Latent autoimmune diabetes in adults (LADA) accounts for 2%-12% of all cases of diabetes. Patients are typically diagnosed after 35 years of age and are often misdiagnosed as type II Diabetes Mellitus (DM). Glycemic control is initially achieved with sulfonylureas but patients eventually become insulin dependent more rapidly than with type II DM patients. Although they have a type II DM phenotype, patients have circulating beta (β) cell autoantibodies, a hallmark of type I DM. Alternative terms that have been used to describe this condition include type 1.5 diabetes, latent type I diabetes, slowly progressive Insulin Dependent Diabetes Mellitus, or youth onset diabetes of maturity. With regards to its autoimmune basis and rapid requirement for insulin, it has been suggested that LADA is a slowly progressive form of type I DM. However, recent work has revealed genetic and immunological differences between LADA and type I DM. The heterogeneity of LADA has also led to the proposal of criteria for its diagnosis by the Immunology of Diabetes Society. Although many workers have advocated a clinically oriented approach for screening of LADA, there are no universally accepted criteria for autoantibody testing in adult onset diabetes. Following recent advances in immunomodulatory therapies in type I DM, the same strategy is being explored in LADA. This review deals with the contribution of the genetic, immunological and metabolic components involved in the pathophysiology of LADA and recent approaches in screening of this distinct but heterogeneous clinical entity.

Prostasin is a glycophosphatidylinositol-anchored protein which is found in prostate gland, kidney, bronchi, colon, liver, lung, pancreas, and salivary glands. It is a serine protease with trypsin-like substrate specificity which was first purified from seminal fluid in 1994. In the last decade, its diverse roles in various biological and physiological processes have been elucidated. Many studies done to date suggest that prostasin is one of several membrane peptidases regulating epithelial sodium channels in mammals. A comprehensive literature search was conducted from the websites of Pubmed Central, the US National Library of Medicine's digital archive of life sciences literature and the National Library of Medicine. The data was also assessed from journals and books that published relevant articles in this field. Understanding the mechanism by which prostasin and its inhibitors regulate sodium channels has provided a new insight into the treatment of hypertension and some other diseases like cystic fibrosis. Prostasin plays an important role in epidermal growth factor receptor (EGFR) signal modulation. Extracellular proteases have been implicated in tumor metastasis and local tissue invasion because of their ability to degrade extracellular matrices.

The data on plasma homocysteine and endogenous insulin in type 2 diabetes mellitus with nephropathy and relationship to body mass index (BMI) is particularly from the Indian subcontinent. A prospective study was carried out in 50 patients of type 2 diabetes mellitus with overt nephropathy (Group A). The results were compared with 25 diabetics without nephropathy (Group B), and 25 age and sex matched healthy controls (Group C). Microenzyme immunoassay and ELISA estimated the plasma homocysteine and insulin, respectively. The mean values of plasma homocysteine were significantly elevated in diabetic nephropathy (21.3+/-7.2 micromol/L) and diabetics without nephropathy (19.4+/-7.1) when compared to healthy control (11.5+/-2.3). The insulin levels and BMI were significantly higher in diabetics as compared to controls. There was no correlation between homocysteine and insulin, homocysteine and BMI, and homocysteine with the degree of renal failure.

While movement disorders are frequently encountered after brain injuries, and may create a host of complicated problems for the clinician, only a few cases of Parkinsonism associated with hydrocephalus have ever been described in the literature. Parkinsonism-like syndrome complicating hydrocephalus is a rare disorder, especially when associated with nontumoral aqueductal stenosis. Yet as this case report discusses, hdyrocephalus-induced Parkinsonism may be responsive to levodopa-carbidopa administration. This report describes a perplexing case of persistent akinesis following corrective surgery for aqueductal stenosis and the subsequent response to levodopa-carbidopa administration. We present the case of a 28-year-old male with a history of non-tumoral aqueductal stenosis diagnosed at age 12. As a child, he underwent a ventriculo-peritoneal shunt placement for obstructive hydrocephalus followed by multiple shunt revisions over the next several years. Sixteen years after his initial shunt placement, the patient presented with a decline in mental status. A third ventriculocisternostomy was performed rather than another shunt revision. Following surgery, the patient remained obtunded, and displayed profound hypokinesis, best described as freezing in movement. Upon admission to a rehabilitation unit 2 weeks later, he had made only minimal progress. A SPECT (single-photon emission computed tomography) brain scan revealed decreased basal ganglia perfusion. Levodopa/carbidopa therapy was initiated and within 2 weeks, the patient showed improvement in speed of movement, facial expression and verbal output. Eight weeks later, the patient could independently complete his basic activities of daily living and demonstrated little, if any, disordered movement. This report illustrates how dopaminergic agents may be useful in cases of hypokinesis following corrective surgery for aqueductal stenosis. SPECT may further aid in the diagnosis and management of Parkinsonism-like syndromes in brain injuries.

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