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The typical patient with post-traumatic hypopituitarism is a young adult male presenting months to years after an automobile accident, following which he was unconscious for several days. He will probably have sustained a fracture of the base of the skull and on recovery is likely to have permanent visual or other neurological sequelae. Temporary or permanent diabetes insipidus may have occurred. The features of panhypopituitarism such as weight loss, fatigue, faintness, loss of libido, and impotence may have been ascribed to depression or the "postconcussion syndrome" and often inappropriate treatment and rehabilitation advised. The striking feature on review of the literature is that the pathological consequences of head injury to the pituitary and hypothalamus have been well described, while only 47 cases of traumatic hypopituitarism have been reported. The most likely reason for this disparity is that head injury of sufficient severity to cause hypothalamic and pituitary damage commonly led to death. More patients now survive, owing to the availability of intensive care; accordingly, most cases have been reported in the last 15 years. However, several patients are described in whom the initiating head injury was not associated with a skull fracture or followed by coma. We recommend that patients with major head injury (defined by post-traumatic amnesia greater than 24 hours), and in particular those with fractures of the base of the skull or diabetes insipidus should be closely monitored for symptoms and signs of endocrine dysfunction and appropriate dynamic pituitary-function tests performed.
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PMID:Post-traumatic hypopituitarism. Six cases and a review of the literature. 301 25

Fifty-nine patients with both clinical evidence of thyroid dysfunction and patent diabetes mellitus were investigated in our diabetology department. Patients with euthyroid goitre and iatrogenic or pituitary hypothyroidism were excluded from the study. Among the 45 diabetics with hyperthyroidism, 32 had Graves' disease and 13 had toxic adenoma; 71% were insulin-treated. Hyperthyroidism had passed unnoticed in 7 of these 32 patients because fatigue and loss of weight, which initially were the predominant or sole symptoms, are extremely frequent in uncontrolled diabetes. These symptoms, as well as polyuria, polyphagia and even sweating are common to both diseases. Considerable deterioration in the control of glycaemia was observed in 63% of the insulin-treated patients when hyperthyroidism developed, with a 17 to 212% (mean 82%) increase in insulin dosage in 53%. There was no correlation between the degree of hyperthyroidism and the loss of control. Following treatment of the hyperthyroidism, control was improved in 63%, with an 11-83% (mean 44%) decrease in insulin dosage in 59% of them. Insulin therapy could be withdrawn in only one of the 32 insulin-treated patients. Non-iatrogenic primary hypothyroidism was found in 0.2% of the diabetics investigated. This incidence was significantly higher than the calculated probability of the two diseases occurring by chance in the same patient. Eleven out of 14 patients were insulin-treated. When hypothyroidism developed, 73% of them had their insulin dosage reduced, with a high frequency of hypoglycaemic disorders: repeated "malaise" in 55% and coma in 27%. A higher proportion of vitiligo was also noted: 14% in the total patient population reported, and 18% in insulin-treated patients.
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PMID:[Effect of clinical hyperthyroidism and hypothyroidism on patent diabetes. 59 cases]. 315 40

In a consecutive series of 100 neck explorations for primary hyperparathyroidism, 42 patients were 60 years of age or older; in this group of elderly patients the surgical cure rate was 100%. These patients were reviewed retrospectively by means of a structure interview. Twenty-one patients had had preoperative neuromuscular symptoms that ranged from coma to subjective muscular weakness. These patients had significantly-higher preoperative serum calcium and parathyroid hormone levels than did 21 patients without neuromuscular symptoms (P = 0.003 and P = 0.046, respectively). Most of the neuromuscular symptoms improved in the postoperative period. In particular, 15 of 17 patients with muscle weakness reported a significant improvement, while 14 of 15 patients who suffered from fatigue and lethargy reported an improvement. An improvement also occurred in the level of day-to-day function in eight patients. While surgery for primary hyperparathyroidism generally is undertaken for a specific indication, such as severe hypercalcaemia or renal stones, it appears from this study that neuromuscular symptoms also may improve, particularly in elderly patients.
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PMID:Neuromuscular symptoms in elderly patients with hyperparathyroidism: improvement with parathyroid surgery. 339 14

