Baseda disease – palpitations, hypertrophy and bulging of the eyes
Baseline disease is a specific autoimmune disease that affects the thyroid gland. It develops after the pathologically enhanced function of the gland. It is characterized by a specific symptom complex that allows patients to be recognized from the first physical examination. The condition proceeds with pronounced tachycardia – accelerated activity of the heart muscle, hypertrophy of the gland, which appears enlarged and enlarged, and characteristic protrusion of the eyeballs.
Psychotrauma at an early age or increased nervous tension during the work process in a chronic order play a large role in triggering the disease. Also, some specialists in endocrinology share about familial predisposition in the disease. The disease is named after von Basedow, who was a German physician who participated in all the studies about the disease. He was the first to describe the pathogenesis and etiology of the disease, and later presented the full clinical picture. In his honour in 1840 they named the disease after him.
The disease affects women more often than men. It manifests itself at the age between 30 and 50 years. Until very recently, it was thought that the disease was impossible to link to an existing pregnancy. Subsequently, after teamwork, psychiatrists, endocrinologists and obstetricians proved that stress in pregnancy or the occurrence of urinary tract infections may be linked to the manifestation of Baseline disease in pregnancy.
How does the disease develop in the body?
Baseline disease is an autoimmune disease in which antibody production against the TSH hormone begins. Sometimes antibodies in the blood plasma against T3 and T4 hormones are also found. Antibodies bind to TSH receptors and stimulate the production of T3 and T4. It is the increase in these two hormones that causes the manifestation of clinical symptoms of hyperthyroidism and goiter.
Increased production of these hormones accelerates tissue metabolism and oxygen consumption. The intensity in the production of thyroid hormones leads to so-called excess or hypermetabolism, which neutralizes very quickly the glucose or fat molecules that have entered the body. This causes the release of even more heat energy, which leads to some of the specific symptoms. Thus, nervous excitability is increased, which in turn explains other common symptoms in the clinical picture of patients.
2. What are the symptoms of the disease?
Symptoms are characteristic of the disease. The disease can proceed latently with the manifestation of only one symptom, which is usually atypical , or with the whole complex of clinical data. Among the most common symptoms are exophthalmos – protrusion of the eyeballs, frequent sweating and fluid loss, weight loss, tachycardia, muscle weakness, and constant fatigue.
Among the rarer symptoms can be noted elevated blood pressure – hypertension, which is often an atypical debut symptom when the disease is triggered. This masks the clinical finding and delays the diagnosis in time. Emotional instability and problems with sleep and memory are also typical symptoms for sufferers of the disease.
The clinical picture is objectified by pronounced goiter in an average of 80% of patients. The gland has a soft consistency on palpation, painless and with a smooth surface. On auscultation of the gland, a systolic noise is detected from the pushing of blood through the aortic valve.
Patients are mostly restless and tense, have accelerated thought activity and poor memory. They are characterized by logorrhea. Some of them share about insomnia and emotional lability. A characteristic feature is the protrusion of the eyeballs. The exophthalmos is symmetrical and moderately pronounced. Looking down, there is upper eyelid lag, delayed convergence, hyperpigmentation of the eyelid skin and very slow and infrequent blinking – a symptom of Stewag.
Patients usually report weight loss in addition to maintained or increased appetite. This is explained by the increased production of thyroid hormones, which play a major role in the body’s fat and carbohydrate metabolism. In women, oligo or amenorrhea is often observed, which in practice is objectified by a delay and thinning of menstrual cycles.
Often observed in patients manifestations of tachycardic crises and extrasystoles. Usually, the degree of development of the disease also determines the values of the accelerated pulse. In moderately severe forms of the disease, a frequency of between 100-120 beats per minute is maintained. In severe cases, sometimes the pulse rate can reach up to 180 beats per minute, which is a life-threatening condition.
3. How is the diagnosis made?
Diagnosis is a slow process and aims to examine many clinical features to prove the development of the disease. Laboratory diagnosis shows a strong decrease in TSH and respectively an increase in T3 and T4. Low amounts of cholesterol, leukopenia with lymphocytosis, elevated calcium, decreased potassium and impaired or decreased glucose tolerance are also recorded.
At the onset of the disease, diagnosis is difficult. It is facilitated by a complete database of clinical and laboratory data, as well as the manifestation of specific symptomatic entities for the disease.
Treatment of the disease is complex. Beta-blockers are used to regulate cardiac activity, vitamins, sedative and anxiolytic drugs. To normalize hormonal genesis in the gland, some antithyroid drugs are administered, which block the production of thyroid. Some thyreostatics and corticosteroids may also be administered. Some endocrinologists recommend their drug-resistant patients undergo a subtotal thyroidectomy, which actually reduces hormone production because part of the gland is removed.