The drug itself is also known to be nephrotoxic, opening up the possibility of spontaneous emergence of toxicity at doses that were previously well-tolerated. Lithium toxicity can be mistaken for other syndromes associated with antipsychotic use, such as serotonin syndrome because lithium increases serotonin metabolites in the cerebrospinal fluid.There are several drug interactions with lithium. Interactions can occur from typical antipsychotics or atypical antipsychotics. In particular, certain drugs enhance lithium levels by increasing renal re-absorption at the proximal tubule. These drugs are angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs and thiazide diuretics. Diagnosis
The diagnosis is generally based on symptoms and supported by a lithium level blood level. Blood levels are most useful six to twelve hours after the last dose. The normal serum lithium level in those on treatment is between 0.6-1.2 mEq/L. Some blood tubes contain lithium heparin which may result in falsely positive results.When lithium toxicity is suspected tests may include:

fingerstick glucose
serum lithium concentration
basic metabolic panel to assess renal function
serum acetaminophen and salicylate concentrations to rule out other sources of acute ingestion
urine pregnancy tests to ensure management does not cause abortionImaging tests are not helpful. Treatment
If the persons lithium toxicity is mild or moderate, lithium dosage is reduced or stopped entirely. If the toxicity is severe, lithium may need to be removed from the body. The removal of lithium is done in a hospital emergency department. It may involve:

Gastric lavage. A tube is placed through the nose or mouth into the stomach. The tube is used to remove lithium that has not been digested yet.
Non-bullous pemphigoid
In some patients, pemphigoid starts off with cutaneous manifestations of BP without bullae, as the only sign of the disease. Pruritic eczematous, papular, or urticaria-like skin lesions may also persist for weeks to months. Bullous phase
The bullous stage of BP shows vesicles and bulla, appearing on apparently normal or erythematous skin, predominantly at  the flexural aspects of the extremities and the lower trunk. Mucosal lesions, which typically are erosions of the oral mucosa, are present in 10 to 30 percent of patients. Occasionally, the blister fluid becomes blood-tinged. The blisters are tense, about 1–4 cm in diameter, leaving eroded and crusted areas, together with urticarial and infiltrated papules and plaques in an annular or figurate pattern.Homology between bullous pemphigoid antigens in the skin and neuronal antigens in the central nervous system has been proposed as a cause for the observed link between bullous pemphigoid and neurologic disease, along with a genetic predisposition. Patients with bullous pemphigoid usually present with two or more other chronic diseases such as neurological disorders(dementia, Parkinsons disease, or stroke). However, further studies are necessary to explore the relationship between these disorders. Cause
The pathogenetic mechanism of blister formation is known, the trigger to the formation of the antibodies to the hemidesmosome antigens is still unknown. Most of the bullous pemphigoid cases are due to autoantibodies (mostly IgG) directed at antigens (BP180 and BP230) arranged at the dermal-epidermal junction.