Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cushing's syndrome may be caused by pituitary ACTH, ectopically produced ACTH, adrenocortical tumor or medication. Cushing's disease, due to excessive pituitary ACTH resulting in adrenocortical hyperplasia, remains a complex endocrine disorder for which no single treatment is wholly satisfactory. Twenty-two patients with surgically treated Cushing's syndrome are presented: Four with benign adrenocortical adenoma, two with adrenocortical carcinoma and 16 with adrenocortical hyperplasia. The four benign adenomas were excised with the one death due to respiratory failure and sepsis. Both patients with carcinoma and liver metastases died of their tumors. Of the 16 patients with adrenocortical hyperplasia and Cushing's disease, eight underwent subtotal adrenalectomy and thereafter eight had total intra-abdominal adrenalectomy with autotransplantation of adrenal tissue to the thigh. There was one operative death. Total adrenalectomy has now replaced subtotal resection in most clinics. All eight of the patients who had adrenal autotransplantation exhibited biopsy or functional evidence of some degree of graft survival. On patient stopped steroid replacement permanently and another developed recurrent Cushing's syndrome from the grafts. Of a total of 26 reported patients with adrenal autotransplants surveyed, 22 exhibited evidence of graft survival, 16 were able to discontinue steroid replacement therapy and three eventually developed recurrent Cushing's syndrome from the transplants. There is now strong evidence that most patients with Cushing's disease harbor a pituitary basophil ademona, and in the future the initial surgical attack may be directed to the pituitary rather than to the adrenals.
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PMID:Surgical management of Cushing's syndrome with emphasis on adrenal autotransplantation. 68 95

A 36-year-old patient developed marked pigmentation, marked myopathy and severe hypokalaemic alkalosis which at first pointed towards an ectopic ACTH syndrome. The dexamethasone test at a high dose indicated cortisol suppression. A mediastinal tumour was seen radiologically, but the sella was of normal size. Computed tomography provided indirect signs of a sellar space-occupying lesion which suggested an ectopic production of corticotropin-releasing factor (CRF) as cause of the Cushing's syndrome. CRF concentration in antecubital venous blood was markedly elevated to 280 ng/l. The mediastinal tumour was excised and proved to be a carcinoid histologically. Postoperatively the CRF concentration fell to 70 ng/l. An extract of the carcinoid contained 15.5 ng/g wet-weight of CRF and 254 ng/g wet-weight of beta-endorphin. The patient died 5 weeks postoperatively of sepsis with bilateral pneumonia. At autopsy the hypophysis was of normal size but showed nodular ACTH-cell hyperplasia. This was thus a case of Cushing's syndrome resulting from ectopic CRF production in a mediastinal carcinoid tumour.
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PMID:[Cushing's syndrome in CRF-producing mediastinal carcinoid]. 230 1

In a 60-year-old woman Cushing's syndrome was induced by an ACTH producing bronchial carcinoid. In spite of the presence of an ectopic ACTH syndrome, the clinical, radiological and biochemical findings and the positive dexamethasone suppression test were compatible with Cushing's disease. Selective enucleation of an adenoma or total hypophysectomy was therefore felt to be indicated. Following total hypophysectomy, however, the Cushing's syndrome persisted and this suggested the possibility of an ectopic ACTH syndrome. As tumor localization was impossible, bilateral adrenalectomy was planned, but before this could be done the patient had to be hospitalized for staphylococcal septicemia and died. Autopsy revealed a subpleurally located bronchial carcinoid as the source of ACTH.
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PMID:[Cushing's syndrome in bronchial carcinoid: suppressible ectopic ACTH selection]. 714 63

Most staghorn calculi are infection stones composed of struvite and/or carbonate apatite. Sometimes, cystine, uric acid, whewellite and brushite stones also assume a staghorn configuration when located in the kidney. It is very important in stone crushing to know the composition and architecture of the stones. Struvite stones show a concentric laminal structure and are fragile because of wide interstices of crystals and rich organic matrix. These stones usually contain many bacterial colonies in the interstices of crystals and bacteria break out of the stones when they are crushed. Therefore, perioperative administration of antibiotics is necessary for prevention of bacteremia and sepsis. Whewellite stones and uric acid stones have a smooth surface and reveal compact radial and laminal structure especially in the peripheral layer. They are very hard and are refractory to crushing, and the fragments are large. Cystine stones show a compact radial monomineral texture and are very hard. The fragments made by crushing are large. Therefore, combination therapy of stone crushing and irrigation of alkali solution may be useful for treatment of cystine stones as well as uric acid stones. Calcium phosphate stones, hydroxyapatite or brushite stones, are rare and are formed in hyperparathyroidism, Cushing syndrome and renal tubular acidosis. Hydroxyapatite stones are rich in matrix and fragile. Brushite stones reveal radiate structure and are hard. There is no general method of treatment for staghorn calculi but we should select the most reasonable method including open surgery for each case taking into consideration the stone composition, predisposing factors and possibility of stone residue and recurrence.
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PMID:[Treatment of staghorn calculi on the basis of composition and structure]. 826 80

