Author:
Amelicheva Alena Aleksandrovna medical editor
Quick Transition Treatment of Addison's Disease
Addison's disease (hypocorticism, chronic adrenal insufficiency) is a rare disease characterized by insufficient production of the glucocorticoid hormone cortisol and the mineralocorticoid hormone aldosterone by the adrenal glands.
Most often, hypocortisolism, which affects both men and women, occurs at the age of 30-50, but the onset (first clinical manifestation) of the disease can be observed at any age.
The worldwide prevalence of Addison's disease is 40-60 patients diagnosed with AD per 1 million people.
Causes
Typically, Addison's disease occurs due to damage or destruction of the adrenal cortex as a result of the development of an autoimmune process (the immune system perceives the adrenal cortex as foreign, attacks and destroys it) or another autoimmune disease that the patient has.
Other causes of the disease include:
- tuberculosis (mainly in developing countries);
- other (secondary, for example fungal) infections;
- malignant tumors (with the spread of tumor cells from the primary focus, lymphoma);
- bleeding in the adrenal glands (adrenal infarction);
- genetic predisposition (in rare cases).
Deficiency of glucocorticoid and mineralocorticoid hormones caused by decreased function of the adrenal cortex is called primary adrenal insufficiency. If the adrenal glands are unable to produce these hormones for other reasons (for example, due to pituitary gland abnormalities or dysfunction), we are talking about secondary adrenal insufficiency.
Which bones and joints are susceptible to osteochondropathy?
pathological processes can develop in various bone structures. Osteochondropathies are susceptible to:
- Long tubular bones (epiphyses):
femur (head), II-III metatarsal bones, clavicle (sternal end), fingers (phalanx);
- Short tubular bones:
navicular bone of the foot, lunate carpal, patella, vertebral body, talus, sesamoid bones, tarsus.
- Apophyses:
tibia, apophyseal rings of the vertebrae, humerus, pubis. Osteochondropathy of the calcaneal tuber is often diagnosed.
Depending on the location of the lesion, several types of disease are distinguished - Legg-Calvé-Perthes disease, Keller-I and II, Scheuermann-Mau, Calve, partial osteochondropathy, damage to the knee, elbow joint, calcaneus, etc.
Symptoms
Addison's disease progresses slowly over several months. Symptoms may vary from person to person. The first clinical manifestations are often nonspecific, that is, similar to the symptoms of other common diseases.
Usually in the initial stages of the disease the patient does not feel any symptoms. Unfortunately, the onset of AD is associated with 90% damage to the adrenal cortex.
Symptoms of Addison's disease include:
- increased fatigue;
- decreased energy;
- general malaise;
- hyperpigmentation of the skin, affecting the palmar sweets, phalanges of the fingers, scars, mucous membranes of the oral cavity, friction points;
- skin pigmentation disorder (vitiligo);
- decreased appetite and weight loss;
- dehydration;
- low weight and retarded physical development (in children);
- craving for salt or salty foods;
- nausea, vomiting;
- abdominal pain, diarrhea;
- fainting;
- muscle and joint pain;
- irritability, decreased concentration, depression;
- alopecia areata;
- hair loss in some areas of the body, dry skin, decreased libido, menstrual irregularities (in women);
- hypoglycemia (decreased blood glucose concentration);
- postural hypotension (a sharp decrease in blood pressure when body position changes).
Sometimes Addison's disease, which has not manifested itself before, can occur suddenly and acutely - for example, in the absence of necessary treatment or as a result of exposure to stress factors (accident, injury, surgery), infection, or other disease. In this case, we are talking about a life-threatening condition - the so-called. Addisonian crisis or acute adrenal insufficiency. Characteristic signs: severe weakness, confusion, pain in the back, legs and abdomen, vomiting and diarrhea, low blood pressure, hyperkalemia, hyponatremia.
Forms of the disease
The disease can develop in the area of the bone epiphysis.
