Tuberculosis - I.T. Pyatnochka 2005

Complications of tuberculosis
Amyloidosis of internal organs

Amyloidosis is a systemic disease affecting various Organs and Tissues, characterized by impaired Protein METABOLISM and extracellular deposition of amyloid (a glycoprotein complex) within them, leading to organ dysfunction.

The Etiology of amyloidosis remains undetermined. Among patients who have died from Pulmonary Tuberculosis, amyloidosis is diagnosed in 10-20% of cases. The triggering and determining factors for the development and progression of amyloidosis in pulmonary tuberculosis patients—aside from widespread inflammatory and destructive processes (secondary amyloidosis)—include antiproteinase deficiency, carriage of certain genes (M₃, S, Z) and the α₁-proteinase inhibitor (genetic amyloidosis), predominantly occurring in older age groups (senile amyloidosis).

The Pathogenesis of amyloidosis is not yet fully understood. It most frequently develops in chronic destructive forms of pulmonary tuberculosis, chronic Pleural Empyema, and similar conditions. Contributing factors include intoxication, Hypoxia, and vitamin deficiency. Amyloidosis predominantly affects the Spleen, Liver, Kidneys, and Adrenal Glands, and much less frequently the Tongue, Stomach, and myocardium.

There are four stages of amyloidosis: preclinical, proteinuric, edematous-hypotonic, and azotemic.

Morphological verification of the Diagnosis is of critical importance, as there are currently no pathognomonic clinical signs or Laboratory tests for amyloidosis.

Preclinical stage of amyloidosis. Clinical data can only suggest the potential development of amyloidosis in chronic destructive forms of pulmonary tuberculosis. The diagnosis is confirmed by the results of liver and Kidney biopsies.

The proteinuric stage is characterized by persistent proteinuria, minor Hematuria, and cylindruria. Both stages (I and II) exhibit an elevated ESR, dysproteinemia, and increased fibrinogen levels.

The edematous-hypotonic stage is marked by impaired renal concentration function, presenting as hyposthenuria, cylindruria, lower extremity edema, and occasionally ascites.

The azotemic stage of amyloidosis is nephrosclerotic. The kidneys become partially contracted, urinary excretion is impaired, Blood nitrogen levels rise, and uremia develops.

The Treatment of amyloidosis as a complication of pulmonary tuberculosis involves adequate antimycobacterial therapy and, in some cases, surgery. Under these conditions, the regression of amyloidosis is possible.

The dietary regimen for patients with Renal Amyloidosis is identical to that for Chronic Glomerulonephritis. Additionally, patients with amyloidosis are advised to consume raw liver on a long-term basis (100-120 g daily). In stages I–III of amyloidosis, Chemotherapy must be combined with delagil (0.25 g once daily for an extended period); kontrikal at 10,000–20,000 IU in 300–500 ml of isotonic sodium chloride solution administered as an intravenous drip once daily; vitamin E (tocopherol acetate) 1–2 capsules (0.5 ml of a 20% solution) two to three times daily, or intramuscularly 1 ml of a 5%, 10%, or 30% oil solution daily; and albumin 100–200 ml as an intravenous drip 1–2 times a week. Vitamins C, B₁, and B₆; sulfhydryl group Donors (Methionine 0.5–1 g three times daily, unitiol 5% solution 5–10 ml intramuscularly daily or every other day, course of treatment 25–30 weeks); hepatoprotectors (syrepar 2–4 ml once daily intramuscularly or intravenously (slowly), course of treatment 1.5–2 months; Essentiale 2–3 capsules three times daily or 10–20 ml as an intravenous drip in a 5% glucose solution, course of treatment 3 months; thiotriazoline 2 ml of a 2.5% solution intramuscularly 3 times daily or 0.1–0.2 g 3 times daily, course of treatment 20–30 days; lewolin 1 capsule 3 times daily; lipokain, etc.) are also indicated.