Differential diagnosis in primary aldosteronism

The diagnosis of primary aldosteronism (PA) is based on the finding of the combination of elevated urinary and/or plasma aldosterone and suppressed renin activity in patients with hypertension and hypokalemia. However, PA consists of a number of subsets, and diagnostic criteria for a correct identification of surgically remediable forms are of great interest. The methods and the results concerning our series of 113 patients with PA are presented in this review. Aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were the most frequent forms, 51 and 44%, respectively. They had similar blood pressure levels, but hypokalemia was most frequently found in APA. Urinary and upright plasma aldosterone were similar, but supine plasma aldosterone was lower in IHA. Plasma aldosterone response to upright posture and angiotensin II infusion was absent in most cases of APA and present in IHA, but occasionally renin-responsive adenoma were found. Captopril failed to decrease plasma aldosterone in most patients with APA, and in a subgroup of patients with IHA. Patients with adenoma also had higher values of the aldosterone precursor 18-hydroxy-corticosterone, and of atrial natriuretic peptide, probably as a consequence of a greater degree of volume expansion. Among morphological studies, CT scan and adrenal radiocholesterol scintiscan provided similar results (85% accuracy): adrenal veins catheterization clarified almost all the remaining cases. Among the subsets of PA, 3 familiar cases of dexamethasone-suppressible hyperaldosteronism were recognized, with characteristically high levels of aldosterone, 18-hydroxy-corticosterone, 18-hydroxy-cortisol and 18-oxo-cortisol, due to the genetic abnormalities of the 11-18 hydroxylase system. Isolated cases of primary adrenal hyperplasia (with all functional tests resulting compatible with APA, but no tumour at surgery) and aldosterone producing carcinoma (1 case) have also been reported in the present study.     

Early diagnosis of dementia: neuroimaging

BACKGROUND [corrected] AND PURPOSE: We reviewed Stroke Clinic data to determine the extent of risk factor modification achieved in patients with cerebrovascular disease over 2 years. METHODS: Visits to the Stroke Clinic of a tertiary medical center from July 1, 1994, through June 30, 1996, were reviewed. Obesity, smoking, hypertension, hyperlipidemia, hyperglycemia, and lifestyle changes were noted in patients with >/=2 visits (n=61) and measures (number varied) of these parameters. RESULTS: Fifty-six patients (92%) had primary care physicians. In the 49 patients with >/=2 weight measurements, 33 (67%) were moderately or severely overweight by weight-height correlation. Forty-four patients (90%) remained in the same weight category. Of the 60 patients with available blood pressure data, 50 (83%) were hypertensive. At their last visits, 43 of the 50 (86%) were receiving medications, and 22 of the 43 treated (51%) were controlled. Serum glucose remained elevated in 14 of 47 patients (30%) and in 11 of 16 diabetic patients (69%). Thirty-six of 47 patients (55%) had elevated lipid measurements. None of the 21 smokers quit during the study period. Few patients modified dietary and exercise practices. Of 61 patients, 29 (48%) sustained vascular events during the study, with 17 of these 29 patients (59%) having strokes or transient ischemic attacks. CONCLUSIONS: Although most patients were asked to quit smoking, received advice regarding diet and exercise, and were medicated for hypertension, elevated glucose, and cholesterol levels, their risk factor profiles showed little improvement during the 2-year period. More effective methods of controlling stroke risk factors are needed.     

Differential ulcus cruris diagnosis

Most leg ulcers are of venous or arterial origin (85%). Advanced chronic venous insufficiency is the most common underlying condition (65%), followed by advanced peripheral arterial occlusive disease (10%), and combined chronic venous insufficiency and peripheral arterial occlusive disease (10%). Chronic ulcers in diabetic feet (5%) are of great socio-economic importance, as well. They are a consequence of diabetic polyneuropathy which in part of the patients may be combined with peripheral arterial occlusive disease, usually of the calf arteries. However, a leg ulcer can also be caused by a large array of other underlying conditions, such as ulcerating skin tumours, trauma followed by disturbed wound healing, infectious ulcerations, ulcerations in angiodysplasias, vasculitic ulcerations, pyoderma gangrenosum, cholesterol-embolism, idiopathic livedo reticularis with ulceration, primary and secondary antiphospholipid-antibody-syndrome, coumarin-necrosis, calciphylaxis in chronic renal insufficiency, necrobiosis lipoidica, different forms of panniculitis, hematologic disorders, autoimmun diseases and autoimmun-bullous dermatoses. The following article discusses the differential diagnosis, examination and treatment of leg ulcers in these less common underlying conditions.     

