Azathioprine-associated Acute Pancreatitis in Rheumatoid Arthritis / 대한내과학회지

Drug-induced pancreatitis is now recognized as a distinct, although uncommon, entity. Azathioprine has been incriminated as a causative agent of acute pancreatitis. We report a 36-year-old female who developed acute pancreatitis in the course of treatment with azathioprine for rheumatoid arthritis. She was admitted due to epigastric pain, radiating to the back, for four days. Serum amylase and lipase levels were 226U/L (normal : 30-110U/L) and 1300U/L(normal : 23-300U/L), respectively. The abdominal ultrasonogram and CT scan revealed diffuse enlargement of the pancreas. We diagnosed it as acute pancreatitis. There was no history of alcohol use or gallbladder disease. We considered drugs, especially azathioprine, as the cause of acute pancreatitis. The patient was treated conservatively with intravenous fluid and analgesics. The symptoms subsided within three days. Thirteen days later, azathioprine was resumed. After six hours, the patient complained of epigastric pain. The elevated level of serum lipase(542U/L) confirmed the recurrence of pancreatitis. Her symptoms subsided when azathioprine intake stopped, and the serum lipase level returned to normal within four days.

A Case of Graves' Disease Associated with Guillain-Barre Syndrome / 대한내분비학회지

Graves disease, an autoimmune endocrine disorder, which causes defects in cellular and humoral immunity, is associated with insulin-dependent diabetes mellitus, Addisons disease, pemicious anemia, and rheumatoid arthritis. Graves disease is associated with various neuro-muscular disorders, such as myopathy, exophalmous oculopathy, periodic paralysis, myastenia gravis and rarely Guillain-Barre syndrome. Guillain-Barre syndrome is considered as an autoimmune disease which can occur concurrently with other autoimmune disorders. This syndrome is characterized by segmental demyelination and axonal degeneration in electrophysiology due to autoantibody to nervous systems via cellular and humoral autoimmunity. In Graves disease, the exact mechanism of the associated Guillain-Barre syndrome is not well understood but it is considered that the autoimmunity is the leading cause of development of both diseases. A 37 year-old man had suffered from thyrotoxic symptoms and progressive symmetrical muscular paralysis. In nerve conduction velocity studies, the result shows peripheral neuropathy; axonopathy; myelinopathy; motor nerve and sensory nerve derangement; right first sacral nerve neuropathy; and decreased CMAP amplitude. The patient was treated with propylthiouracil and high dose intravenous immunoglobulin (400mg/kg/day for Sdays). He responded to the therapy well and became euthyroid state with improvement of muscle weakness. We report a case of Graves' disease associated with Guillain-Barre syndrome with brief review of literature which shows a possible relationship between both diseases.

Acute Renal Failure in Rhabdomyolysis Associated with Furosemide Induced Hypokalemia / 대한신장학회잡지

Though hypokalemia often goes unrecognized as a cause of rhabdomyolysis, its causal relation for acute renal failure can be considered in cases of extreme hypokalemia when combined with rhabdomyolysis. We present the case of a 21-year-old female in whom acute renal failure was developed by myoglobinuria which was associated with furosemide induced hypokalemia. She had taken 2 grams of furosemide daily over 6 months before developing rhabdomyolysis. Initial neurologic examination revealed painful quadriplegia and laboratory findings showed markedly elevated blood CPK, LDH and AST levels with azotemia. Arterial blood gas analysis showed pH 7.439, serum Na 128mEq/L, K 1.5mEq/L, Cl 87mEq/L, HCO3- 12.6mmol/L and calculated anion gap of 29.9 which indicated that she was under the condition of mixed metabolic alkalosis and metabolic acidosis. Though intravenous infusion of potassium chloride improved muscle strength, azotemia and acidemia persisted for several days. This case suggest that large amount of furosemide, when used for a long time, can be result in the acute renal failure by rhabdomyolysis which was caused by hypokalemia.