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This article is reprinted under the authorization of the author, please do not reprint without permission
.
Primary hyperparathyroidism (PHPT) is a set of clinical syndromes caused by excessive secretion of parathyroid hormone (PTH) caused by primary lesions of parathyroid tissue, including hypercalcemia, renal calcium reabsorption, and urine Increased phosphorus excretion, kidney stones, nephrocalcinosis, and increased absorption of cortical bone
.
It can occur at any age, but it is most common in adults.
The peak incidence is 30-50 years old.
It is more common in postmenopausal women.
The incidence of women is about 4 times that of men
.
As an endocrine disease, this disease was considered uncommon in the past.
In fact, according to data from the West, the number of diagnosed PHPT is increasing year by year, and it has become a relatively common endocrine disease.
However, the clinical manifestations of PHPT are complicated.
It harms multiple organs and is related to various systems.
It is often not specific, and the disease is insidious, which brings great difficulties to the diagnosis of the disease.
It is very easy to cause misdiagnosis or missed diagnosis.
If the treatment is delayed, it can cause irreversible damage to the patient.
, Even life-threatening
.
The following summarizes and analyzes the clinical misdiagnosis of PHPT, hoping to help improve clinicians' understanding of the disease
.
1.
Common misdiagnosis of PHPT 1.
Misdiagnosed as a "neurological disease", such as cerebrovascular disease, psychosis, dementia, etc.
➤ Hypercalcemia caused by PHPT affects the stability of the central nervous system, and the toxicity of high calcium to brain cells can be Interfering with the electrophysiological activities of brain cells, causing patients to have a variety of neuropsychiatric symptoms, including anxiety, affective disorders, personality changes, and confusion, which are easily misdiagnosed as psychosis; ➤Severe hypercalcemia (5 mmol/l) may cause drowsiness, Confusion, stupor, and coma may be misdiagnosed as cerebrovascular disease; some patients may show memory loss, cognitive impairment, personality changes, depression, etc.
, especially in elderly patients, and it is easy to be misdiagnosed as Alzheimer’s and depression And so on, clinicians should remain vigilant
.
2.
Misdiagnosed as "digestive system disease", such as chronic gastritis, gastric ulcer, pancreatitis, etc.
PHPT can cause a series of pathological changes in the digestive system, which are also closely related to hypercalcemia.
The main mechanism is: ➤Hypercalcemia can cause Neuromuscular excitability decreases, gastrointestinal smooth muscle tension decreases, and peristalsis is slow.
The main clinical manifestations are loss of appetite, abdominal distension, anorexia, constipation, etc.
, which are easily misdiagnosed as chronic gastritis and gastrointestinal dysfunction; ➤High blood calcium can stimulate the stomach Mucosal G cells secrete gastrin, which increases the secretion of gastric acid, and eventually peptic ulcers, upper abdominal pain, melena and other symptoms appear.
Clinically, some patients with recurrent peptic ulcers should be highly alert to PHPT; ➤High blood calcium promotes pancreatic juice secretion Activating trypsinogen, leading to the pancreas self-digestion and causing pancreatitis, long-term deposition of calcium ions in the pancreas can cause pancreatic duct calcification or formation of pancreatic duct stones, which can lead to acute attacks of chronic pancreatitis
.
The possibility of PHPT should be considered in clinical encounters with such patients
.
3.
Misdiagnosed as a "urinary system disease", such as urinary tract infection, kidney stones, chronic renal insufficiency, etc.
Hypercalcemia caused by PHPT makes calcium deposits in the renal parenchyma, which can cause interstitial nephritis, salt-loss nephropathy, calcium Substance deposition and renal calculi decline in renal tubular concentration, and eventually develop into renal failure, and are also prone to urinary tract infections, manifested as polydipsia, polydipsia, nocturia, polyuria and other phenomena
.
Kidney stones and renal parenchymal calcification cause recurrent renal colic and hematuria
.
Clinically, there are many misdiagnosed as simple urinary tract infections and kidney stones
.
Renal colic, ureter spasm, gross hematuria, and even gravel-like stones in the urine
.
Patients with recurrent urinary calculi should think of the possibility of PHPT
.
4.
Misdiagnosed as a "skeletal system disease", such as rheumatoid arthritis, primary osteoporosis, bone tumors and other hyperparathyroidism, excessive secretion of PTH will cause abnormal calcium and phosphorus metabolism, increased bone absorption, and Osteoporosis occurs earlier, faster, and more severely, with systemic diffuse and progressively worsening bone and joint pain.
