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Author: Yang Xia, Hong Yunchuan, Tianjin Medical University General
Hospital
Case Review A 63-year-old male patient was admitted to the hospital mainly due to "intermittent hemoptysis for 2 years"
.
History of present illness: The patient had hemoptysis without obvious incentives 2 years before admission, with a daily volume of about 30ml, no chest pain, expectoration, dyspnea, skin and mucous membrane hemorrhage, hematuria, no low-grade fever, night sweats, fatigue, etc.
Chest CT in other hospitals on December 2020: The round high-density shadow at the apex of the left lung was considered: pneumonia, and the hemoptysis improved after anti-infective treatment (specifically unknown)
.
After that, there was still intermittent hemoptysis, about ten times, the nature was the same as before, and no special diagnosis and treatment was given
.
One week before admission, hemoptysis occurred again, the amount was about 50ml, and the nature was the same as before.
Then, he went to the outpatient department of our hospital.
A complete chest CT showed that the calcification of the upper lobe of the left lung was the main nodule, and the tumor lesions were to be excluded, and further examination was recommended
.
In order to further check the admission to our hospital
.
Since the onset of the disease, the patient's spirit has been slightly worse, sleep, diet can be normal, urine and bowel movements are normal, and there is no change in weight
.
Past history: a 20-year history of "hypertension" with a blood pressure of up to 160/110 mmHg, oral administration of "amlodipine, fosinopril", and the blood pressure can be controlled
.
20 years of history of "type 2 diabetes", oral administration of "metformin, acarbose, dapagliflozin", subcutaneous injection of "insulin glargine" before going to bed to lower blood sugar, and blood sugar control can be achieved
.
Denied a history of heart disease
.
Denied a history of infectious diseases
.
Denied surgery, trauma, blood transfusion history
.
Denied things, drug allergies
.
Personal history: 10 years of smoking history, 10 cigarettes per day on average, 30 years of quitting smoking
.
Denies history of alcoholism
.
No history of exposure to industrial toxicants, dust and radioactive substances
.
Family History: Denied family history of genetic disease
.
2021.
7.
5 Chest CT: calcification in the upper lobe of the left lung as the main nodule, except for tumor lesions, and micronodules in the upper lobe of the left lung
.
2021.
7.
11 Enhanced chest CT: calcified nodules in the upper lobe of the left lung, with multiple short burr shadows on the edge, except for malignant transformation of scars secondary to old lesions, and micronodules in the upper lobe of the left lung
.
Physical examination on admission: body temperature 36.
4°C, pulse 75 beats/min, respiration 17 beats/min, blood pressure 131/77mmHg
.
Conscious, steady breathing, to the point, articulate clearly, and cooperate in physical examination
.
There was no yellowing of the skin and mucous membranes of the whole body, no superficial lymphadenopathy, soft neck, no sense of resistance, and no jugular vein filling
.
The position of the trachea is in the middle, the shape of the thorax is normal, there is no widening of the intercostal space, the lungs are voiceless on percussion, the breath sounds are voiceless, a small amount of fine moist rales can be heard in the left lung, and no wheezing is heard
.
There was no enlargement of the heart border percussion, the heart sounds were fine, the rhythm was uniform, and there was no murmur
.
The abdomen was flat, with no abdominal tenderness, no abdominal rebound tenderness, no palpable liver, no palpable spleen, and negative hepatic jugular venous return sign
.
Both lower extremities are not swollen
.
Auxiliary examination: perfect chest CT enhancement after admission (Figure 2)
.
Blood routine: WBC 7.
64*10^9/L, HGB 137g/L, NEUT% 66.
8%, LYM% 20.
5%
.
Biochemistry: LDH 137U/L, ALB 39g/L, BUN 8mmol/L, CREA 91umol/L
.
CRP 0.
39mg/dl
.
ESR 17mm/h
.
D-dimer: 397ng/ml
.
