1/10. Hypoglycemic coma masquerading thyrotoxic storm.A 59-year-old woman was hospitalized in hypoglycemic coma. Although hypoglycemia was promptly reversed, she was in a somnolent, restless state with tachycardia, tremor, profuse sweating, and high body temperature. Thyrotoxic storm was highly suspected and vigorous antithyroid regimens gradually brought her up to normal mental and cardiovascular states in several days. However, profound generalized myopathy necessitated the maintenance with a respirator. One month later, an episode of angina pectoris was followed by generalized convulsion, coma, and death in a few days. neuroimaging study disclosed posterior leukoencephalopathy syndrome. This case is instructive in that hypoglycemic coma may masquerade the major symptomatology of thyrotoxic storm, and that profound myopathy and angiopathic or angiospastic processes of the brain and the heart may interfere with the outcome.- - - - - - - - - - ranking = 1keywords = sweat (Clic here for more details about this article) |
2/10. Adrenal crisis presenting as hypoglycemic coma.An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. plasma levels of ACTH and cortisol remained undetectable. renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.- - - - - - - - - - ranking = 0.021244944921774keywords = gland (Clic here for more details about this article) |
3/10. coma blisters in a case of fatal theophylline intoxication.A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.- - - - - - - - - - ranking = 13.610212294374keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
4/10. Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.- - - - - - - - - - ranking = 0.021244944921774keywords = gland (Clic here for more details about this article) |
5/10. Drug-induced sweat gland necrosis in a non-comatose patient: a case presentation.BACKGROUND: coma-induced bullae and sweat gland necrosis is a rare clinicopathological entity often associated with drug-induced coma. SUBJECT: We report a case with clinical and histopathologic findings characteristic of blisters and sweat gland necrosis occurring in a non-comatose patient. CONCLUSIONS: skin blisters with underlying sweat gland necrosis is an entity previously reported to occur in comatose patients, our findings open new questions about the role of the drugs in the pathogenesis of those conditions.- - - - - - - - - - ranking = 95.271486060617keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
6/10. Carboxyatractyloside poisoning in humans.OBJECTIVE: Cocklebur (xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside carboxyatractyloside, which is highly toxic to animals. We describe nine cases of carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND methods: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.- - - - - - - - - - ranking = 1keywords = sweat (Clic here for more details about this article) |
7/10. Multiple bullae and paresis after drug-induced coma.Two cases of bullous skin lesions and paresis following coma due to the ingestion of many antipsychotic drugs were reported. Histological examination showed an intra-epidermal blister in case 1 and degeneration of sweat glands in both cases. An immunofluorescence study showed massive deposits of IgM and C3 in the dermal vessels. As similar deposits of immunoglobulin and complement were not observed in patients with ordinary lesions such as decubitus, a different mechanism in the formation of the bullous skin lesion other than pressure is suggested.- - - - - - - - - - ranking = 13.610212294374keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
8/10. coma blisters: report and review.coma blisters are self-limited lesions that occur in the setting of coma of various causes, but are most commonly associated with barbiturate overdose. Examination of a skin biopsy specimen demonstrates the characteristic presence of eccrine sweat duct necrosis. Although the exact cause of coma blisters remains unknown, they are not related to underlying infections or rheumatologic disorders, and do not contraindicate the continued therapeutic use of barbiturates.- - - - - - - - - - ranking = 1keywords = sweat (Clic here for more details about this article) |
9/10. diazepam-induced coma with bullae and eccrine sweat gland necrosis.Bullous skin lesions that indicate sweat gland necrosis have been known to occur in drug-induced coma resulting from barbiturates and in carbon monoxide poisoning. To our knowledge, this is the first cases in which diazepam is implicated in causing bullous lesions over pressure points, and the first case showing on biopsy specimen eccrine sweat gland and sweat duct necrosis. Penile and oral lesions are being described here for the first time to our knowledge. The following mechanisms could be responsible for the skin lesions: hypoxia, local pressure, hyperthermia with excessive sweating, and a specific toxic effect on the eccrine gland. With the increasing use of the benzodiazepines, such lesions could be seen more frequently in the future.- - - - - - - - - - ranking = 83.682518711165keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
10/10. Case report: interferon induced coma in Sheehan's syndrome.A 54-year-old woman who was being treated with 10 million units (mu) of natural interferon (IFN)-alpha per day for chronic active hepatitis c at a local clinic, developed coma on the fourth day of treatment. On admission to Yamagata University Hospital, she was still in a state of semicoma with severe hyponatraemia (122 mEq/L) and hypochloraemia (89 mEq/L). After the administration of electrolytes, her condition improved remarkably. Endocrinological loading tests showed a hypofunction of the anterior pituitary gland. In consideration of these results, and her past experiences of haemorrhage during childbirth and subsequent amenorrhoea, we diagnosed her illness as a coma as a result of Sheehan's syndrome which had become overt during IFN therapy. She recovered completely after treatment with hydrocortisone and l-thyroxine.- - - - - - - - - - ranking = 0.021244944921774keywords = gland (Clic here for more details about this article) |
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