Subject(s)
Polychondritis, Relapsing/complications , Respiratory Insufficiency/etiology , Aged , Bronchi , Bronchoscopes , Cough/etiology , Fever/etiology , Humans , Male , Polychondritis, Relapsing/diagnostic imaging , Polychondritis, Relapsing/drug therapy , Radiography , Respiratory Insufficiency/diagnostic imaging , Respiratory Insufficiency/drug therapy , Trachea/diagnostic imagingABSTRACT
BACKGROUND: The prevalence and clinical implications of vitamin D deficiency have never been studied in patients with underlying neuromuscular diseases complicated with chronic respiratory failure. The aim of this study is to demonstrate the prevalence of vitamin D deficiency, its relationship with other bone markers, and mode of nutrition. MATERIALS AND METHODS: Serum 25-hydroxyvitamin D (25[OH]D) levels along with calcium, serum albumin, and phosphorus levels were obtained from 57 patients with chronic respiratory failure due to underlying neuromuscular diseases. These levels were obtained during their first visit to a chronic respiratory diseases clinic. Data with regard to nutrition, respiratory muscle function, and level of mobility were also obtained at the same time. RESULTS: Seventy-five percent of patients had serum 25(OH)D levels ≤ 30 ng/mL. There is a negative correlation between parathyroid hormone and 25(OH)D levels (P = .006) and corrected calcium levels (P = .066). Serum 25(OH)D levels varied with the mode of nutrition. Patients on enteral nutrition had the highest serum levels of 25(OH)D, whereas combined oral and tube feeds had the lowest 25(OH)D levels (P = .006). CONCLUSION: Low serum 25(OH)D levels are highly prevalent in patients with neuromuscular disease and chronic respiratory failure. The route of nutrition has an impact on these levels.
Subject(s)
Neuromuscular Diseases/complications , Respiratory Insufficiency/metabolism , Vitamin D Deficiency/diagnosis , Vitamin D Deficiency/epidemiology , Adult , Calcium/blood , Eating , Enteral Nutrition , Feeding Methods , Female , Humans , Male , Middle Aged , Parathyroid Hormone/blood , Phosphorus/blood , Prevalence , Respiratory Insufficiency/etiology , Respiratory Insufficiency/nursing , Vitamin D/analogs & derivatives , Vitamin D/blood , Vitamin D Deficiency/bloodABSTRACT
Objective. Acute thyrotoxic bulbar palsy is rare, severe, and rapidly progressive. We describe a case of thyrotoxicosis with bulbar palsy, encephalopathy, and pyramidal tract dysfunction. Case Report. 64-year-old white male with toxic multinodular goiter presented with rapid atrial fibrillation. He had mild tremor, normal cranial nerve examination, 4/5 strength in all extremities, normal reflexes, and down going plantars. TSH was low at 0.09 (normal: 0.34-5.6 uIU/mL), and free T4 was high at 5.22 (normal: 0.47-1.41 ng/dL). Despite optimal AV nodal blockade, he had persistent rapid atrial fibrillation. He later developed cervical dystonia, rigidity, clonus, dysarthria, dysphagia, vocal cord palsy, and absent gag reflex. Thyroid storm was suspected. Neuroimaging and cerebrospinal fluid cultures were nondiagnostic. Acetylcholine receptor antibodies were negative. Swallow ability was impaired with heavy secretions. Remarkable improvement in symptoms was noted after initiation of treatment for thyroid storm. Conclusion. Pyramidal tract symptoms and bulbar palsy may occur with thyrotoxicosis. Cranial nerve involvement and encephalopathy raise a question of primary brain mechanism causing bulbar palsy. This is reversible with prompt treatment of thyroid storm.
