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ACETOLAZAMIDE USING IN IDIOPATHIC INTRACRANIAL HYPERTENSION
Akhmadov Jakhongir Akmal ugli
Asian International University, Bukhara, Uzbekistan
https://doi.org/10.5281/zenodo.15242502
Abstract.
The management of patients with idiopathic intracranial hypertension (IIH) has
been guided primarily by informed opinion, clinical experience, and a small number of primarily
retrospective studies. Given the results of the IIH Treatment Trial (IIHTT), there is now evidence
supporting the use of acetazolamide for patients with IIH, especially with visual loss.
Acetazolamide, a compound developed in the 1950s as a diuretic drug and presently used as an
antiglaucoma, antiepileptic and diuretic agent, is effective in the treatment of IIH. is a low
nanomolar inhibitor of Carbonic anhydrase(CA) isoforms involved in cerebrospinal fluid (CSF)
secretion. Inhibition of brain/choroid plexus CA II, IV, VA and XII leads to a decreased CSF
fluid secretion and control of the intracranial pressure.
Keywords:
acetazolamide, carbonic anhydrase, intracranial hypertension, cerebral fluid
secretion, pressure, convoluted tubule.
ИСПОЛЬЗОВАНИЕ АЦЕТОЛАЗАМИДА ПРИ ИДИОПАТИЧЕСКОЙ
ВНУТРИЧЕРЕПНОЙ ГИПЕРТЕНЗИИ
Аннотация.
Лечение пациентов с идиопатической внутричерепной гипертензией
(ИВГ) в первую очередь основывалось на информированном мнении, клиническом опыте и
небольшом количестве преимущественно ретроспективных исследований. Учитывая
результаты исследования лечения ИВГ (IIHTT), в настоящее время имеются
доказательства, подтверждающие применение ацетазоламида у пациентов с ИВГ,
особенно с потерей зрения. Ацетазоламид, соединение, разработанное в 1950-х годах как
диуретическое средство и в настоящее время используемое как противоглаукомное,
противоэпилептическое и диуретическое средство, эффективно при лечении ИВГ.
является низконаномолярным ингибитором изоформ карбоангидразы (КА), участвующих
в секреции спинномозговой жидкости (СМЖ). Ингибирование мозгового/хориоидального
сплетения КА II, IV, VA и XII приводит к снижению секреции СМЖ и контролю
внутричерепного давления.
Ключевые слова:
ацетазоламид, карбоангидраза, внутричерепная гипертензия,
секреция мозговой жидкости, давление, извитой каналец.
Introduction:
Acetazolamide is a carbonic anhydrase inhibitor, hence causing the
accumulation of carbonic acid. In short, under normal conditions, the net effect of carbonic
anhydrase in the urinary lumen and cells of the proximal convoluted tubule is to acidify the urine
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and transport bicarbonate (HCO
3
−
) into the div. Another effect is excretion of Cl
−
as it is
needed to maintain electroneutrality in the lumen, as well as the reabsorption of Na
+
into the
div.
Mechanism:
Under normal conditions in the proximal convoluted tubule of the kidney,
most of the carbonic acid (H
2
CO
3
) produced intracellularly by the action of carbonic anhydrase
quickly dissociates in the cell to bicarbonate (HCO
3
−
) and an H
+
ion (a proton), as previously
mentioned. The bicarbonate (HCO
3
−
) exits at the basal portion of the cell via sodium (Na
+
)
symport and chloride (Cl
−
) antiport and re-enters circulation, where it may accept a proton if
blood pH decreases, thus acting as a weak, basic buffer. The remaining H
+
left over from the
intracellular production of carbonic acid (H
2
CO
3
) exits the apical (urinary lumen) portion of the
cell by Na
+
antiport, acidifying the urine. There, it may join with another bicarbonate (HCO
3
−
)
that dissociated from its H
+
in the lumen of the urinary space only after exiting the proximal
convoluted kidney cells/glomerulus as carbonic acid (H
2
CO
3
) because bicarbonate (HCO
3
−
) itself
can not diffuse across the cell membrane in its polar state. This will replenish carbonic acid
(H
2
CO
3
) so that it then may be reabsorbed into the cell as itself or CO
2
and H
2
O (produced via a
luminal carbonic anhydrase). As a result of this whole process, there is a greater net balance of
H
+
in the urinary lumen than bicarbonate (HCO
3
−
), and so this space is more acidic than
physiologic pH. Thus, there is an increased likelihood that any bicarbonate (HCO
3
−
) that was left
over in the lumen diffuses back into the cell as carbonic acid, CO
2
, or H
2
O.
Thus, by disrupting this process with acetazolamide, urinary Na
+
and bicarbonate
(HCO
3
−
) are increased, and urinary H
+
and Cl
−
are decreased. Inversely, serum Na
+
and
bicarbonate (HCO
3
−
) are decreased, and serum H
+
and Cl
−
are increased. H
2
O generally follows
sodium, and so this is how the clinical diuretic effect is achieved, which reduces blood volume
and thus preload on the heart to improve contractility and reduce blood pressure, or achieve other
desired clinical effects of reduced blood volume such as reducing edema or intracranial
pressure.
Methods:
For studying of acetozalamide effect 40 participants with IIH wa selected and
mild visual loss who received a low-sodium weight-reduction diet. Participants were enrolled in
4 clinis in Bukhara and followed up for 3 months ( january 2025 - march 2025).Prospective
evaluation and data collection of high intracranial pressure CSF leaks was performed. Subjects
underwent CSF diversion and postoperative assessment of pressure changes via a standard
protocol. Lumbar drains or ventriculostomies were clamped on postoperative day 2 for 4 hours
prior to assessment with a manometer. Acetazolamide (500 mg) was administered orally
immediately following the recording and CSF pressure was measured after 4 hours. Data
regarding demographics, etiology of CSF leak, div mass index (BMI), location and size of
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defect, and clinical follow-up were also collected.
Outcomes and measures.
0
5
10
15
20
25
30
35
40
Intracranial pressure
decreased patients
Vision loss restored
patients
Weight lost
no effect observed
Conclusion
This study provides some of the first direct evidence of decreased intracranial pressure
associated with the oral administration of acetazolamide, especially symptom with vision loss. In
combination with the excellent endoscopic repair outcomes noted in a high risk population, this
evidence supports the routine use of acetazolamide in patients with high intracranial pressure
CSF leaks.
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