The bone pain in the weight-bearing part is more prominent, and the lower limbs and lumbar spine are more obvious.
Skeletal deformities and pathological conditions may occur Fractures, short stature, difficulty walking, or even being unable to stand are easily misdiagnosed as rheumatoid arthritis or primary osteoporosis
.
In the later stage, it manifests as fibrocystic osteitis.
X-ray or CT examination often shows obvious osteoporosis, severe or even obvious bone destruction, and "giant cell tumor" appears in the long bone backbone, ribs, jaw or clavicle, which is easy to be misdiagnosed For bone tumors
.
Among them, after joint pain, decreased bone density and fragility fractures are misdiagnosed as primary osteoporosis, if given active calcium treatment, the symptoms of hypercalcemia will be aggravated
.
2.
How to avoid the misdiagnosis of PHPT Due to the lack of understanding of PHPT, most patients with PHPT are treated in rheumatology, endocrinology, gastroenterology, orthopedics, urology and other departments with certain system symptoms, and some clinicians are also lacking The overall understanding of the disease, especially when the symptoms are not typical in the early stage, often only pay attention to the local symptoms and ignore the overall performance, which is easy to be misdiagnosed and mistreated
.
When a certain clinical symptom is prominent, the typical manifestations of hyperparathyroidism are often masked
.
Therefore, clinicians need to improve their sensitivity to this disease, and should consider the possibility of primary hyperparathyroidism when clinically encountering the following clinical manifestations: 1.
Recurrent or active urinary calculi or renal calcium salt deposition Disease
.
2.
Osteoporosis of unknown cause, especially accompanied by subperiosteal cortical bone resorption and/or alveolar bone plate resorption and bone cyst formation
.
3.
"Giant cell tumors" of long bones, ribs, jaws or clavicles, especially multiple ones
.
4.
Unexplained nausea, vomiting, unhealed peptic ulcer, intractable constipation or recurrent pancreatitis
.
5.
Unexplainable psychoneurological symptoms, especially those accompanied by thirst, polyuria, and bone pain
.
6.
Positive family history and mothers of infants with neonatal tetany
.
7.
Long-term use of lithium preparations and hypercalcemia
.
8.
Hypercalciuria with or without hypercalcemia
.
9.
Those who have hypercalcemia when supplementing calcium, vitamin D preparations or using thiazide diuretics
.
Once primary hyperparathyroidism is suspected, complete the necessary laboratory tests, including the measurement of electrolytes, parathyroid hormone, urine calcium, urine phosphorus, etc.
, when there is hypercalcemia accompanied by blood parathyroid hormone If the level is higher than normal or higher than the normal range, it is necessary to consider the diagnosis of primary hyperparathyroidism, and then use ultrasound, radionuclide, neck and mediastinal CT and other relevant localization examinations to understand parathyroid disease Complete positioning diagnosis of the site
.
Third, PHPT treatment of primary hyperparathyroidism, surgical resection of the primary lesion is the first choice
.
Medical treatment and long-term follow-up can be considered for patients who are inoperable or who refuse surgery
.
When blood calcium>3.
5mmol/L, no matter whether there are clinical symptoms or not, effective measures should be taken immediately to lower blood calcium levels
.
Drugs, including therapeutic expansion principle, promote urinary calcium excretion, inhibiting bone resorption, etc.
, commonly used drugs, including bisphosphonates, estrogen, cinacalcet the like
.
References: [1] Wang Ou, Xing Xiaoping, Meng Xunwu, et al.
Analysis of the clinical characteristics of asymptomatic primary hyperparathyroidism[J].
Chinese Journal of Osteoporosis and Bone Mineral Diseases.
2010, 3( 01): 18-22.
[2] Liu Yang, Zhu Yingying, Shi Ying, et al.
Diagnosis and treatment of primary hyperparathyroidism[J].
Chinese Journal of Laboratory Diagnosis.
2015, 19(02): 230-232.
[3] Li Zitao, Ma Zhijun, Liu Zhen, Shen Guoshuang.
Surgical treatment and misdiagnosis analysis of 18 cases of primary hyperparathyroidism [J].
Chinese Journal of New Clinical Medicine, 2019, 12(10):1098-1102.
[4 ]Ma Lu, Liu Qi, Liu Xiang, Ding Ya, Zhe Zhanfei.
Analysis of diagnosis and treatment of 9 cases of primary hyperparathyroidism and literature review[J].
Progress in Modern Chinese General Surgery,2021,24(05):415- 417.
