TPP patients are usually between 20 and 40 years of age, similar to the age distribution for thyrotoxicosis. Isolated cases were reported in paediatric age group. The paralytic attacks are characterized by transient, recurrent episodes of muscle weakness. Attacks involve proximal more than the distal muscles, with an initial involvement of the lower limbs and subsequently the truncal muscles, and finally all four limbs. The degree of weakness varies from mild weakness to total flaccid paralysis and hyporeflexia. Some patients may experience prodromal symptoms of aches, cramps, or stiffness in the affected muscles. Weakness usually affects skeletal muscles only. However, total paralysis of respiratory, bulbar, and ocular muscles has been reported in severe cases. Recovery is usually complete, but the duration of paralysis can vary from a few hours in a mild attack to 36– 72 h in a severe attack. Electromyographic studies have confirmed the myopathic changes with intact peripheral nerve function. The presentation of TPP may be confused with Guillain- Barre syndrome, acute spinal cord compression, myelitis, and hysteria. The attacks of weakness are similar to those of familial hypokalaemic periodic paralysis (FHPP) except for the presence of hyperthyroidism. While FHPP is an autosomal dominant condition affecting mainly Caucasians, TPP is a sporadic disease found mainly in Asian males, and familial cases of TPP are extremely rare.

High carbohydrate loads and strenuous exercise are well recognized precipitating factors for TPP. The paralytic attacks do not occur during exercise but occur during the resting period that follow strenuous exercise, and the attacks may be aborted by continuation of exercise. In subtropical cities such as Hong Kong, attacks are most common during the seasons of summer and fall. This seasonal variation is probably associated with an increased intake of sugary drinks as well as outdoor activities and exercise in these weather conditions. In tropical cities such as Singapore, sea sonal variation is not seen. Attacks usually occur in the middle of the night or early morning, which coincides with a period of rest following a heavy meal or exercise. Paralysis can be induced in these patients with high carbohydrate loads with or without insulin infusion, strenuous exercise, or even thyroxine therapy. However, attacks cannot be induced once the patient has become euthyroid. Although high carbohydrate loads and strenuous exercise are well recognized precipitating factors for TPP, they were implicated in only 16 and 10 out of 135 cases in a prospective observational study, respectively. Other precipitation factors include trauma, stress, alcohol consumption (especially binge drinking), acute urinary tract infection, and drugs (such as steroids and non- steroidal anti- inflammatory drugs).

Hypokalaemia is the hallmark of TPP. Plasma potassium concentrations have been reported to be as low as 1.1 mmol/ L. Some patients may have a near to normal plasma potassium concentration if they are admitted during the recovery phase of the attack. Mortality due to cardiac arrhythmia associated with the hypokalaemia has been reported. The complication of rhabdomyolysis may occur in a severe attack. Potassium concentration returns to normal when the patient recovers spontaneously from the weakness. The degree of hypokalaemia and the severity of weakness have no cor relation with the severity of hyperthyroidism and the serum thyroid hormone concentration. Indeed, many patients have relatively few symptoms of hyperthyroidism and TPP may be their only manifestation of thyrotoxicosis. Apart from hypokalaemia, patients may also experience mild to moderate hypophosphataemia and hypomagnesaemia. These are also a result of intracellular shift as these electrolyte abnormalities would return to normal spontaneously when the patient recovers from the paralysis.

The underlying cause of hyperthyroidism in the majority of TPP patients is Graves’ disease. However, TPP can also be associated with thyroiditis (either spontaneous or induced by interferon therapy), toxic nodular goitre, toxic adenoma, TSH- secreting pituitary tumour, and even overdosage of thyroid hormone. TPP is usually the early presentation of the underlying thyroid disease. In the case of Graves’ disease, TPP can also be a presenting feature of relapse of the disease. Paralysis only occurs when the patient is thyrotoxic but not euthyroid.

Muscle biopsies from patients with TPP have revealed a variety of abnormalities. The most consistent finding is proliferation and focal dilation of the sarcoplasmic reticulum and transverse tubular system, with prominent vacuoles arising from the sarcoplasmic reticulum. It is uncertain whether these vacuoles represent coalescence of dilated sarcoplasmic reticulum or sequestrated areas of focal myofibrial necrosis.

اخر الاخبار

اخبار العتبة العباسية المقدسة

للاطلاع على تجربته الإعلامية.. قسم الإعلام يستقبل وفدًا من جامعة واسط

المتولي الشرعي للعتبة العباسية المقدسة يطلع على واقع العمل في مصنع النور لإنتاج الألواح الشمسية

دار علوم نهج البلاغة تقدم المحاضرة التاسعة ضمن محفل نهج البلاغة الأسبوعي في بغداد

ضمن برامجه التوعوية.. قسم الشؤون الدينية ينظم محاضرة إرشادية لملاكات الحزام الأخضر الجنوبي

المزيد

الآخبار الصحية

عدد مرات التبرز يكشف أسرارا عن صحة الأمعاء

علامات جينية طويلة الأمد تتركها الرضاعة الطبيعية في دم الطفل

هل يمكن إعادة برمجة الجهاز المناعي لإنتاج أجسام مضادة نادرة؟

دراسة: أدوية الزهايمر "لا تحدث فرقا يذكر لدى المرضى"

المزيد

الآخبار التكنلوجية

روسيا تطور تقنية جديدة لتعديل خصائص البلاديوم

الصين: طاقم مهمة شينتشو-21 سيبقى في الفضاء شهرا آخر

"أبل" تهدد بحذف تطبيق "غروك" من متجرها وتكشف السبب

"أبل" تهدد بحذف تطبيق "غروك" من متجرها وتكشف السبب

المزيد

مواضيع ذات صلة

Absent Intrinsic Factor Secretion and Pernicious Anemia

Subclinical Hyperthyroidism

Nutritional Causes of Folate Deficiency

Neurologic Dysfunction with Cobalamin Deficiency

Sclerosing Thyroiditis (Riedel’s Thyroiditis) : Clinical Features

Infectious Thyroiditis

Leukopenia

Morphologic Expression of Megaloblastosis

Presentations Associated with Sideroblastic Anemia or Porphyrinuria

Sideroblastic Anemia and Porphyrinuria Caused by Drugs

Addison’s Disease

Cushing’s Disease