Glucocorticoids signal enhanced proteolysis in various instances of muscle atrophy and increased gene expression of components of the lysosomal, Ca(2+)-dependent, and/or ubiquitin-proteasome proteolytic pathways in both rat skeletal muscle and myotubes. Cushing's syndrome is characterized by chronic excessive glucocorticoid production, which results in muscle wasting. We report here no change in messenger RNA levels for cathepsin D (a lysosomal proteinase), m-calpain (a Ca(2+)-activated proteinase), ubiquitin, 14-kDa ubiquitin-activating enzyme E2, and 20S proteasome subunits (i.e. critical components of the ubiquitin-proteasome proteolytic process) in skeletal muscle from such patients. Thus, in striking contrast with animal studies, glucocorticoids did not regulate the expression of muscle proteolytic genes in Cushing's syndrome. In humans, messenger RNA levels, for at least ubiquitin and proteasome subunits, are elevated in acute situations of muscle wasting, such as head trauma or sepsis. Because Cushing's syndrome is a chronic catabolic condition, we suggest that the lack of regulation of proteolytic genes in such patients may represent an adaptive regulatory mechanisms, preventing sustained increased protein breakdown and avoiding rapid muscle wasting.
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PMID:Glucocorticoids do not regulate the expression of proteolytic genes in skeletal muscle from Cushing's syndrome patients. 928 62

We report the emergency and prolonged use of etomidate to control circulating cortisol levels in a patient with Cushing's syndrome secondary to ectopic ACTH production from a pancreatic islet cell tumor. Duodenal perforation and peritonitis complicated an episode of salmonella septicemia, precluding the use of conventional oral medical adrenolytic therapy. Endogenous cortisol secretion was abolished by parenteral etomidate, allowing serum cortisol levels to be controlled with an iv infusion of hydrocortisone over an 8-week period in intensive care before definitive pancreatic surgery.
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PMID:Emergency and prolonged use of intravenous etomidate to control hypercortisolemia in a patient with Cushing's syndrome and peritonitis. 976 61

We report a case with an initial diagnosis of adenocarcinoma of the prostate in whom Cushing's syndrome developed. The disease did not respond to estrogen treatment and the patient died of severe septicemia. Histopathologic examination of the autopsy specimens revealed a small cell carcinoma intermingled with a moderately differentiated adenocarcinoma in the prostate and widespread metastases of small cell carcinoma. Immunoreactivity for neuroendocrine differentiation was found only in the small cell carcinoma. Determination of different tumor markers in plasma samples showed markedly elevated levels of prostate-specific antigen as well as carcinoembryonic antigen prior to treatment, with no significant changes after treatment. The concentration of the neuroendocrine marker chromogranin A was initially within the normal range, but increased during estrogen treatment, whilst neuron-specific enolase was moderately elevated throughout the observation period.
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PMID:Cushing's syndrome in prostate cancer. An aggressive course of prostatic malignancy. 1059 2