Differential osteoporosis diagnosis in the woman

Bone mineral density of a woman in the second half of her life depends on the amount of bone made during growth and its subsequent rate of loss. Although the rate of bone loss did receive more attention in the study of pathogenesis of osteoporosis, it is becoming increasingly clear that insufficient accumulation of skeletal mass by young adulthood predisposes a person to low bone mass and subsequently to fractures later in life as age related and menopause-related bone loss ensue. In this article we 1) explain the role of inadequate peak bone mass as a major risk factor for osteoporosis and 2) give an overview of factors leading to osteoporosis by decreasing bone mass. Special emphasis has been put on iatrogenic osteoporosis which is frequently neglected because of the fact that the responsible agents often are not known as to be deleterious to the skeleton: among others, glucocorticoids, thyroid hormones and antiepileptics adversely affect bone.     

Differential diagnosis of dysphagia in children

Dysphagia in children often presents a difficult diagnostic challenge. A systematic approach in each individual can help with diagnosis and treatment. An overview of the differential diagnosis and the diagnostic and treatment options available is provided.     

Differential diagnosis and therapy in Adie's syndrome

In general, Adie's syndrome does not represent a serious diagnostic problem. In cases of cerebrospinal syphilis the Argyll-Robertson phenomenon or even absolute pupillary rigidity will be observed. Positive syphilis reactions will clarify these cases. The erroneous diagnosis of brain tumour may arise because of anisocoria. However, if pupillotonia can be ascertained by means of conjunctival instillation of drugs no further invasive diagnostics will be necessary. In some cases of Adie's syndrome concomitant emotional instability may be present. This dysautonomic reaction type of personality will hardly ever be confounded with the psychological disturbances encountered in brain tumours. Therapy is restricted to symptomatic measures. Pupillotonia can be influenced by strychnine and thymoxamine. Headache and facial neuralgia respond to the usual therapeutic schemes. Sweating disorder cannot be influenced. Neuropharmacological treatment may become necessary in periods of acute emotional disturbance.     

Differential diagnosis of pulmonary tuberculosis

Differential diagnosis of pulmonary tuberculosis is discussed. Chest X-ray findings of pulmonary tuberculosis may be greatly varied, because tuberculosis may cause three different lesions: an exudative lesion, a proliferative lesion, and a fibrotic lesion, and because it may invade all the structure. Thus, the differential diagnosis of pulmonary tuberculosis includes very many diseases. The most important differential diagnosis of nodule is tuberculoma and lung cancer. The clue of the diagnosis is the feature of the nodule and surrounding structure, such as pleural indentation, or knotching. There is, however, the limitation of the diagnosis by imaging: some tuberculoma may show the identical feature with the pulmonary adenocarcinoma. It is important to gather the pathological or bacteriological evidences by means of suitable procedures.     

Differential diagnosis of orofacial pain

Orofacial pain, especially if the problem is chronic, presents a diagnostic and management challenge to all health practitioners. This paper suggests how clinicians might simplify the diagnosis of orofacial pain. First, the pain is classified into one of the three basic pain categories: somatic, neuropathic, or psychogenic pain. Somatic pain results from noxious stimulation of normal neural structures. Neuropathic pain is caused by a structural abnormality in the nervous system. Psychogenic pain arises from psychic causes; there is no apparent physiologic or organic basis for the pain. The next step is to determine the tissue system from which the pain arises: intracranial, extracranial, musculoskeletal, neurovascular, neurogenous, or psychological. Finally, some of the more common orofacial pain syndromes within each category are discussed.     

Differential diagnosis of pleural effusion

The results of following up 598 patients diagnosed as having pleural exudate were used to analyze the potentialities of complex radiation and clinical differential diagnoses of this abnormality. The authors identified 4 most common nosological entities (tuberculosis, pleuropneumonia, cancer, mesothelioma) among patients of diagnostic hospitals. The diagnostic algorithm should be derived by taking into account the current techniques applicable to each disease form. With this, valid diagnosis may be made in 98.5% of cases.     

Differential diagnosis of Alzheimer's disease

The differential diagnosis of Alzheimer's disease has dramatically changed since the evolution of the diagnostic strategies (with definition of neuropsychological, behavioural, and imaging patterns) and disposal of cholinergic drugs indicated in Alzheimer's disease. The question is no more centred on exclusion of the traditional reversible dementias or depression. It is centred on the distinction between Alzheimer's disease and other degenerative diseases still often misdiagnosed with Alzheimer's disease such as frontotemporal dementias, dementia with Lewy bodies, and some focal atrophies that do not have the same physiopathology and should not be treated with anticholinesterase drugs. Besides, better knowledge on the links between cerebrovascular pathology and Alzheimer's disease, remind us that both pathologies may coexist and should be taken into account.