Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
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We report a newborn girl (36th week of gestation, birth weight 1,054 g) with Cushing's syndrome secondary to nodular adrenocortical hyperplasia with normal plasma ACTH levels. From birth she was hypertensive, hyperglycaemic and slightly hirsuit. Hypercortisolaemia (>1,380 nmol/l) was accompanied by normal plasma ACTH levels (8.64-23.9 pg/ml). A 48-h dexamethasone suppression test decreased plasma cortisol by 35%, indicating some degree of ACTH dependency. However, there was no ACTH rise on CRF test. MRI showed enlarged adrenal glands with a possible cyst on the right; the pituitary gland was normal. At the age of 6 weeks she underwent bilateral adrenalectomy. Histology showed enlarged adrenals with multiple non-pigmented nodules (up to 5 mm) in both glands. However, over the next few weeks she developed liver failure and sepsis. She died at the age of 3 months. Post mortem examination confirmed the diagnosis. Nodular adrenocortical hyperplasia may present at birth with severe Cushing's syndrome and unsuppressed ACTH levels, indicating some degree of ACTH dependency in this condition.
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PMID:Prenatal Cushing's syndrome secondary to nodular adrenocortical hyperplasia with unsuppressed plasma ACTH levels. 1645 60

Adrenalectomy continues to play an important role in the management of Cushing's syndrome (CS). Untreated CS causes considerable physical and mental morbidity and mortality. However, little information is available on the effect of adrenalectomy in ameliorating functional disabilities in CS patients. Our study assesses the long-term outcome of adrenalectomy in patients with CS. This is a retrospective analysis of CS patients managed during 1990-2005 at a tertiary care center. We analyzed the clinical presentation, endocrine evaluation, and surgical management preoperatively and following adrenalectomy. The subjects were 37 patients with CS (age 24.5 +/- 15 years, range 1-60 years; male:female 1.0:1.2). There were various etiologies--unilateral adrenocortical adenoma (n = 11), adrenocortical carcinoma (n = 13), pituitary ACTH-secreting adenoma with failed transsphenoidal surgery (n = 4), ectopic unidentified ACTH source (n = 7), bilateral adrenal macronodular hyperplasia (n = 1), primary pigmented nodular adrenal hyperplasia (n = 1) --for which the patients underwent adrenalectomy: unilateral (n = 22), bilateral (n = 13), or adrenonephrectomy (n = 2). Two patients died during the perioperative period owing to chest infection and sepsis. At the median follow-up of 60 months (range 6-144 months), the patients exhibit significant persistence of obesity (41%), proximal muscle weakness (44%), menstrual irregularity (8%), hypertension (31%), and insulin-dependent diabetes (29%). Hirsutism and psychological abnormalities persisted to a lesser extent. All patients had biochemical cure of CS following surgery evidenced by the 8 a.m. basal cortisol < or = 5 microg/dl. The hypothalamic-pituitary-adrenal axis recovered as shown by normalization of the short synacthen-stimulated cortisol level (peak level > or = 20 microg/dl) after a median follow-up of 9 months (range 6-18 months). Incomplete clinical recovery following adrenalectomy emphasizes the need of early recognition and prompt treatment of CS. Surgery for adrenocortical adenoma is safe and effective; however, survival of patients with CS due to adrenocortical carcinoma remains poor. Bilateral adrenalectomy provides early control of hypercortisolism in selected cases of unlocalized ectopic ACTH syndrome or failed transsphenoidal surgery. Even though functional recovery is incomplete after adrenalectomy, quality of life improves considerably.
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PMID:Outcome of adrenalectomy for Cushing's syndrome: experience from a tertiary care center. 1753 56