PCT was normal
.
Fasting blood sugar: 13.
70mmol/L, blood sugar 2h after breakfast: 25.
6mmol/L, blood sugar after lunch: 16.
50mmol/L, blood sugar 2h after dinner: 20.
60mmol/L
.
Sputum smear, sputum culture: Streptococcus viridans, no fungal hyphae and yeast-like buns, no bacteria, acid-fast bacilli (0)
.
Lung tumor markers: CEA, CYFRA21-1, SCC, ProGRP, NSE showed no obvious abnormality
.
Cardiac ultrasonography, abdominal ultrasonography, and lower extremity vascular ultrasonography showed no obvious abnormality
.
To further improve the bronchoscopy: the large airway, the left main bronchus, the posterior segment of the left upper lobe apex, and the basal segment of the left lower lobe can be seen with fresh bloodstains (the apical segment of the left upper lobe is highlighted)
.
No tumor was seen under the microscope
.
Alveolar lavage fluid NGS: Streptococcus pneumoniae (number of detected sequences: 3), Aspergillus flavus (number of detected sequences: 14), human rhinovirus type A (number of detected sequences: 1)
.
BALF x-pert: (-)
.
BALF GM: 3.
14 (≥1 is positive)
.
Treatment: After admission, the patient was given intermittent hemoptysis and hemostasis treatment.
The patient's previous antibiotic treatment seemed to be effective.
Moxifloxacin was given to fight infection, supplemented by phlegm reduction and blood sugar control
.
Voriconazole antifungal therapy was added according to the auxiliary examination results
.
Further treatment: The patient’s chest imaging could not rule out fungal infection complicated with tumor lesions.
After the family’s surgical treatment, left upper lobectomy under general anesthesia under left thoracoscopic surgery, systematic lymph node dissection, lysis of complex thoracic adhesions, and closed thoracic drainage were performed.
.
Pathological results: 1.
(Left upper lobe) pulmonary mycosis, cystic degeneration in the center of the lesion, containing a large number of molds, peripheral fibrosis and chronic inflammation, local alveolar epithelial and bronchial epithelial hyperplasia; immunohistochemical staining showed: epithelium Positive for CK7, TTF-1 and P40, negative for CEA; special staining: PAS and silver hexamine showed mold
.
2.
(Group 5, Group 7, Group 9, Group 10, Group 11) Reactive lymph node hyperplasia
.
Postoperative anti-inflammatory, fluid replacement, pain relief and other treatments were given, and the patient recovered smoothly
.
The final diagnosis was: invasive pulmonary aspergillosis, hypertension grade 3 (very high risk), and type 2 diabetes
.
Discussion Invasive non-aspergillosis (IPA) occurs in severely immunocompromised patients, especially those with neutropenia due to hematological malignancies, chemotherapy, or immunosuppressive therapy
.
According to the route of transmission, it can be divided into: vascular invasion and airway invasion, and the two can coexist in the same patient
.
Angioinvasive aspergillosis (AGIA) is histologically characterized by the invasion of fungal hyphae into small and medium-sized blood vessels, resulting in thrombosis and vascular occlusion, followed by tissue necrosis and systemic spread
.
Early IPA can present as small nodules and/or small pleural wedge-shaped changes surrounded by a ground-glass halo (halo sign) representing alveolar hemorrhage (peak 5 days)
.
As the disease progresses, nodules may become cavitated and necrotic parenchyma will separate from the adjacent lung, forming an air crescent similar to that seen in Aspergillus (10-15 days), forming what is thought to be a Typical angioinvasive aspergillosis
.
Airway invasive aspergillosis is the massive inhalation of Aspergillus spores and the growth of hyphae on the bronchial mucosa, causing acute tracheo-bronchitis and pneumonia without evidence of vascular invasion
.
Around the involved airway, there is usually a variable-sized hemorrhagic area and/or tissue pneumonitis
.
