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*Read only for medical professionals.
It's not just gout! A patient with joint redness, swelling, heat and pain accompanied by blood pressure that has not been able to drop came to the outpatient clinic.
If it were you, how would you investigate the cause, diagnose and treat it? Case Review A 57-year-old middle-aged man was admitted to the hospital mainly because of "episodic polyarticular redness, swelling, heat and pain for 20 years, aggravation and fever for 2 days"
.
History of present illness: The patient developed redness, swelling, heat and pain in the first metatarsophalangeal joint of the right foot after drinking and eating seafood 20 years ago.
He went to a local hospital and found that uric acid was significantly elevated (specifically unknown), and was diagnosed with "gouty arthritis".
After being discharged from the hospital, he continued to take "colchicine, special medicine (diclofenac sodium, vitamin B1, wild papaya tablets, Weiyou, dexamethasone)" orally, and stopped taking the medicine automatically after the symptoms improved
.
After being injured by fire 10 years ago, he began to experience red, swollen and hot pain in the ankle joints and knee joints of both lower extremities.
Each time lasted about 2-7 days and occurred twice a year.
There was no fever, morning stiffness, skin changes, no joint deformities, and no subcutaneous nodules.
, After taking "colchicine" and taking "dexamethasone" for intermittent attacks, the symptoms improved after treatment, and the symptoms recurred, and the frequency of attacks gradually increased, 6-8 times a year
.
Two months ago, after soaking my feet in hot water, my knees and ankles were red, swollen, and hot.
I went to a local hospital for treatment with traditional Chinese medicine (the specific ingredients are unknown), but the treatment effect was not good
.
In the past 1 week, he felt that the swelling and pain of both knees and ankles were worse than before, accompanied by local redness and swelling, increased skin temperature, limited activity, and no morning stiffness
.
Fever started 2 days ago, up to 38.
5°C, without medication, considering acute gouty arthritis to be admitted to our department, poor spirit, normal appetite, no cough and expectoration, no chest tightness, no abdominal pain, no diarrhea, normal urine and stool , there was no significant change in body weight
.
Past history: average physical fitness
.
Denied high blood pressure, diabetes, heart disease history
.
He denied the history of hepatitis; allergy to sulfonamides, denied the history of food allergy; denied the history of trauma and blood transfusion; the history of vaccination is unknown
.
Denied family history of hereditary disease
.
Deny the history of travel and residence in high-risk areas of new coronary pneumonia, and deny the history of contact with confirmed cases
.
Physical examination: body temperature 39.
0℃, pulse 111 times/min, respiration 19 times/min, blood pressure 201/153mmHg, weight 73kg, height 174cm, body mass index (BMI) 24.
1kg/m2, waist circumference: 95cm, hip circumference: 100cm , Waist-to-hip ratio: 0.
95
.
Clear, sleepy, and admitted to the hospital in a wheelchair
.
Bloody face, multiple subcutaneous petechiae can be seen on the front chest, no palpable enlargement of superficial lymph nodes
.
Cardiopulmonary abdominal examination showed no obvious abnormality
.
The knee joints and ankle joints were red and swollen, the movement was limited, the skin temperature was significantly increased, the percussion pain was obvious, and the formation of tophi was visible in both feet
.
Preliminary diagnosis: 1.
Gout 1.
1 Acute gouty arthritis was admitted to the hospital, the condition was analyzed and the laboratory related tests were completed: potassium 3.
3mmol/L↓, blood sugar 6.
43mmol/L↑
.
Creatinine 119μmol/L↑, cystatin C1.
53mg/L↑, uric acid 544μmol/L↑
.
Urine microalbumin/creatinine 36.
4mg/gCr↑, urine microalbumin 26.
4mg/L↑, 24-hour uric acid: 1400mg/24h, urine routine: red blood cell 42.
7/μI↑, bacterial count 35277/μI↑
.
Infection index: procalcitonin 1.
10ng/ml↑, blood routine: leukocyte 19.
75*109/L↑, neutrophil #16.
06*109/L↑, monocyte #1.
56*109/L↑, neutrophil Cells% 81.
3%↑, lymphocytes% 10.
3%↓, eosinophils% 0.
3%↓; C-reactive protein 288.
0mg/L↑ Knee ultrasound: bilateral knee joint effusion, synovial hyperplasia with calcification
.
Energy reconstruction of both lower extremities: multiple tophi formation on both knees, ankles and feet, accompanied by gouty arthritis manifestations
.
Lung CT: Small nodules in the apical segment of the upper lobe of the right lung, the outer basal segment of the lower lobe, and the lower lingual segment of the upper lobe of the left lung, follow-up is recommended
.
Abdominal ultrasound: fatty liver; multiple kidney stones
.
Improve rheumatism, rheumatoid, vasculitis four items, anti-soluble antigen (ENA) spectrum and other rheumatic immune examinations, and preliminarily exclude rheumatic immune diseases
.
In summary, the preliminary diagnosis considers: 1.
gout 1.
1 acute gouty arthritis; 1.
2 hyperuricemia; 1.
3 gouty nephropathy; 1.
4 double kidney stones; 1.
5 formation of subcutaneous tophi Kalemia 4.
Fatty liver 5.
Pulmonary nodules 6.
Sinus tachycardia 7.
Impaired glucose tolerance How should these 3 issues be considered? Q1: Acute gouty arthritis is usually aseptic inflammation, but the patient was accompanied by obvious chills and high fever when he was admitted to the hospital, the infection index was significantly increased, and the procalcitonin was 1.
10ng/ml.
