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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Choosing appropriate antimicrobial therapy for patients with pneumonia requires knowledge of the etiologic agents seen in specific kinds of patients at specific times and places. For community-acquired pneumonia, there is an important difference in the agents seen in the normal and the compromised host. The normal host most often presents with viral, mycoplasmal, or pneumococcal pneumonia. The exact place of Chlamydia pneumoniae is still under study. A normal host who aspirates is at risk of anaerobic pneumonia. Normal hosts with influenza may acquire superinfection with Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus. Under specific epidemiologic conditions, community-acquired pneumonia may be due to Legionella species, Yersinia pestis, Francisella tularensis, Coxiella burnetii, Chlamydia psittaci, a mycotic agent, or tuberculosis. Patients with chronic bronchitis and emphysema are predisposed to H. influenzae, Moraxella catarrhalis, and S. pneumoniae infections. HIV-infected patients are likely to have Pneumocystis carinii pneumonia and pneumonia due to cytomegalovirus, S. pneumoniae, and H. influenzae. Patients with diabetes, nursing-home patients, hospitalized patients, immuno-compromised patients, and patients with recent antibiotic therapy are predisposed to pneumonia due to Gram-negative aerobic bacilli of enteric and environmental origin. Initial therapy should be directed at the likely organism or organisms based on hospital susceptibility surveillance. In the normal host with community-acquired pneumonia, the therapy will often be penicillin G or erythromycin. In the patient predisposed to Gram-negative pneumonia, a third-generation cephalosporin with or without an aminoglycoside is the usual choice.
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PMID:Pneumonia. Patient profiles, choice of empiric therapy, and the place of third-generation cephalosporins. 173 Jan 86

Azotemia and diabetes mellitus are now well-known adverse reactions associated with Pentamidine treatment, especially since its prescription in case of Pneumocystis carinii pneumonia. We report the case of a 2 year-old boy, treated for kala-azar with pentamidine and N-methyl glucamine antimoniate who developed adverse effects, characterized by a nephrotic syndrome associated with the classic acute tubular necrosis, and transient diabetes mellitus.
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PMID:[Transitory acute kidney insufficiency and insulin-dependent after treatment of kala-azar with pentamidine and N-methylglucamine antimony]. 185 38

Patients with acquired immunodeficiency syndrome (AIDS) are at risk from many endocrine complications. Pentamidine has been recognised for its potential to cause symptomatic, and even life-threatening hypoglycaemia. We report two cases of diabetes mellitus presenting with ketoacidosis 3 to 4 months after pentamidine therapy for Pneumocystis carinii pneumonia (PCP), and review our experience of dysglycaemia in 58 patients with AIDS treated with pentamidine. These cases emphasise the potential for severe pancreatic toxicity in patients with AIDS. Hyperglycaemia during pentamidine therapy may be a marker for patients at increased risk of developing diabetes mellitus.
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PMID:Diabetes mellitus presenting with ketoacidosis following pentamidine therapy in patients with acquired immunodeficiency syndrome. 190 May 21

Serious and occasionally fatal reactions to pentamidine have been reported and with the increased use of the drug in immunocompromised patients they are likely to become more frequent. We report the development of acute pancreatitis and permanent diabetes mellitus in an AIDS patient treated with intravenous pentamidine for Pneumocystis pneumonia. The literature on pentamidine induced pancreatic damage is reviewed.
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PMID:Survival from pentamidine induced pancreatitis and diabetes mellitus. 195 14