Ectopic adrenocorticotropin (ACTH) secretion accounts for less than 10% of all causes of endogenous Cushing's syndrome (CS) and is usually associated with neuroendocrine tumors and small cell carcinoma of the lung. We report the case of a 62-year-old man with CS due to ectopic ACTH production by small cell carcinoma of the prostate. He presented with severe hypercortisolism and associated symptoms. Plasma neuron specific enolase (NSE) was grossly elevated. Despite performing a laparoscopic bilateral adrenalectomy, the patient died as a result of sepsis with multi-organ failure. Post-mortem immunohistochemical staining of prostate tumor tissue showed ACTH expression. ACTH staining was also performed in four additional patients with small cell carcinoma of the urinary tract without CS. None of these additional cases showed a positive staining for ACTH. Although a rare cause of ectopic ACTH production, neuroendocrine prostate carcinoma should be considered in male patients with Cushing's syndrome, in particular in those with an occult source of ACTH overproduction.
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PMID:Cushing's syndrome due to ectopic ACTH production by (neuroendocrine) prostate carcinoma. 1832 2

Cushing's syndrome results from lengthy and inappropriate exposure to excessive concentrations of either endogenous or exogenous glucocorticoids. This study described 30 patients with a novel type of severe exogenous Cushing's syndrome in a group of intravenous drug users due to illicit use and dependence on a new opioid combination, Norjizak. Thirty consecutive patients (2 women and 28 men) who presented with a novel type of severe exogenous Cushing's syndrome and other complications were admitted to the emergency departments of Qom and Isfahan University of Medical Sciences, Isfahan, Iran, between September 2005 and September 2007 were enrolled. All participating patients were intravenous drug users who used a narcotic drug called Norjizak, a combination of different opioids with dexamethason or benzodiazepines. Patients were first evaluated and managed based on the current illness, and then entered into a detoxification program by a medical team. Clinical data were collected by an open interview and the patient's files using a standard form. High-performance liquid chromatography was used to determined glucocorticoid existence in the brand. The major complaints and clinical findings were withdrawal symptoms, severe edema, osteoporotic fracture, impairment in glucose tolerance, decreased libido, and sepsis (including necrotizing pneumonia, cutaneous infection, multivalvular endocarditis, osteomyelitis, and urogenital infection). Most patients had started with 2 or 3 vials per day and then increased the dose compulsively to maximum of approximately 15 to 20 vials per day. The concentration of Dexamethhasone disodium phosphate in each 2 mL vial was 0.4 to 1 mg/mL. Heroin was also found in them. We are witnessing a special exogenous Cushing syndrome due to the mixing of opiates and dexamethasone. Norjizak syndrome is the clinical condition of poisoning with a second material when it is combined with opiates due to compulsive dose increment and long duration.
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PMID:A case series of abuse of a new opioid combination, Norjizak. 1934 Jun 81

Cushing's syndrome is a condition caused by high levels of glucocorticoids, or most commonly as a result of prolonged exposure to exogenous steroids. Clinical features include diabetes, hypertension, obesity, skin atrophy, immune suppression and delayed wound healing. We report a patient with iatrogenic Cushing's syndrome, in whom long-term topical steroid therapy was used to treat varicose eczema, which contributed to the development of type 2 diabetes, morbid obesity, sleep apnoea and chronic wound sepsis. In this case, repeated hospital admissions and systemic antibiotics were associated with considerable comorbidity. Aggressive local treatment, consisting of potassium permanganate soaks and irrigating gels, was highly effective in reducing the amount of exudate, pain and preventing from further deterioration of the patient's legs.
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PMID:Cushing's syndrome and chronic venous ulceration--a clinical challenge. 2107 30

Pulmonary cryptococcosis usually occurs as an opportunistic infection in immunocompromised patients. Endogenous Cushing's syndrome is associated with cortisol excess and can predispose to development of cryptococcal infections. We report a case of diabetic patient with ACTH secreting pituitary tumour who developed a cavitating lung mass. Computed tomography-guided biopsy of the lesion revealed mucicarminophilic budding forms of cryptococcus. Broncheoalveolar lavage culture grew Cryptococcus neoformans. There was radiological response to treatment with liposomal Amphotericin, but patient ultimately succumbed to septicemia and multiorgan failure. Opportunistic infections with organisms like Cryptococcus neoformans, should be considered in patients with endogenous Cushing's syndrome and a pulmonary infiltrate.
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PMID:Endogenous excess cortisol production and diabetes mellitus as predisposing factors for pulmonary cryptococcosis: a case report and literature review. 2126 83