Pathology develops in tubular bones in the following areas:
- epiphyses - zone of bone tissue growth;
- apophyses - bone protrusions with muscles and ligaments located next to the epiphyses.
Osteochondropathy is a clinical process with a characteristic change of phases. There are 5 stages in the development of pathology:
- aseptic necrosis;
- impression fracture and fragmentation;
- resorption of necrotic tissue;
- regeneration;
- recovery.
Osteochondropathy of the talus (Diaz syndrome)
This disease is rare, mainly in children during periods of intensive growth. The talus is part of the ankle joint and serves to evenly distribute body weight to all structural elements of the foot. With Diaz syndrome, in addition to necrotization of bone tissue, damage to the articular cartilage occurs. Lack of treatment exacerbates further destruction of cartilage tissue. The pathology is accompanied by pain in the ankle joint, lameness, soreness and swelling of the lower leg.
Gaglund-Schinz disease
A child may experience pain while running.
Osteochondropathy of the calcaneal tuberosity is more often observed in girls. The pain is most pronounced during intense movements - running, jumping, fast walking. Usually the disease goes away as you grow older, but heel pain persists for a very long time, sometimes until the teenager has completely grown. A characteristic feature of this type of disease is increased sensitivity of the back of the foot. Over time, the pain intensifies - this forces the patient to rely on his fingers when walking, which is why the gait is distorted.
Keller's disease I
It is diagnosed more often in boys 3-9 years old. The disease represents osteochondropathy of the scaphoid bone with damage to the epiphyseal zones, usually on one leg. Soreness and swelling of the back of the inner edge of the foot forces the child to step on the outer side when walking. In adults, the disease is rarely detected, mainly due to injuries and heavy work overload. In such cases, necrosis develops on already formed bone, so treatment should be completed as early as possible to avoid complications.
Keller's disease II
With this pathology, walking barefoot causes discomfort to a person.
The disease represents chondropathy of the heads of the 2nd and 3rd metatarsal bones, but cases with multiple or bilateral lesions are possible. A feature of multiple lesions is static deformation of the foot - flat feet, dysplasia, valgus deformity of the big toe, an increase in the size of the head of the bones, shortening of the fingers. When palpating, the patient feels pain at the base of the fingers. Unpleasant sensations appear when walking barefoot and wearing shoes with soft soles.
Renander-Muller disease
The development of aseptic necrosis of the sesamoid bone of the first metatarsophalangeal joint is more common in young women. The pathology is manifested by characteristic, gradually increasing pain at the base of the fingers, especially when stepping on the foot. The images show structural changes in the sesamoid bone with fragmentation. For this area, differential diagnosis is necessary, since the studied areas of necrosis, taken for osteochondropathy, may be the consequences of fractures.
Disease of the tuberosity of the fifth metatarsal bone
Some doctors compare this pathology with a slowdown in ossification. But the process always proceeds painlessly and in the same plane. Therefore, pain and x-rays showing the location of fragments of the fifth metatarsal tuberosity in two planes are important indicators for diagnosis, as well as thickening at the site of the lesion and swelling of the soft tissues, causing the patient to limp.
Diagnostics
The diagnosis is established based on the patient’s medical history, complaints and symptoms, and the results of laboratory and instrumental diagnostics (CT, MRI).
Blood tests are aimed at determining the levels of sodium, potassium, cortisol and adrenocorticotropic hormone (ACTH), which stimulates the production of hormones by the adrenal cortex, as well as identifying specific antibodies associated with Addison's disease.
The patient may be prescribed an ACTH stimulation test, during which adrenocorticotropic hormone is administered (to stimulate cortisol production). If stimulation does not produce normal levels of cortisol, this indicates adrenal damage or dysfunction.
An insulin-induced hypoglycemic test is also performed , which helps to establish the relationship between the characteristic symptoms of Addison's disease and pituitary gland abnormalities or dysfunction. During this test, the patient is injected with fast-acting insulin, and blood sugar levels are measured before and after the injection.
To assess the function of the adrenal glands and their structural features, additional imaging is performed using CT and MRI. These studies help clarify the characteristic changes observed during the development of Addison's disease.
