1, digestive system adverse reactions: common, manifestations: nausea, vomiting, abdominal distension, diarrhea, etc. (protease inhibitors, desoxynivalenol and zidovudine). Within the first 2 months after treatment, but most are not serious, symptomatic treatment. If taken with food, certain digestive adverse reactions can be reduced.
2. Bone marrow suppression: caused by zidovudine, manifestation: anemia and/or granulocytopenia. The incidence of anemia is 1-4% and granulocytopenia is 2-5%. Patients with low baseline CD4 are susceptible. discontinue AZT if Hb or Hct falls >25% from baseline levels. consider discontinuing AZT if granulocyte count is below 750. （Consider discontinuing AZT if granulocyte counts are below 750 (switch from AZT to TDF). In severe cases: hospitalization (blood transfusion, EPO, GSF).
3. rash: The rash is mainly caused by NVP, with an incidence of 15%, and usually occurs within the first 3 months after treatment. efV can also cause a rash, but it is less common. Grading of rash: Grade 1/2 mild or moderate (erythema, itching, diffuse maculopapular rash, dry desquamation); Grade 3/4 severe or potentially life-threatening (blistering, wet desquamation, ulceration, mucosal involvement, suspected S-J syndrome, toxic epithelial necrolysis, erythema multiforme, gangrene, desquamative dermatitis). If a mild to moderate (grade 1 or 2) rash develops during the NVP introduction period, the introduction period should be extended until the rash improves. If a mild to moderate (grade 1 or 2) rash develops after the NVP introduction period, continue the antiviral and administer antihistamines. If moderate to severe rash is associated with fever, liver function tests should be performed. All antiviral therapy drugs should be discontinued at any stage of grade 3 or 4 rash. (NVP/EFV for LPV/r).
4. Hepatotoxicity: more common, variable in severity. Elevated transaminases to hepatic necrosis. The former incidence is 8-15% and can be caused by any PIs and NNRTIs. Hepatic necrosis due to NVP occurs within 6 to 18 weeks after NVP treatment. The onset is sudden, with flu-like manifestations, fever, rash, gastrointestinal symptoms, and elevated eosinophils. Hepatic necrosis tends to occur in patients with high CD4 (11% in women with CD4 >250 and 6% in men with CD4 >400). After normalization of ALT and resolution of symptoms, HAART can be started with EFV-containing antiviral regimens, but preferably with LPV/r. After prolonged antiviral therapy and co-infection with HBV or HCV, ALT >200 can be continued with antiviral therapy, but Monitor ALT and changes in hepatitis symptoms closely, every 10-14 days. Any patient with ALT > 400 or with jaundice, petechiae, petechiae, hemorrhage, fluttering tremor, etc., should stop all antiviral therapy immediately, be hospitalized and treated symptomatically.
5. Hypersensitivity reactions: caused by abacavir (ABC), incidence 6-7%. (Class I MHC-HLA-B*5701 gene positive). Time of occurrence: median – day 9 after drug administration, 90% within the first 6 weeks. Presentation: high fever, diffuse rash, nausea, headache, diarrhea, arthralgia, laryngitis, dyspnea, abnormal liver function. Treatment: immediate discontinuation, hospitalization, no further use, supportive treatment, hormones and antihistamines are ineffective, most symptoms disappear after 48 hours of discontinuation.
6. Peripheral neuritis: mainly caused by ddI and d4T. It often appears after 3 months of treatment, with an incidence of 10-30%. Peripheral neuritis can also be caused by HIV itself or other viruses, especially in patients with low CD4 counts. In mild or moderate patients, antiviral therapy can still be continued with the addition of vitamin B complex and symptomatic management. If severe symptoms occur, d4T, ddI should be stopped and other NRTI drugs should be used instead.
