on the phosphatidylinositol cycle; stabilisation of the levels of neuroprotective proteins; normalisation of the values of some cytosolic endopeptidases; etc. In any case, it has yet to be determined which of these is the principal factor responsible for lithium's therapeutic action, while at the same time the possibility cannot be totally ruled out that its precise mechanism of action is still to be discovered.
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PMID:[Lithium: 55 years of history in the therapy of bipolar affective disorder]. 1726 94

Lithium is derived from the Greek word "lithia" which means "stone." Since its discovery by the Swedish chemist Arfedsson in the year 1817, it has been used for treatment of gout, hypertension, uremia, and rheumatism. Currently, lithium is the treatment of choice for the long-term control of mania and to prevent relapse in bipolar disorder. It has a narrow therapeutic index (0.6-1.2 mEq/L). Lithium overdose has been associated with a wide range of cardiovascular complications including cardiac arrhythmias and interstitial myocarditis. We present a review of published cases relevant to lithium-related cardiotoxicity.
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PMID:Sinus node dysfunction in association with chronic lithium therapy: a case report and review of literature. 1935 46

Uric acid and purines (such as adenosine) regulate mood, sleep, activity, appetite, cognition, memory, convulsive threshold, social interaction, drive, and impulsivity. A link between purinergic dysfunction and mood disorders was first proposed a century ago. Interestingly, a recent nationwide population-based study showed elevated risk of gout in subjects with bipolar disorder (BD), and a recent meta-analysis and systematic review of placebo-controlled trials of adjuvant purinergic modulators confirmed their benefits in bipolar mania. Uric acid may modulate energy and activity levels, with higher levels associated with higher energy and BD spectrum. Several recent genetic studies suggest that the purinergic system - particularly the modulation of P1 and P2 receptor subtypes - plays a role in mood disorders, lending credence to this model. Nucleotide concentrations can be measured using brain spectroscopy, and ligands for in vivo positron emission tomography (PET) imaging of adenosine (P1) receptors have been developed, thus allowing potential target engagement studies. This review discusses the key role of the purinergic system in the pathophysiology of mood disorders. Focusing on this promising therapeutic target may lead to the development of therapies with antidepressant, mood stabilization, and cognitive effects.
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PMID:Purinergic system dysfunction in mood disorders: a key target for developing improved therapeutics. 2544 63

Purinergic system plays a role in the regulation of many psychological processes, including mood and activity. It consists of P1 receptors, with adenosine as the agonist, and P2 receptors, activated by nucleotides (e.g., adenosine 5'-triphosphate - ATP). Propounded disturbances of uric acid in affective disorders were related to the introduction of lithium for the treatment of these disorders in the 19th and 20th century. At the beginning of the 21st century, new evidence was accumulated concerning a role of uric acid in the pathogenesis and treatment of bipolar disorder (BD). In patients with BD, higher prevalence of gout and increased concentration of uric acid have been found as well as the therapeutic activity of allopurinol, used as an adjunct to mood stabilizers, has been demonstrated in mania. In recent years, the research on the role of the purinergic system in the pathogenesis and treatment of affective disorders and schizophrenia focuses on the role of adenosine (P1) receptors and nucleotide (P2) receptors. Activation of adenosine receptors is related to an antidepressant activity. Alterations of P2 receptors are also significant for the pathogenesis of affective disorders. The role of purinergic system in schizophrenia is related to the effect of adenosine and nucleotide receptors on dopaminergic and glutamatergic neurotransmission. A lot of data indicate that schizophrenia is related to a deficit of adenosine system. Changes in the purinergic system are also significant for psychopathological symptoms of schizophrenia and for the action of antipsychotic drugs.
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PMID:Disturbances of purinergic system in affective disorders and schizophrenia. 3152 98