Differential diagnosis
Most often, Addison's disease is differentiated (distinguished) from the following diseases:
- secondary adrenal insufficiency caused by a decrease in the production of adrenocorticotropic hormone by the pituitary gland;
- congenital adrenal hyperplasia (a group of hereditary pathologies arising due to impaired cortisol biosynthesis);
- adrenoleukodystrophy (hereditary degenerative disease of the central nervous system, which is transmitted in an X-linked recessive manner and is associated with adrenal insufficiency);
- autoimmune polyendocrine syndrome type 2 (Schmidt syndrome, a rare autoimmune disease in which there is a sharp decrease in the function of several endocrine organs: adrenal glands, thyroid gland, parathyroid glands, gonads, pancreas);
- autoimmune polyendocrine syndrome type 1 (a rare genetic syndrome APECED, which is characterized by lesions of the skin and mucous membranes by Candida fungi, decreased function of the parathyroid glands and autoimmune insufficiency of adrenal function).
Treatment of Addison's disease
Treatment of Addison's disease is based on the use of drug therapy aimed at replacing glucocorticoid and mineralocorticoid hormones. Oral administration of hydrocortisone and fludrocortisone is recommended; the dosage of the drugs is selected individually. Therapy is carried out throughout life.
Androgen replacement therapy (testosterone or androstenedione) may be offered to some patients. Patients receiving this treatment report a decrease in symptoms of fatigue, an improvement in mood and psycho-emotional state in general, and an increase in libido (in women), however, these treatment approaches are still being studied.
Treatment for Addisonian crisis includes intravenous hydrocortisone, fluids, electrolytes, and blood pressure medications.
Features and benefits of treatment for Addison's disease at the Rassvet Clinic
Timely diagnosis and effective treatment of rare syndromes and diseases are the areas of interest of all doctors at the Rassvet Clinic.
Our endocrinologists are highly qualified doctors, well trained and have extensive practical experience.
Patients with suspected Addison's disease undergo all necessary diagnostic tests to confirm or exclude the diagnosis. If necessary, an adequate treatment regimen is selected individually.
Recommendations from an endocrinologist at the Rassvet clinic for patients with Addison’s disease
In addition to taking replacement therapy drugs, the patient needs to ensure that he gets enough salt (sodium) from the diet, especially during exercise, fever or gastrointestinal upset.
The dosage of medications taken may be temporarily increased if the patient experiences stress associated with surgery, infectious or other diseases. If the patient is unable to take the necessary medications orally due to nausea and vomiting, injections are prescribed.
It is important for patients with Addison's disease to know that taking steroids in their case is not associated with serious side effects, since the lack of hormone production is compensated. With the correct dosage of medications, there are practically no side effects.
Patients with Addison's disease must always carry a medical document indicating the presence of the disease with them in cases of emergency medical care.
Addison's disease cannot be prevented, but there is an effective treatment for it. With timely diagnosis, proper selection of therapy, and compliance with measures to prevent acute adrenal insufficiency, life expectancy in patients with this disease does not decrease.
Up to 12 weeks
— Andrey Georgievich, today experts are talking not just about COVID-19, but also about its protracted form. Please explain to our readers what is meant by the term “long Covid”.
- This condition does not affect everyone. In some patients, symptoms of coronavirus infection may persist for up to 12 weeks. This is long-Covid, that is, prolonged Covid, when all the signs of intoxication and damage to various functional systems of the body remain, despite the therapy.
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If after 12 weeks the patient is bothered by excessive weakness, drowsiness, decreased performance, depression, memory impairment, and impaired concentration, then these manifestations are called post-Covid, and this condition can last a year or even more.
— What symptoms characterize long-covid?
- Absolutely the same as in the acute period. It all depends on which organs and systems are affected by the coronavirus infection.
Most often, the respiratory system suffers, and damage to other organs and systems is also observed: digestive, cardiovascular, nervous, endocrine and others.
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