Dysregulation of growth hormone in acquired generalized lipodystrophy.
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Adult↗
Biomedical subjects
Azmi T Ahmad
Publications and source records attributed to Azmi T Ahmad.
Sleepwalking associated with hyperthyroidism.
OBJECTIVE: To report several cases of hyperthyroidism in patients presenting with the unusual symptom of sleepwalking and to discuss the possible pathophysiologic basis for this novel association. METHODS: After encountering and reporting the first case of new-onset somnambulism in a patient presenting with thyrotoxicosis at our institution, we routinely inquired about the sleep history of patients with thyrotoxicosis, questioning both the patients and family members when applicable. Those patients who actually had sleepwalking episodes coinciding with the onset of thyrotoxicosis underwent close follow-up, and the relationship between the sleepwalking and the results of thyroid function tests was analyzed. In addition, we reviewed the literature on psychiatric disorders and sleep problems, and the pathophysiologic rationale for a cause-and-effect relationship is discussed. RESULTS: We collected 8 cases of patients with new-onset sleepwalking episodes that coincided with the start of thyrotoxicosis. The disappearance of the sleepwalking with successful achievement of euthyroidism supports a cause-and-effect relationship. This hypothesis is further supported by the absence of a family history, the adult onset, and the relapse of sleepwalking in 2 of the patients when their thyrotoxicosis became poorly controlled as a result of noncompliance with medications and its subsequent disappearance with reachievement of euthyroidism. Of note, such a presentation was seen only in patients with thyrotoxicosis caused by diffuse toxic goiter or Graves' disease and never in patients with other causes of thyrotoxicosis. CONCLUSION: New-onset sleepwalking could be caused by thyrotoxicosis or, more specifically, by thyrotoxicosis resulting from diffuse toxic goiter. The mechanism is hypothesized to be related to the combination of prolongation of non-rapid eye movement sleep and the associated fatigue. Specific inquiry about this unusual presentation of thyrotoxicosis is encouraged, and more studies are needed to confirm and evaluate its extent.
Adolescent↗
Pituitary enlargement in patients with primary hypothyroidism.
OBJECTIVE: To assesses the frequency and degree of pituitary hyperplasia in patients with primary hypothyroidism, the association of pituitary enlargement with disease severity, and the response to treatment. METHODS: Between April 2002 and August 2004 at the National Center for Diabetes, Endocrinology and Genetics in Amman, Jordan, 53 patients (49 female and 4 male subjects) with primary hypothyroidism and serum thyrotropin (thyroid-stimulating hormone or TSH) levels of > or = 50 microIU/mL were encountered. Initial and follow-up investigations included thyroid function tests, serum prolactin levels, and magnetic resonance imaging (MRI) of the pituitary. Visual field examination was requested for all patients with pituitary enlargement (and adequately completed in 24). RESULTS: Pituitary enlargement on MRI was found in 37 of the 53 patients (70%), with 31 of the 37 patients (84%) having TSH levels of > or = 100 microIU/mL. After thyroxine treatment, 85% of the patients with pituitary enlargement who underwent a follow-up MRI showed a decrease in size of the gland. About half of the patients were referred to our facility with the diagnosis of hypothyroidism; presenting features in the rest of the patients included galactorrhea, menstrual irregularities, learning disability, short stature, precocious puberty, ovarian hyperstimulation syndrome, headaches, visual field defects, and dry ichthyotic skin. CONCLUSION: The association between pituitary gland enlargement and primary hypothyroidism should be kept in mind when pituitary hyperplasia is detected on MRI, before unwarranted and drastic interventions are initiated.
Adolescent↗
Diabetic foot disease.
OBJECTIVE: To review the spectrum of foot problems in patients with diabetes and the underlying etiologic factors. METHODS: In this review, the term "diabetic foot disease" (DFD) will be used (previously referred to as simply "diabetic foot"). The relevant anatomy of the foot is discussed, the clinical evaluation and severity of DFD are outlined, and the role of both systemic control and local measures in the management of DFD is addressed. RESULTS: DFD is linked with a wide variety of etiologic associations, pathologic forms, and clinical severity. The causes of DFD include such factors as diabetic neuropathy, vascular insufficiency, and the presence of underlying bone deformity. The pathologic forms range from superficial skin lesions, soft tissue infections, joint swellings, and deformities to frank necrosis and gangrene. The clinical severity ranges from mild, self-resolving disease to fulminant, rapidly progressive disease that usually eventuates in amputation. The heterogeneity of patients whose illness is grouped collectively under the diagnosis of DFD has contributed to the persisting confusion and controversy regarding the optimal classification system for diabetes-related foot problems and their appropriate management. CONCLUSION: Optimal management of DFD involves a multimodality approach directed at regular foot care, blood glucose control, and early recognition of foot problems. Appropriate surgical management, administration of systemic antibiotics, and off-loading techniques are necessary to prevent the progression of DFD.
Coronary Disease↗