Among them, non-specific tracheal wall thickening may be the only manifestation, while patchy peribronchial consolidation, centrilobular nodules, and tree-in-bud signs are all non-specific and indistinguishable from bronchopneumonia caused by other microorganisms
.
At present, there are few reports of IPA cases with "calcification" as the main manifestation.
Some scholars once believed that one of the characteristics of Aspergillus niger infection is the presence of calcium oxalate crystals detected by pathological examination (1)
.
In addition, studies have shown that there is a high proportion of mucous impaction with high density (calcification) in ABPA patients.
It has been reported in the literature that nearly 50% of patients can have such manifestations, but the proportion of actual clinical encounters is not high
.
The current traditional methods for detecting fungi include direct microscopy, culture, and histopathological diagnosis, but these methods have problems such as long diagnosis time, low sensitivity or specificity, and delay in diagnosing the condition of patients
.
Galactomannan (GM), a thermostable polysaccharide on the cell wall of Aspergillus, can be detected in blood early in Aspergillus infection
.
Studies have shown that the sensitivity of BALF-GM test for diagnosing pulmonary aspergillosis is higher than that of serum GM test
.
With the continuous maturity and popularization of next-generation sequencing (NGS) technology, when the BALF GM test is combined with NGS, the reliability of the results increases significantly
.
In this case, we can also see that the BALF GM test and NGS results are completely consistent with the pathological results
.
Considering clinically mainly calcification with multiple short burr shadow nodules at the edge, the possibility of special pathogen infection should be excluded before considering tumor lesions
.
Clinically, the combined application of bronchoalveolar lavage fluid GM test and bronchoalveolar lavage fluid NGS has guiding value in the diagnosis of invasive pulmonary aspergillosis
.
Reference 1.
Edson Marchiori, Bruno Hochhegger, Gláucia Zanetti.
Calcified intracavitary mass: a rare presentation of aspergilloma.
J Bras Pneumol.
2019 Mar 25;45(2):e20180396.
Hospital
Case Review A 63-year-old male patient was admitted to the hospital mainly due to "intermittent hemoptysis for 2 years"
.
History of present illness: The patient had hemoptysis without obvious incentives 2 years before admission, with a daily volume of about 30ml, no chest pain, expectoration, dyspnea, skin and mucous membrane hemorrhage, hematuria, no low-grade fever, night sweats, fatigue, etc.
Chest CT in other hospitals on December 2020: The round high-density shadow at the apex of the left lung was considered: pneumonia, and the hemoptysis improved after anti-infective treatment (specifically unknown)
.
After that, there was still intermittent hemoptysis, about ten times, the nature was the same as before, and no special diagnosis and treatment was given
.
One week before admission, hemoptysis occurred again, the amount was about 50ml, and the nature was the same as before.
Then, he went to the outpatient department of our hospital.
A complete chest CT showed that the calcification of the upper lobe of the left lung was the main nodule, and the tumor lesions were to be excluded, and further examination was recommended
.
In order to further check the admission to our hospital
.
Since the onset of the disease, the patient's spirit has been slightly worse, sleep, diet can be normal, urine and bowel movements are normal, and there is no change in weight
.
Past history: a 20-year history of "hypertension" with a blood pressure of up to 160/110 mmHg, oral administration of "amlodipine, fosinopril", and the blood pressure can be controlled
.
20 years of history of "type 2 diabetes", oral administration of "metformin, acarbose, dapagliflozin", subcutaneous injection of "insulin glargine" before going to bed to lower blood sugar, and blood sugar control can be achieved
.
Denied a history of heart disease
.
Denied a history of infectious diseases
.
Denied surgery, trauma, blood transfusion history
.
Denied things, drug allergies
.
Personal history: 10 years of smoking history, 10 cigarettes per day on average, 30 years of quitting smoking
.
Denies history of alcoholism
.