Can bacterial infection be considered? A1: The patient has no clear respiratory tract, digestive tract and other symptoms, and the urine routine also indicates bacteria but few urine white blood cells, which are not consistent with the infection indicators
.
Therefore, considering the possibility of intra-articular infection in combination with the patient's history of post-fire joint trauma, empirical antibiotics were given, and the blood count and PCT were significantly lower than before, suggesting that the anti-infective treatment was effective
.
Q2: The patient has no history of hypertension or diabetes, and no family history of hereditary hypertension or diabetes.
Why is the abnormal glucose tolerance diagnosed? A2: After the patient was admitted to the hospital, the blood pressure was measured several times at about 200/140 mmHg, and two kinds of antihypertensive drugs were used.
The blood pressure still fluctuated greatly.
The fasting and 2-hour postprandial blood glucose monitoring revealed abnormal glucose tolerance, so the diagnosis was clear
.
Q3: Why was the patient's admission blood sugar and blood pressure abnormal and complicated with hypokalemia? Is it related to gout? A3: Combined with the patient's history of long-term discontinuation of oral dexamethasone, and the physical examination after admission showed a bloody appearance, scattered subcutaneous petechiae on the chest, combined with hypokalemia, refractory hypertension, abnormal glucose tolerance, fatty liver, etc.
Consider the possibility of drug-induced Cushing's syndrome
.
Improve corticosteroids, 24-hour urinary free cortisol and other tests, if no definite abnormality is found, instruct the patient to stop glucocorticoid therapy, strictly low-purine diet, quit smoking and limit alcohol, drink more water, and use colchicine and etoricoxib in an acute attack.
Other drugs, regular outpatient follow-up during the remission period, and low-dose uric acid-lowering drugs
.
After discharge, the patient's antihypertensive drugs were gradually reduced to amlodipine 5 mg once a day, and then completely stopped.
Blood pressure was controlled steadily, blood glucose was monitored within the normal range, and serum potassium was measured multiple times
.
Consider the diagnosis of drug-induced Cushing's syndrome
.
What is drug-induced Cushing's syndrome? Cushing's syndrome, also known as hypercortisolism, is mainly manifested as: full moon face, bloody appearance, central obesity, acne, purple striae, hypertension, secondary diabetes and osteoporosis, etc.
Long-term use of glucocorticoids Or alcohol abuse can also cause clinical manifestations similar to Cushing's syndrome, known as extrinsic, drug-induced or Cushing-like syndrome
.
The laboratory examination of drug-induced Cushing syndrome often needs to improve the urine free cortisol and circadian corticosteroid rhythm examination, but the diagnosis is mainly based on clinical symptoms
.
Treatment: Gradual withdrawal of glucocorticoids is the most effective method
.
Conclusion: This case was caused by a history of long-term discontinuation of oral glucocorticoids due to irregular treatment of gout outside the hospital and lack of relevant professional knowledge
.
If clinically encountered with unexplained hypertension, abnormal blood sugar and electrolyte disorders, abnormal lipid metabolism, etc.
, drug-induced Cushing's syndrome should be considered.
Such patients are more common in clinical practice and should be paid attention to
.
Acute gouty arthritis is admitted to the hospital.
If procalcitonin is too high, bacterial infection should be considered, or antibiotics may be used as appropriate
.
Too little to see enough? Don't worry ~ pay attention to the "Medical Endocrine Channel Video Number" to see the endocrinology medical team of the Southern Theater General Hospital bring you a "special program" of 420 people's attention to gout day.
From April 17th to April 24th, every day at 11:00 every day The daily "Medical Questions and Answers" solves common misunderstandings about gout.
Today's "Medical Questions and Answers" Second Question: In daily life, what foods are least recommended for gout patients? Can't find the content of the first question of "Medical Questions and Medical Answers"? Click into the article and turn to the end of the article to see it! ↓↓↓ I don’t want to have a gout attack, and “drinking” is also a knowledge! References: [1] Endocrinology and Metabolic Diseases Professional Committee of the Chinese Medical Doctor Association Integrative Medicine Physician Branch, Ni Qing, Wang Yangang.
Guidelines for the diagnosis and treatment of hyperuricemia and gout syndrome (2021-01-20) [J].
World Chinese Medicine, 2021, 16(2): 183-189.
[2] Feng Wenwen, Cui Dai, Yang Tao.
Interpretation of the main points of "China's guidelines for the diagnosis and treatment of hyperuricemia and gout (2019)" [J].
Journal of Clinical Internal Medicine, 2020, 37(7):528-531.
[3]Gao Yuxia,Wang Ruixia,Lun Guanfen,et al.
Pharmaceutical care of patients with long-term use of glucocorticoids[J].
Chinese Journal of Hospital Pharmacy,2013,33(10):830- 836.
[4] Endocrinology Branch of Chinese Medical Association.
Expert consensus on Cushing's syndrome (2011) [J].
Chinese Journal of Endocrinology and Metabolism, 2012, 28(2): 96-102.
Reviewing expert Li Jia Southern Theater General Hospital Director of the Department of Endocrinology, MD, postgraduate tutor Vice Chairman of the Clinical Endocrine Drug Evaluation Branch of the China Medical Education Association Chairman of the Osteoporosis Prevention and Rehabilitation Committee of the Guangdong Provincial Geriatric Health Association Chairman of the Guangdong Provincial Medical Association Endocrine Branch Youth Member of the Guangzhou Medical Association Diabetes Branch The chairman has published more than 40 papers in SCI and core journals.
Editor-in-chief, editor-in-chief, and translation of 5 monographs.
In recent years, he has presided over 5 national natural and provincial and ministerial-level funds.