.
Primary hyperparathyroidism (PHPT) is a set of clinical syndromes caused by excessive secretion of parathyroid hormone (PTH) caused by primary lesions of parathyroid tissue, including hypercalcemia, renal calcium reabsorption, and urine Increased phosphorus excretion, kidney stones, nephrocalcinosis, and increased absorption of cortical bone
.
It can occur at any age, but it is most common in adults.
The peak incidence is 30-50 years old.
It is more common in postmenopausal women.
The incidence of women is about 4 times that of men
.
As an endocrine disease, this disease was considered uncommon in the past.
In fact, according to data from the West, the number of diagnosed PHPT is increasing year by year, and it has become a relatively common endocrine disease.
However, the clinical manifestations of PHPT are complicated.
It harms multiple organs and is related to various systems.
It is often not specific, and the disease is insidious, which brings great difficulties to the diagnosis of the disease.
It is very easy to cause misdiagnosis or missed diagnosis.
If the treatment is delayed, it can cause irreversible damage to the patient.
, Even life-threatening
.
The following summarizes and analyzes the clinical misdiagnosis of PHPT, hoping to help improve clinicians' understanding of the disease
.
1.
Common misdiagnosis of PHPT 1.
Misdiagnosed as a "neurological disease", such as cerebrovascular disease, psychosis, dementia, etc.
➤ Hypercalcemia caused by PHPT affects the stability of the central nervous system, and the toxicity of high calcium to brain cells can be Interfering with the electrophysiological activities of brain cells, causing patients to have a variety of neuropsychiatric symptoms, including anxiety, affective disorders, personality changes, and confusion, which are easily misdiagnosed as psychosis; ➤Severe hypercalcemia (5 mmol/l) may cause drowsiness, Confusion, stupor, and coma may be misdiagnosed as cerebrovascular disease; some patients may show memory loss, cognitive impairment, personality changes, depression, etc.
, especially in elderly patients, and it is easy to be misdiagnosed as Alzheimer’s and depression And so on, clinicians should remain vigilant
.
2.
Misdiagnosed as "digestive system disease", such as chronic gastritis, gastric ulcer, pancreatitis, etc.
PHPT can cause a series of pathological changes in the digestive system, which are also closely related to hypercalcemia.
The main mechanism is: ➤Hypercalcemia can cause Neuromuscular excitability decreases, gastrointestinal smooth muscle tension decreases, and peristalsis is slow.
The main clinical manifestations are loss of appetite, abdominal distension, anorexia, constipation, etc.
, which are easily misdiagnosed as chronic gastritis and gastrointestinal dysfunction; ➤High blood calcium can stimulate the stomach Mucosal G cells secrete gastrin, which increases the secretion of gastric acid, and eventually peptic ulcers, upper abdominal pain, melena and other symptoms appear.
Clinically, some patients with recurrent peptic ulcers should be highly alert to PHPT; ➤High blood calcium promotes pancreatic juice secretion Activating trypsinogen, leading to the pancreas self-digestion and causing pancreatitis, long-term deposition of calcium ions in the pancreas can cause pancreatic duct calcification or formation of pancreatic duct stones, which can lead to acute attacks of chronic pancreatitis
.
The possibility of PHPT should be considered in clinical encounters with such patients
.
3.
Misdiagnosed as a "urinary system disease", such as urinary tract infection, kidney stones, chronic renal insufficiency, etc.
Hypercalcemia caused by PHPT makes calcium deposits in the renal parenchyma, which can cause interstitial nephritis, salt-loss nephropathy, calcium Substance deposition and renal calculi decline in renal tubular concentration, and eventually develop into renal failure, and are also prone to urinary tract infections, manifested as polydipsia, polydipsia, nocturia, polyuria and other phenomena
.
Kidney stones and renal parenchymal calcification cause recurrent renal colic and hematuria
.
Clinically, there are many misdiagnosed as simple urinary tract infections and kidney stones
.
Renal colic, ureter spasm, gross hematuria, and even gravel-like stones in the urine
.
Patients with recurrent urinary calculi should think of the possibility of PHPT
.
4.
Misdiagnosed as a "skeletal system disease", such as rheumatoid arthritis, primary osteoporosis, bone tumors and other hyperparathyroidism, excessive secretion of PTH will cause abnormal calcium and phosphorus metabolism, increased bone absorption, and Osteoporosis occurs earlier, faster, and more severely, with systemic diffuse and progressively worsening bone and joint pain.
