ctopic secretion of growth hormone-releasing hormone (GHRH) is a rare cause of acromegaly. [1][2][3][4][5] The most common tumors secreting GHRH are bronchial carcinoids and pancreatic islet cell tumors. Differential diagnosis of pituitary adenoma is necessary to avoid unnecessary pituitary surgery and damage to the pituitary gland. Rarely, that syndrome is secondary to a carcinoid bronchial tumor. We present a case of a synchronous GHRH-secreting bronchial carcinoid and a pituitary adenoma in a patient with acromegaly.
Furthermore, the bowel was silent and abdominal compartment syndrome with a measured pressure of 25 cmH 2 O (on 8th day), developed. CT of the abdomen, on 8th day, revealed multiple peritoneal and extraperitoneal fluid collections with infectious extension to the retroperitoneum. Surgical drainage was performed; the abdomen remained open. A slow progressive recovery was followed. Closure of the abdominal walls was performed on 25th day. The patient remained in the ICU for 39 days. Serum antistreptolycin O (ASO) titer was 580 IU/ml on the 6th day (normal range, 0-180 IU/ml), rising to 2,750 IU/ml on the 21st day. Although erythema and edema of the posterior pharynx were present and the tonsils were enlarged upon admission to the ICU, swabs cultures obtained from the throat grew only commensals.He was discharged home on the 50th day on oral penicillin ( Fig. 1A). Usual laboratory findings were all in normal values. An extensive search for immunodeficiency (including assays of immunoglobulins and IgG subclasses, serum complement levels, and white cell burst) and HIV were negative. Three months later the fever and weakness reoccurred. A new abdominal CT revealed a prevesical abscess and a large abscess in the right lower abdominal quadrant. In addition, diffuse obscurity of the retroperitoneum in combination with thickening of the obturator internus muscle, possibly indicating infectious extenPrimary peritonitis caused by group A streptococci (GAS) is quite unexpected in previously healthy adults without underlying disease [1, 2,3]. Moreover, primary peritonitis due to a combination of GAS and E. coli has not been previously reported in the literature.A 40-year-old, previous healthy man, presented to an outboard clinic with 2-day history of fever 39°C, ephidrosis, and a sore throat; only antifebrile medication was prescribed. Five days later, he was admitted to a regional hospital with clinical and laboratory findings of acute peritonitis. The patient underwent urgent laparotomy. Diffuse peritonitis with a large amount of fine intra-peritoneal cloudy fluid was found; no bowel perforation was established. Broad-spectrum antibiotics (Metronidazole, netilmicin, piperacillin/tazobactam) were initiated. Two days later, the patient was led to the operating room for second time, as his condition was still unstable, requiring noradrenaline; again, no focus of infection or intestine perforation could be identified. The patient continued to deteriorate due to severe sepsis, and finally was intubated on the 4th day after the first operation, and transferred to the ICU.Upon admission to the ICU, a soft-tissue inflammation with extensive skin erythema, edema, and tenderness -with no sharply demarcated margins from the surrounding uninvolved tissue -extending to the right abdominal wall and the right thigh was evident. Although necrotizing fasciitis was considered [4], undermining of the skin was not demonstrated. Meanwhile, GAS (sensitive to penicillin) and E. coli were cultured in all peritoneal pus samples, obtained at the time...
We present a case of a 52-year-old male patient who died from massive hematemesis as a result of perforation of a benign peptic ulcer into the descending thoracic aorta, 1 year after esophagectomy for esophageal cancer and gastric tube interposition. We also review the literature for mechanisms of ulceration in intrathoracic gastric grafts and for complications of such ulcers.
Calcification of coronary vessels progresses rapidly in hemodialysis (HD) patients and comprises a strong predictor of cardiovascular events. The aim of this prospective study was to evaluate the coronary artery calcification (CAC) in patients with end stage renal disease undergoing regular HD and to determine the effect of renal transplantation (RT) in the progression of CAC, using the Agatston technique for calcium scoring. The study included 20 patients with end-stage renal disease undergoing a regular HD treatment (16 males, 4 females) 54.1 ± 9.5 years old who had just received a renal transplant and 16 more HD patients (11 males, 5 females) 54.4 ± 13.8 years old as control group. The baseline evaluation showed a very high prevalence of CAC in both groups, which was positively correlated with age (p < 0.001) and CRP (p = 0.03). The second (follow-up) evaluation showed a significant slower progression of calcification after RT. In both groups, high calcium score values in the follow-up evaluation had a strong positive correlation with baseline calcium score (p < 0.001).
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