Of 18 AIDS patients with Pneumocystis carinii pneumonia treated with pentamidine mesylate parenterally, four developed serious to severe hypoglycaemia, three hypoglycaemia followed by insulin-requiring diabetes, and two others diabetes alone. Hypoglycaemia (blood glucose 2.1 +/- 0.2 (+/- SE) mmol l-1) occurred 9 (2-22) days after starting treatment, and diabetes (initial blood glucose 30 +/- 6 mmol l-1) after 60 (20-90) days. The other patients remained euglycaemic. The dysglycaemic patients (hypo- and hyper-glycaemic) had a higher pentamidine dosage (p less than 0.01), and higher serum creatinine levels at end of treatment (p less than 0.001), consistent with drug accumulation and dose-dependent toxicity. Plasma C-peptide levels were low in the diabetic patients, in the basal state (0.25-0.28 nmol l-1) and following stimulation by IV glucagon (0.35-0.40 nmol l-1), vs 0.80 +/- 0.06 nmol l-1 (basal) and 1.83 +/- 0.16 nmol l-1 (stimulated) in 23 healthy control subjects (mean +/- SE). Islet cell or insulin antibodies were not detected. Serum amylase levels rose abnormally in the dysglycaemic group, and pancreatitis was proved in one, and suspected in another patient. None of 28 similar AIDS patients whose P. carinii pneumonia was treated with cotrimoxazole showed blood glucose disturbance.
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PMID:Hypoglycaemia and diabetes mellitus following parenteral pentamidine mesylate treatment in AIDS patients. 214 64

Insulin-dependent diabetes mellitus occurred following intravenous pentamidine treatment of two AIDS patients with Pneumocystis carinii pneumonia. Both patients also experienced drug-induced nephrotoxicity. Patients receiving pentamidine must be observed for multisystem dysfunction, including the onset of severe diabetes mellitus. Dosage adjustment or alternative therapy should be considered with the onset of toxicity.
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PMID:Insulin-dependent diabetes mellitus associated with pentamidine. 278 86

The feasibility of on-site primary care services and their use by human immunodeficiency virus HIV-seropositive and seronegative injecting drug users within an outpatient methadone maintenance program are examined. A 16-month prospective study was conducted within an ongoing cohort study of HIV infection at a New York City methadone program with on-site primary care services. The study group consisted of 212 seropositive and 264 seronegative drug injectors. A computerized medical encounter data base, with frequencies of primary care visits and with diagnoses for each visit, was linked to the cohort study data base that contained information on patients' demographic characteristics, serologic status, and CD4+ T-lymphocyte counts. Eighty-one percent of the drug injectors in the study voluntarily used on-site primary care services in the methadone program. Those who were HIV-seropositive made more frequent visits than those who were seronegative (mean annual visits 8.6 versus 4.1, P < .001), which increased with declining CD4+ T-lymphocyte counts; 79 percent of those who were seropositive with CD4 counts of less than 200 cells per cubic millimeter received on-site zidovudine therapy or prophylaxis against Pneumocystis carinii pneumonia, or both. Common primary care diagnoses for patients seropositive for HIV included not only conditions specific to the human immunodeficiency virus but also bacterial pneumonia, tuberculosis, genitourinary infections, asthma, dermatologic disease, psychiatric illness, and complications of substance abuse; those who were seronegative were most frequently seen for upper respiratory infection, psychiatric illness, complications of substance abuse, musculoskeletal disease, hypertension, asthma, and diabetes mellitus. Vaginitis and cervicitis,other gynecologic diseases, and pregnancy were frequent primary care diagnoses among both seropositive and seronegative women.
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PMID:Utilization of on-site primary care services by HIV-seropositive and seronegative drug users in a methadone maintenance program. 839 79