This review addresses the practical usage of intravenous etomidate as a medical therapy in Cushing's syndrome. We reviewed the relevant literature, using search terms 'etomidate', 'Cushing's syndrome', 'adrenocortical hyperfunction', 'drug therapy' and 'hypercortisolaemia' in a series of public databases. There is a paucity of large randomised controlled trials, and data on its use rely only on small series, case study reports and international consensus guideline recommendations. Based on these, etomidate is an effective parenteral medication for the management of endogenous hypercortisolaemia, particularly in cases with significant biochemical disturbance, sepsis and other serious complications such as severe psychosis, as well as in preoperative instability. We suggest treatment protocols for the safe and effective use of etomidate in Cushing's syndrome.
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PMID:Etomidate in the management of hypercortisolaemia in Cushing's syndrome: a review. 2293 Apr 88

Edwardsiella tarda is very seldom a cause for gastroenteritis in humans. This organism can also cause extraintestinal infections, such as soft tissue infections, meningitis, peritonitis, osteomyelitis, endocarditis and hepatobiliary tract disease, particularly in the setting of compromised immunity. We describe, for the first time a case of E. tarda sepsis with multiple liver abscesses associated with Cushing's syndrome as a result of recreational aquatic exposure.
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PMID:Edwardsiella tarda sepsis with multiple liver abscesses in a patient with Cushing's syndrome. 2288 7

The risk of sepsis with a hip or knee implant does not seem to be increased by prior joint injections, as long as the injection and surgery are separated by at least two months. Calcifications have been reported after intradiscal injection in the coccygeal region for coccydynia. Complete rest for 24 hours after injection of triamcinolone hexacetonide into the knee had no effect on systemic diffusion of the product. Patients infected by HIV who are treated with ritonavir are at much greater risk for Cushing syndrome after epidural injection. Problems with menstruation after corticosteroid injection seem to be related to a transient decrease in estradiol levels, without alterations in FSH and LH levels. The risk of central serous chorioretinopathy and acute necrosis of the retina after injection is not known, even by ophthalmologists. Transient dysphonia occurs in 12% of patients receiving corticosteroid injections. The impressive Tachon's syndrome seems to be the venous counterpart to Nicolau's syndrome for arteries. Injections into C1-C2 should be abandoned because of the neurological risks. Since serious neurological events after foraminal injections could be the result of an overly fast injection into the arterialized radicular veins rather than in the arteries, only slow injections with products having a low risk of embolism or vascular complications should be allowed. Dexamethasone-based preparations seem to contain no particles or crystals, and have not induced any neurological accidents in various animal models, even after direct administration into vertebral or carotid arteries.
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PMID:Side effects of corticosteroid injections: what's new? 2335 13

Atrophy occurs in specific muscles with inactivity (for example, during plaster cast immobilization) or denervation (for example, in patients with spinal cord injuries). Muscle wasting occurs systemically in older people (a condition known as sarcopenia); as a physiological response to fasting or malnutrition; and in many diseases, including chronic obstructive pulmonary disorder, cancer-associated cachexia, diabetes, renal failure, cardiac failure, Cushing syndrome, sepsis, burns and trauma. The rapid loss of muscle mass and strength primarily results from excessive protein breakdown, which is often accompanied by reduced protein synthesis. This loss of muscle function can lead to reduced quality of life, increased morbidity and mortality. Exercise is the only accepted approach to prevent or slow atrophy. However, several promising therapeutic agents are in development, and major advances in our understanding of the cellular mechanisms that regulate the protein balance in muscle include the identification of several cytokines, particularly myostatin, and a common transcriptional programme that promotes muscle wasting. Here, we discuss these new insights and the rationally designed therapies that are emerging to combat muscle wasting.
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PMID:Muscle wasting in disease: molecular mechanisms and promising therapies. 2554 88


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