No history of exposure to industrial toxicants, dust and radioactive substances
.
Family History: Denied family history of genetic disease
.
2021.
7.
5 Chest CT: calcification in the upper lobe of the left lung as the main nodule, except for tumor lesions, and micronodules in the upper lobe of the left lung
.
2021.
7.
11 Enhanced chest CT: calcified nodules in the upper lobe of the left lung, with multiple short burr shadows on the edge, except for malignant transformation of scars secondary to old lesions, and micronodules in the upper lobe of the left lung
.
Physical examination on admission: body temperature 36.
4°C, pulse 75 beats/min, respiration 17 beats/min, blood pressure 131/77mmHg
.
Conscious, steady breathing, to the point, articulate clearly, and cooperate in physical examination
.
There was no yellowing of the skin and mucous membranes of the whole body, no superficial lymphadenopathy, soft neck, no sense of resistance, and no jugular vein filling
.
The position of the trachea is in the middle, the shape of the thorax is normal, there is no widening of the intercostal space, the lungs are voiceless on percussion, the breath sounds are voiceless, a small amount of fine moist rales can be heard in the left lung, and no wheezing is heard
.
There was no enlargement of the heart border percussion, the heart sounds were fine, the rhythm was uniform, and there was no murmur
.
The abdomen was flat, with no abdominal tenderness, no abdominal rebound tenderness, no palpable liver, no palpable spleen, and negative hepatic jugular venous return sign
.
Both lower extremities are not swollen
.
Auxiliary examination: perfect chest CT enhancement after admission (Figure 2)
.
Blood routine: WBC 7.
64*10^9/L, HGB 137g/L, NEUT% 66.
8%, LYM% 20.
5%
.
Biochemistry: LDH 137U/L, ALB 39g/L, BUN 8mmol/L, CREA 91umol/L
.
CRP 0.
39mg/dl
.
ESR 17mm/h
.
D-dimer: 397ng/ml
.
PCT was normal
.
Fasting blood sugar: 13.
70mmol/L, blood sugar 2h after breakfast: 25.
6mmol/L, blood sugar after lunch: 16.
50mmol/L, blood sugar 2h after dinner: 20.
60mmol/L
.
Sputum smear, sputum culture: Streptococcus viridans, no fungal hyphae and yeast-like buns, no bacteria, acid-fast bacilli (0)
.
Lung tumor markers: CEA, CYFRA21-1, SCC, ProGRP, NSE showed no obvious abnormality
.
Cardiac ultrasonography, abdominal ultrasonography, and lower extremity vascular ultrasonography showed no obvious abnormality
.
To further improve the bronchoscopy: the large airway, the left main bronchus, the posterior segment of the left upper lobe apex, and the basal segment of the left lower lobe can be seen with fresh bloodstains (the apical segment of the left upper lobe is highlighted)
.
No tumor was seen under the microscope
.
Alveolar lavage fluid NGS: Streptococcus pneumoniae (number of detected sequences: 3), Aspergillus flavus (number of detected sequences: 14), human rhinovirus type A (number of detected sequences: 1)
.
BALF x-pert: (-)
.
BALF GM: 3.
14 (≥1 is positive)
.
Treatment: After admission, the patient was given intermittent hemoptysis and hemostasis treatment.
The patient's previous antibiotic treatment seemed to be effective.
Moxifloxacin was given to fight infection, supplemented by phlegm reduction and blood sugar control
.
Voriconazole antifungal therapy was added according to the auxiliary examination results
.
Further treatment: The patient’s chest imaging could not rule out fungal infection complicated with tumor lesions.
After the family’s surgical treatment, left upper lobectomy under general anesthesia under left thoracoscopic surgery, systematic lymph node dissection, lysis of complex thoracic adhesions, and closed thoracic drainage were performed.
.
Pathological results: 1.