7. lactic acidosis: lactic acidosis is rare but can be fatal and can be caused by any NRTI, resulting from mitochondrial toxicity of the drug. Studies have shown that the sequence of drugs causing mitochondrial toxicity is: d4T+ddI, d4T, ddI, AZT. manifestations: fatigue, nausea, vomiting, abdominal pain, muscle pain and weight loss, often with shortness of breath and shortness of breath in late stages. Blood lactate levels correlate with prognosis: 0-2mmol/L normal, 5-10mmol/L mortality 7%, 10-15mmol/L mortality over 30%, >15mmol/L mortality over 60%. Risk factors for lactic acidosis include: (1) pregnancy (2) ddI+d4T combination (3) concomitant use of metformin (4) alcohol abuse. Judgment criteria: elevated serum lactate and decreased blood PH. The anion gap (AG) can also be calculated after the onset of symptoms , AG = (Na+)C(Cl- + HCO3-). If AG > 12, the patient should be evaluated immediately and discontinuation of all antiviral therapy drugs may be considered. If AG> 16, antiviral therapy should be discontinued immediately. Therapeutic measures: rehydration, alkaline supplementation, high amounts of VitB1, B2, L-carnitine, coenzyme Q, VitC, antioxidants. Full clinical recovery takes 4 to 28 weeks. After the patient has fully recovered, antiviral therapy is restarted. Treatment regimen may include enhanced PIs plus NNRTI, and may also include TDF or ABC. 8. Pancreatitis: Uncommon, but may be very severe. Incidence ddI + d4T>ddI>d4T. Severe upper abdominal pain, nausea and vomiting are present and blood amylase must be tested and imaging methods such as ultrasound, CT or MRI aid in diagnosis. If pancreatitis is diagnosed, stop all antiviral drugs. When the patient’s clinical symptoms disappear and the blood amylase is normal, resume the antiviral, but no more ddI, d4T. Metabolic syndrome: including 2 parts: fat deposition and fat atrophy, the former is mostly caused by protease inhibitors, the latter is mostly caused by NRTI. Incidence 20~80%. Clinical features include centripetal obesity, extremity wasting, peripheral tissue fat consumption, cheek subcutaneous fat loss. There is also usually hyperglycemia and hyperlipidemia and hypertension. It usually appears several months or years after treatment. Diagnosis: 1), patient sensation 2), series of photographs 3), waist/hip ratio: women > 0.85, men > 0.95. 4), ultrasound, CT, MRI . Treatment: 1), low-fat diet, aerobic exercise: beneficial for fat deposition, but aggravate fat atrophy. 2), growth hormone: beneficial for fat deposition. 3), metformin: beneficial for fat deposition and RI resistance. 4), plastic surgery. 5), medication change: PIs for NNRTI. d4T for ABC, TDF, AZT, may have partial effect.
10. Kidney stones: caused by indinavir (IDV). Symptoms: abdominal pain, hematuria, and red blood cells visible on urinalysis. Incidence 5 to 35%, related to IDV peak concentration. Prevention: Drink more than 1.5 liters of water per day. Treatment: Discontinue IDV. 11, CNS adverse reactions: caused by efavirenz (Schidonin, EFV), incidence > 50%, from the first dose of the drug. Performance: nightmares, excessive dreaming, vivid dreams, inattention, dizziness, insomnia, etc. Usually disappear in 2-3 weeks, serious cases can be changed.
12, osteonecrosis, osteoporosis, osteopenia: the mechanism of osteonecrosis is unknown, non-vascular necrosis. It is mainly caused by TDF. The incidence is 100 times that of the general population. It occurs mainly in the femoral head. Risk factors: female, application of glucocorticoids, application of lipid-lowering drugs, application of testosterone, alcohol abuse, hypercoagulable state. Diagnosis: DEXA (dual-energy X-ray absorptiometry) for bone density measurement, X-ray, MRI. Treatment: 1), calcium and VitD supplementation; 2), diphosphonates; 3), weight reduction, crutch support, etc.; 4), surgery.