Because high circulating levels of glucocorticoids impair immunity and predispose to infections, we evaluated whether indices of cortisol (F) production could predict infections in patients with Cushing syndrome (CS) caused by ectopic production of ACTH (EA). Charts of 54 consecutive patients with untreated EA, without underlying diagnosis of small cell carcinoma of the lung, were reviewed, and types of infections, white blood cell (WBC) count, fever, as well as the glucocorticoid indices [0800 h F, daily urine F excretion (UFC), and daily urine 17-hydroxysteroid/g creatinine excretion (17OHS)], were recorded. Thirty-five patients had no or clinically mild infection; the remaining 19 patients had severe, systemic infection (n = 13) and/or sepsis (n = 6), including either bacterial or opportunistic pathogens or both (73.7%, 42.1%, and 13.8%, respectively). The latter group of patients had significantly higher indices of hypercortisolism (F, UFC, and 17OHS) than those with mild or no infections, but these indices did not correlate with temperature or WBC count. Thresholds for identifying severe infection were selected for maximal positive predictive value and were: F, 43.1 microg/dL; UFC, 2000 microg/day; and 17OHS, 35 mg/g creatinine. The most accurate discriminator for severe infection was 17OHS, based on a positive predictive value of 64.7%. Our data strongly suggests that the likelihood for a bacterial or opportunistic infection in CS patients, even without underlying small cell carcinoma of the lung, is greatest in patients with extreme hypercortisolism. The predictive value of total WBC count or the presence of an elevated temperature is not sufficient to identify patients with severe, life-threatening infection.
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PMID:Cortisolemic indices predict severe infections in Cushing syndrome due to ectopic production of adrenocorticotropin. 1115 75

Reactivation of hepatitis B virus (HBV) replication in hepatitis B surface antigen (HBsAg)-positive patients is associated with immunosuppressive therapy. However, the interactions between endogenous glucocorticoid in Cushing's syndrome and HBV-related hepatitis remain unclear. Here, we describe the management of a 32-year-old male HBV carrier with Cushing's syndrome caused by an adrenal cortical adenoma, who developed severe hepatitis B. Repeated episodes of septicemia resulting from hypercortisolemia-related immunosuppression further compromised his hepatic condition. Adrenalectomy could not be performed due to coagulopathy. Lamivudine was not available at that time in Taiwan, and this patient died of hepatic failure and sepsis. At autopsy, his liver showed submassive necrosis with small regenerative nodules. The hepatocytes were positive for HBsAg (membrane and cytoplasmic) and hepatitis B core antigen (nuclear and cytoplasmic). Screening for HBsAg is of crucial significance for immunocompromised individuals. Once positive HBsAg is detected in immunosuppressed patients, liver function and viral status should be closely monitored to enable earlier diagnosis and prompt treatment with the newer nucleoside analogues that actively fight HBV.
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PMID:Submassive liver necrosis in a hepatitis B carrier with Cushing's syndrome. 1209 9

The morphology of canine platelets (changes in size, shape, staining characteristics, degree of activation and clump formation, distribution of granules, appearance of vacuoles on Giemsa-stained smears) was investigated in 20 healthy control and 181 diseased dogs. In the group of the sick dogs 84 animals suffered from disorders affecting directly the haematological parameters or the haematopoietic organs such as bleeding, thymic haemorrhage, haemolytic disorders, lymphoma, immune-mediated thrombocytopenia, and other 97 dogs were affected by other diseases (hepatopathy, nephropathy, hepatic, splenic or intestinal neoplasm, skin diseases, diabetes mellitus, Cushing's syndrome, sepsis). The alterations found in platelet morphology were not specific for any disorder. The most common platelet abnormalities were polychromasia and the presence of giant platelets. These changes occurred in a high number in disorders accompanied by bleeding or haemolysis. Anisocytosis was the most frequent finding in hepatic, splenic or intestinal neoplasms and in certain endocrinopathies. Microcytosis was observed in immune-mediated thrombocytopenia, hepatic neoplasms and endocrine disorders. Extreme platelet activation was common in haemolysis, hepatopathies, neoplastic diseases and sepsis. Vacuolisation was present in thymic haemorrhage, pancreatitis, diabetes mellitus and Cushing's syndrome. A new morphologic phenomenon, i.e. a ring-like formation of granules, was described in the cytoplasm of the platelets both in healthy and diseased animals. In addition, two forms of pathologic granulation were also described for the first time in Giemsa-stained blood smears: the pseudonuclear and the spot-like formation of granules, which were observed especially in disorders affecting the blood cells. The granulation and morphological characteristics of platelets on smears stained by periodic acid-Schiff reaction (PAS) were also studied. Three localisations of granulation were observed, such as peripheral, eccentric and diffuse. The ratio of PAS-positive and -negative platelets was evaluated in several diseases. Our findings support the diagnostic value of platelet evaluation by light microscopy and help clinicians/clinical pathologists to understand why morphologic changes of thrombocytes might be expected in several diseases.
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PMID:Morphological evaluation of canine platelets on Giemsa- and PAS-stained blood smears. 1615 29


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