Pituitary abscess is relatively rare. Only about 80 cases have been reported. Preexisting lesions in pituitary fossa, such as pituitary adenoma, craniopharyngioma and Rathke's cleft cyst, are inclined to be complicated by infection more than the normal pituitary glands are. We reported a case of pituitary abscess caused by infection of Rathke's cleft cyst. A 67-year-old male had general fatigue and loss of appetite 4 months before admission. On admission he was found to have diabetes mellitus, diabetes insipidus, and hypernatremia. These defects were controlled by medication but he gradually became comatose and febrile. CT and MRI revealed an intrasellar lesion with ring enhancement. Lumbar puncture demonstrated an increase of mononuclear cells and protein. Blood chemistry revealed a marked increase of CRP. He was operated on via the transsphenoidal approach, which revealed sphenoid sinusitis and abscess formation in the pituitary gland. Histological examination of the surgical specimen revealed infection of Rathke's cleft cyst but the fluid in the cyst was sterile. By the drainage of the cyst and the use of antibiotics the patient became alert and signs of infection disappeared. He was discharged with a slight hypopituitarism and returned to normal life. Mortality rate of pituitary abscess is decreasing but is still high because of hypopituitarism and severe infection. Accurate diagnosis and operation are necessary. Transsphenoidal surgery is preferable for postoperative drainage of the abscess.
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PMID:[A case of pituitary abscess caused by infection of Rathke's cleft cyst]. 747 22

A 58-year-old woman was admitted to our hospital for impaired consciousness, hyperglycemia and bitemporal hemianopsia. She was diagnosed as having NIDDM one year ago and was treated with diet and glibenclamide (1.25 mg/day) for 6 months. However, she stopped her medical treatment one month ago and then polydipsia and general fatigue were manifested. She was admitted to a hospital five days ago at which time hyperglycemia (405 mg/dl) and anemia (Hb8.0g/dl) were detected. She was transferred to our hospital for control of blood glucose and further examination of bitemporal hemianopsia. She showed typical acromegalic features including enlargement of the nose, lips and tongue, increased heel pad and acral growth. Conscious disturbance was cured by the infusion of saline and the administration of insulin. Endoscopy revealed an active gastric ulcer (A1). Endocrine data disclosed increased GH levels in plasma and urine, whereas plasma IGF-1 levels were low. Plasma GH paradoxically increased following the administration of TRH. A water deprivation test showed an impaired increase in urinary osmolarity, indicating partial central diabetes insipidus (DI). MRI with Gd-contrast revealed a macroadenoma which progressed toward suprasella. She was diagnosed as having acromegaly, partial DI and probable hyperosmolar hyperglycemic nonketotic diabetic pre-coma. Polyuria (5-101/day) due to partial DI was controlled by the administration of DDAVP (10 micrograms/day). The constant subcutaneous administration of octreotide (240 micrograms/day) resulted in normal plasma GH levels and a marked shrinkage of the pituitary tumor. The pituitary tumor was finally removed by the transsphenoidal approach following treatment with octreotide for 4 months. HE staining of the pituitary tumor showed atrophic and acidophilic cells surrounded by hyaloid connective tissue. After the surgery, plasma GH levels were normalized and complications were cured. In conclusion, this is a very rare case of acromegaly associated with diabetic pre-coma and partial DI, and effectively treated with constant subcutaneous infusion of octreotide.
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PMID:[Effective treatment with constant subcutaneous infusion of octreotide in a patient with acromegaly associated with diabetic pre-coma and diabetes insipidus]. 785 21

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 46-year-old man with cardiac failure and statues epileptics]. 794 26

Amantadine has found use primarily as an antiviral agent and in the symptomatic treatment of parkinsonism. However, the use of amantadine for the subjective alleviation of fatigue in multiple sclerosis and in the treatment of agitated aggressive behavior in the traumatic brain injured patient has also been described. Side effects of amantadine are primarily related to the central nervous system and include hallucinations, confusion, and nightmares. Toxic manifestations include acute psychosis, coma, cardiovascular toxicity, and death. Amantadine toxicity is a particular problem in patients with renal insufficiency because 90% of an oral dose is excreted unchanged in the urine. We present a case of amantadine-induced coma in a patient with multiple sclerosis and end-stage renal disease. Moreover, this degree of amantadine toxicity was profoundly apparent at a drug level usually not associated with such a severe presentation.
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PMID:Amantadine-induced coma. 821 67