Glucose homeostasis is maintained by a balance between the release and action of insulin, and the counterregulatory responses mediated principally by glucagon, catecholamines, growth hormone and cortisol. Hence, the effects of a drug on glucose metabolism may be mediated by any of these agents singly or in combination. Host factors, such as inherent glucoregulatory mechanisms, concurrent diseases, organ function and concomitant medications also increase the risk of drug-induced disturbances of glucose homeostasis in susceptible individuals. By far the most important agents causing hypoglycaemia are insulin and the sulphonylureas. Alcohol (ethanol), over-zealous glycaemic control, hypoglycaemic unawareness, detective counterregulation especially in insulin-dependent diabetes mellitus (IDDM), and renal and liver impairment are all important predisposing factors. Although antihyperglycaemic agents such as metformin and alpha-glucosidase inhibitors do not cause hypoglycaemia alone, they may enhance the hypoglycaemic effects of potent hypoglycaemic agents such as insulin and sulphonylureas. On the other hand, the potential hypoglycaemic effects of ACE inhibitors, alpha-blockers, lipid-lowering agents and recombinant human insulin-like growth factor demonstrated in experimental settings, are of potential therapeutic interest. Iatrogenic hypoglycaemia and intensive insulin treatment are associated with hypoglycaemic unawareness which may be obviated by meticulous avoidance of hypoglycaemia. Effective patient education remains an important preventive measure. Oral glucose is used to treat mild hypoglycaemic episodes while more severe episodes are treated by intravenous glucose or glucagon. Nasal glucagon and theophylline are other experimental measures to improve recovery from hypoglycaemia. In refractory hypoglycaemia due to hyperinsulinaemia such as during sulphonylurea overdosage or quinine treatment, the long-acting somatostatin, octreotide, may suppress insulin release and restore euglycaemia. Diuretics, beta-blockers, sympathomimetics, corticosteroids and sex hormones are commonly prescribed drugs which may have adverse effects on carbohydrate metabolism especially in patients with diabetes mellitus or those who are at risk of developing glucose intolerance. Pentamidine was frequently associated with dysglycaemia due to its pancreatic beta-cell cytotoxic effects but is now used less often to treat Pneumocystis carinii pneumonia in immunosuppressed patients. Despite the large number of anecdotal reports of drug-induced disturbances of glucose metabolism, many of the so-called adverse drug reactions were either idiosyncratic or coincidental. Nevertheless, they emphasise the complex nature of glucose homeostasis and its potential interactions with drugs, host factors and disease states. An understanding of these relationships may allow more critical interpretation of these clinical observations, better prediction of drug induced adverse effects on carbohydrate metabolism and the implementation of more rational therapy. Hence, the hypoglycaemic effects of a drug may be turned to a therapeutic advantage in patients with glucose intolerance. Similarly, the hyperglycaemic effect of a drug may help to treat refractory hypoglycaemia.
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PMID:Drug-induced disorders of glucose metabolism. Mechanisms and management. 888 64

Infection with Nocardia spp. is an uncommon but important cause of morbidity and mortality in organ transplant recipients. Cotrimoxazole prophylaxis against urinary tract infection and Pneumocystis carinii pneumonia in these patients usually prevents nocardial infection also. We report the case of a patient on tacrolimus and mycophenolate mofetil who developed drug-induced diabetes mellitus followed by nocardial brain infection. This infection occurred despite conventional cotrimoxazole prophylaxis. Physicians should be aware that newer, more potent and more diabetogenic immunosuppressive regimens may increase the risk of opportunistic infections such as nocardiosis, even in the presence of "adequate" antimicrobial preventive measures.
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PMID:Nocardial infection in a renal transplant recipient on tacrolimus and mycophenolate mofetil. 1044 95

A case is herein reported of pneumocystis carinii pneumonia in a 60-year-old female patient with ectopic production of ACTH at a position 2 cm superior to her right clavicle, revealed in an octreotide scan. Her extremely high plasma ACTH and cortisol levels (460 pg/ml and 80 microg/dl, respectively) were markedly decreased with the combined treatment of octreotide (300 microg/d) and ketoconazole (600 mg/d). As her serum cortisol concentration decreased, pneumocystis carinii pneumonia occurred on the third day of treatment. A secondary E. coli infection was superimposed and the patient died of disseminated intravascular coagulation and adult respiratory distress syndrome. This case suggests that primary prophylaxis for pneumocystis carinii infection should be initiated before cortisol lowering therapy, especially when the plasma cortisol concentration is excessively high, and that early adjunctive glucocorticoid therapy can reduce the acute mortality in patients with endogenous Cushing's syndrome and Pneumocystis carinii pneumonia. This case study would also like to point out that plasma ACTH and cortisol levels were decreased effectively by the combination of octreotide and ketoconazole in this instance of ectopic ACTH syndrome.
Exp Clin Endocrinol Diabetes 2000
PMID:Pneumocystis carinii pneumonia associated with a rapid reduction of cortisol level in a patient with ectopic ACTH syndrome treated by octreotide and ketoconazole. 1082 24


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