(Left upper lobe) pulmonary mycosis, cystic degeneration in the center of the lesion, containing a large number of molds, peripheral fibrosis and chronic inflammation, local alveolar epithelial and bronchial epithelial hyperplasia; immunohistochemical staining showed: epithelium Positive for CK7, TTF-1 and P40, negative for CEA; special staining: PAS and silver hexamine showed mold
.
2.
(Group 5, Group 7, Group 9, Group 10, Group 11) Reactive lymph node hyperplasia
.
Postoperative anti-inflammatory, fluid replacement, pain relief and other treatments were given, and the patient recovered smoothly
.
The final diagnosis was: invasive pulmonary aspergillosis, hypertension grade 3 (very high risk), and type 2 diabetes
.
Discussion Invasive non-aspergillosis (IPA) occurs in severely immunocompromised patients, especially those with neutropenia due to hematological malignancies, chemotherapy, or immunosuppressive therapy
.
According to the route of transmission, it can be divided into: vascular invasion and airway invasion, and the two can coexist in the same patient
.
Angioinvasive aspergillosis (AGIA) is histologically characterized by the invasion of fungal hyphae into small and medium-sized blood vessels, resulting in thrombosis and vascular occlusion, followed by tissue necrosis and systemic spread
.
Early IPA can present as small nodules and/or small pleural wedge-shaped changes surrounded by a ground-glass halo (halo sign) representing alveolar hemorrhage (peak 5 days)
.
As the disease progresses, nodules may become cavitated and necrotic parenchyma will separate from the adjacent lung, forming an air crescent similar to that seen in Aspergillus (10-15 days), forming what is thought to be a Typical angioinvasive aspergillosis
.
Airway invasive aspergillosis is the massive inhalation of Aspergillus spores and the growth of hyphae on the bronchial mucosa, causing acute tracheo-bronchitis and pneumonia without evidence of vascular invasion
.
Around the involved airway, there is usually a variable-sized hemorrhagic area and/or tissue pneumonitis
.
Among them, non-specific tracheal wall thickening may be the only manifestation, while patchy peribronchial consolidation, centrilobular nodules, and tree-in-bud signs are all non-specific and indistinguishable from bronchopneumonia caused by other microorganisms
.
At present, there are few reports of IPA cases with "calcification" as the main manifestation.
Some scholars once believed that one of the characteristics of Aspergillus niger infection is the presence of calcium oxalate crystals detected by pathological examination (1)
.
In addition, studies have shown that there is a high proportion of mucous impaction with high density (calcification) in ABPA patients.
It has been reported in the literature that nearly 50% of patients can have such manifestations, but the proportion of actual clinical encounters is not high
.
The current traditional methods for detecting fungi include direct microscopy, culture, and histopathological diagnosis, but these methods have problems such as long diagnosis time, low sensitivity or specificity, and delay in diagnosing the condition of patients
.
Galactomannan (GM), a thermostable polysaccharide on the cell wall of Aspergillus, can be detected in blood early in Aspergillus infection
.
Studies have shown that the sensitivity of BALF-GM test for diagnosing pulmonary aspergillosis is higher than that of serum GM test
.
With the continuous maturity and popularization of next-generation sequencing (NGS) technology, when the BALF GM test is combined with NGS, the reliability of the results increases significantly
.
In this case, we can also see that the BALF GM test and NGS results are completely consistent with the pathological results
.
Considering clinically mainly calcification with multiple short burr shadow nodules at the edge, the possibility of special pathogen infection should be excluded before considering tumor lesions
.
Clinically, the combined application of bronchoalveolar lavage fluid GM test and bronchoalveolar lavage fluid NGS has guiding value in the diagnosis of invasive pulmonary aspergillosis
.
Reference 1.
Edson Marchiori, Bruno Hochhegger, Gláucia Zanetti.
Calcified intracavitary mass: a rare presentation of aspergilloma.
J Bras Pneumol.
2019 Mar 25;45(2):e20180396.