To explore the pathophysiology of respiratory failure in an experimental pneumonia, a Pasteurella haemolytica broth culture was injected intratracheally into 12 calves, which were then studied over a period of 10 h. Measurements were made of inspired minute ventilation (VE), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory rate (RR) and tidal volume (VT)], transdiaphragmatic pressure (Pdi), occlusion pressure at the airway opening 100 milliseconds after onset of inspiration (Pawo100ms), arterial blood gas tensions and pH and recorded diaphragmatic electromyogram (EMGdi) and rectal temperature (Tr). On and after the third hour after inoculation, the animals varied in respect of clinical signs, Tr, RR, VE, Pawo100ms/EMGdi, and arterial gases and pH. In benign cases, diminished alertness, laboured respiration and fall of arterial oxygen pressure (PaO2) worsened up to 7 h after inoculation, but then progressively improved, VE being maintained at approximately 150% baseline throughout the study (10 h). Neither arterial carbon dioxide pressure (PaCO2) nor pH was altered. Moderate cases resembled benign cases in respect of laboured respiration, VE, PaO2 and PaCO2; however, pH was at first maintained at preinoculation levels, but declined thereafter. In severe cases, the animals were drowsy between hours 3 and 7, and became comatose between hours 8 and 10; in contrast to both benign and moderate cases: (1) RR was reduced by hour 5, (2) there was no trend towards recovery of PaO2 and pH, (3) VE, Pdi, Pawo100ms and Pawo100ms/EMGdi were severely decreased, and (4) PaCO2 increased. These results suggest that pneumonia does not alter ventilatory neuromuscular pump function in calves, unless concomitant cardiovascular collapse occurs. It is not clear whether fatal ventilatory failure is caused mainly by deterioration in ventilatory muscle fibre processes or structures, altered central nervous system adjustment of ventilatory timing, or cardiovascular dysfunction. However, inspiratory pressures fall when excitation to the diaphragm is still growing, which suggests peripheral respiratory muscle fatigue.
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PMID:The relation of ventilatory failure to pulmonary, respiratory muscle and central nervous system disturbances in calves with an experimentally produced pneumonia. 892 32

Prospective registry of newly diagnosed cases of insulin-dependent diabetes mellitus in subjects under 20 years began in 1988 in Aquitaine, Lorraine, Basse- and Haute-Normandie (population base = 2,288,018 inhabitants under 20). The registry gave a complete coverage of the population as the capture-recapture method gave a 98% yield. The mean annual incidence was 7.6/100,000 for the period 1988-1990. A specific survey aimed at describing clinical and biological presentation at diagnosis. The main symptom was polyuria in 98% of the cases, fatigue in 58% and weight loss in 44%. Abdominal pain was reported in 34% of the cases. Diagnosis was ascertained by measurement of plasma glucose, which was > or = 11 mmol/l in 95% of the cases and associated with ketonuria in 84% of the children. Coma in 13% of the children and acidosis (total CO2 < or = 18 mmol/l) in 48% showed the severity at diagnosis. Ketonuria and acidosis were significantly more frequent in the younger age group (0-4 yr). Diagnosis was made by a general practitioner in the majority of the cases; conversely insulinotherapy was initiated at the hospital in 95% of the cases. Initial insulin treatment was 2 daily injections. Following the French experience the collaborative network EURODIAB ACE has undertaken the same survey among the European Registries. Important geographical variations in incidence rates of IDDM in children has been reported across Europe but it is not known whether this interferes with presentation at diagnosis of the disease.
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PMID:[Diagnosis of insulin-dependent diabetes in children: data from the incidence registry]. 893 70

A 41-year-old man died in 1995 during ketoacidotic coma. He suffered from chronic manic depression, used lithium carbonate, and consulted the psychiatrist and the general practitioner (GP) frequently. Diabetes had not been diagnosed. Late in 1994 the situation worsened, the patient complaining of general illness, fatigue, nausea, vomiting, diarrhoea, thirst and excessive drinking of soft drinks. The GP referred the patient to a neurologist who found no neurological disorder but who asked for determination of blood glucose and lithium levels, and of thyroid function. The day afterwards the neurologist went on holiday. The blood glucose level proved to be elevated (16.9 mmol/1) but nobody took any action and the GP was not informed. Six days after returning from his holiday, the neurologist who had an administration backlog, found the laboratory findings only after he had been informed that the patient had just died. The court gave the neurologist a warning. Lessons are that somatic problems should be treated as such, even in a psychiatric patient, and that a good administrative signalling system is a prerequisite for quality in medical practice.
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PMID:[Medical and administrative neglect of high blood glucose levels; comments on a decision by a medical disciplinary tribunal]. 954 47


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