The bone pain in the weight-bearing part is more prominent, and the lower limbs and lumbar spine are more obvious.
Skeletal deformities and pathological conditions may occur Fractures, short stature, difficulty walking, or even being unable to stand are easily misdiagnosed as rheumatoid arthritis or primary osteoporosis
.
In the later stage, it manifests as fibrocystic osteitis.
X-ray or CT examination often shows obvious osteoporosis, severe or even obvious bone destruction, and "giant cell tumor" appears in the long bone backbone, ribs, jaw or clavicle, which is easy to be misdiagnosed For bone tumors
.
Among them, after joint pain, decreased bone density and fragility fractures are misdiagnosed as primary osteoporosis, if given active calcium treatment, the symptoms of hypercalcemia will be aggravated
.
2.
How to avoid the misdiagnosis of PHPT Due to the lack of understanding of PHPT, most patients with PHPT are treated in rheumatology, endocrinology, gastroenterology, orthopedics, urology and other departments with certain system symptoms, and some clinicians are also lacking The overall understanding of the disease, especially when the symptoms are not typical in the early stage, often only pay attention to the local symptoms and ignore the overall performance, which is easy to be misdiagnosed and mistreated
.
When a certain clinical symptom is prominent, the typical manifestations of hyperparathyroidism are often masked
.
Therefore, clinicians need to improve their sensitivity to this disease, and should consider the possibility of primary hyperparathyroidism when clinically encountering the following clinical manifestations: 1.
Recurrent or active urinary calculi or renal calcium salt deposition Disease
.
2.
Osteoporosis of unknown cause, especially accompanied by subperiosteal cortical bone resorption and/or alveolar bone plate resorption and bone cyst formation
.
3.
"Giant cell tumors" of long bones, ribs, jaws or clavicles, especially multiple ones
.
4.
Unexplained nausea, vomiting, unhealed peptic ulcer, intractable constipation or recurrent pancreatitis
.
5.
Unexplainable psychoneurological symptoms, especially those accompanied by thirst, polyuria, and bone pain
.
6.
Positive family history and mothers of infants with neonatal tetany
.
7.
Long-term use of lithium preparations and hypercalcemia
.
8.
Hypercalciuria with or without hypercalcemia
.
9.
Those who have hypercalcemia when supplementing calcium, vitamin D preparations or using thiazide diuretics
.
Once primary hyperparathyroidism is suspected, complete the necessary laboratory tests, including the measurement of electrolytes, parathyroid hormone, urine calcium, urine phosphorus, etc.
, when there is hypercalcemia accompanied by blood parathyroid hormone If the level is higher than normal or higher than the normal range, it is necessary to consider the diagnosis of primary hyperparathyroidism, and then use ultrasound, radionuclide, neck and mediastinal CT and other relevant localization examinations to understand parathyroid disease Complete positioning diagnosis of the site
.
Third, PHPT treatment of primary hyperparathyroidism, surgical resection of the primary lesion is the first choice
.
Medical treatment and long-term follow-up can be considered for patients who are inoperable or who refuse surgery
.
When blood calcium>3.
5mmol/L, no matter whether there are clinical symptoms or not, effective measures should be taken immediately to lower blood calcium levels
.
Drugs, including therapeutic expansion principle, promote urinary calcium excretion, inhibiting bone resorption, etc.
, commonly used drugs, including bisphosphonates, estrogen, cinacalcet the like
.
References: [1] Wang Ou, Xing Xiaoping, Meng Xunwu, et al.
Analysis of the clinical characteristics of asymptomatic primary hyperparathyroidism[J].
Chinese Journal of Osteoporosis and Bone Mineral Diseases.
2010, 3( 01): 18-22.
[2] Liu Yang, Zhu Yingying, Shi Ying, et al.
Diagnosis and treatment of primary hyperparathyroidism[J].
Chinese Journal of Laboratory Diagnosis.
2015, 19(02): 230-232.
[3] Li Zitao, Ma Zhijun, Liu Zhen, Shen Guoshuang.
Surgical treatment and misdiagnosis analysis of 18 cases of primary hyperparathyroidism [J].
Chinese Journal of New Clinical Medicine, 2019, 12(10):1098-1102.
[4 ]Ma Lu, Liu Qi, Liu Xiang, Ding Ya, Zhe Zhanfei.
Analysis of diagnosis and treatment of 9 cases of primary hyperparathyroidism and literature review[J].
Progress in Modern Chinese General Surgery,2021,24(05):415- 417.
